# ent

id: cord-263785-0iift8zy
type: DNA
entity:
  AceQ qPCR Probe Master Mix Kit Vazyme Biotech Nanjing China For haematoxylin eosin staining the collected samples


id: cord-278635-vwdxr1bl
type: TAXON
entity:
  AIV Mycoplasma spp Ornithobacterium rhinotracheale turkey coronavirus astrovirus rotavirus adenovirus parvovirus avian metapneumovirus


id: cord-004400-li1sc47z
type: PROTEIN
entity:
  RNA binding domain RBD 1 73 aa linker region LR 74 88 aa effector domain ED 89 202 aa and C terminal tail CTT 207 237 aa 12 Multiple basic amino acids e g 35R 38R 41K and 46R


id: cord-004400-li1sc47z
type: LAW
entity:
  the Open Access Correspondence lijinxiang caas cn sunjhe sjtu edu cn 1 Shanghai Key Laboratory of Veterinary Biotechnology


id: cord-269531-7gy4epzo
type: GGP
entity:
  Kaposi s sarcoma associated herpesvirus terminal repeat element binding proteins A mass spectrometry based proteomic approach to study Marek s Disease Virus gene


id: cord-269531-7gy4epzo
type: DISEASE
entity:
  human immunodeficiency virus 1 10 13 simian immunodeficiency virus 21 respiratory syncytial virus 22 hepatitis C


id: cord-295661-v3q1spmm
type: ORG
entity:
  Department of Veterinary and Biomedical Sciences College of Veterinary Medicine University of Minnesota


id: cord-278479-vl296i1b
type: SO
entity:
  serotypes APMV 1 through 9 based on Hemagglutination Inhibition HI and Neuraminidase Inhibition NI assays 4 Various strains of APMV 1


id: cord-310194-f5jtufja
type: DNA
entity:
  bovine isotype specific mouse monoclonal antibodies 19 and FITC conjugated polyclonal goat anti mouse antibodies BD Biosciences Total leukocytes


id: cord-266199-smlq11y9
type: DISEASE
entity:
  influenza A virus in swine Assessing production parameters and economic impact of swine influenza PRRS


id: cord-315072-b28yikvj
type: ORG
entity:
  the Medical Research Council s Clinical Sciences Centre CSC Genomics Laboratory Hammersmith Hospital


id: cord-290593-vhmi2559
type: CELL_LINE
entity:
  BHK 21 cells 5 O UKG 2001 C1 Noville O Bulgaria 1 91 O VietNam 7 97 A Brazil 10 93 A Turkey 99 and Asia 1 Turkey 99 were kindly provided by Drs Nigel Ferris and Satya Parida Institute for Animal Health Pirbright UK


id: cord-332881-mkm4ygh6
type: PROTEIN
entity:
  human signaling lymphocytic activation molecule SLAM CD150 Respiratory syncytial virus infection of monocyte


id: cord-326723-jiauk4fq
type: GGP
entity:
  BVDV 2 bovine herpesvirus type 1 BHV 1 bovine parainfluenza 3 virus bovine respiratory syncytial virus bovine adenovirus bovine coronavirus Mannheimia haemolytica Pasteurella multocida Histophilus somni


id: cord-319685-dw0qsl4s
type: ORG
entity:
  the Histology Laboratory Veterinary Laboratory Services School of Veterinary Science and University of Liverpool


id: cord-316908-8ti75mru
type: PROTEIN
entity:
  dynamin II siDyn Sus scrofa 5 CAC CTC ATG ATC AAT AAC A 3 Chlorocebus sabaeus 5 CCT ACA TCA ACA CGA ACC A 3 clathrin heavy chain siCHC Sus scrofa 5 CCC ATA CCA TGA CTG ATG A 3 Chlorocebus sabaeus 5 GAT GAA CCT TAT GCA TGC A 3 EPS 15 siEPS15 Sus scrofa 5 CCT GTG GAT ATT CTT GGA A 3 Chlorocebus sabaeus 5


id: cord-316908-8ti75mru
type: GGP
entity:
  dynamin II siDyn Sus scrofa 5 CAC CTC ATG ATC AAT AAC A 3 Chlorocebus sabaeus 5 CCT ACA TCA ACA CGA ACC A 3 clathrin


id: cord-351881-qea4b0i5
type: DNA
entity:
  Olot 91 strain GenBank Accession Number AGW23409 was synthesized by GenScript Piscataway For generation


id: cord-354114-frdsct44
type: PROTEIN
entity:
  anti RM 7 10 À1 2 5 10 6 10 À2 2 5 10 5 10 À3 2 B1 RM 2 10 10 Undiluted 4 18 F 71 B2 RM 2 10 10 Undiluted 2 18 F 70 2 10 8 10 À2 2 2 10 7 10 À3 2 2 10 6 10 À4 2


# bib

id: cord-000172-um0ds7dh
author: Paul, Mathilde
date: 2009-12-16
txt: ./txt/cord-000172-um0ds7dh.txt
cache: ./cache/cord-000172-um0ds7dh.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821766/
doi: 10.1051/vetres/2009076
summary:
  In this study, we investigated which anthropogenic factors played a role in the risk of HPAI in Thailand using outbreak data from the ''''second wave'''' of the epidemic (3 July 2004 to 5 May 2005 in the country. In this study, we investigated which anthropogenic factors played a role in the risk of HPAI in Thailand using outbreak data from the ''''second wave'''' of the epidemic (3 July 2004 to 5 May 2005 in the country. The risk of HPAI varies spatially according to the anthropogenic characteristics of the different geographical areas of interest, each characterized by a variety of human activities such as poultry farming practices, trade activities and market rules, land use and agro-ecosystems, and veterinary services structure and control. This analysis shows that, when adjusted for the effects of environmental and poultry variables, several anthropogenic factors were significantly associated with an increased risk of HPAI in both chicken and duck populations.

title:
  Anthropogenic factors and the risk of highly pathogenic avian influenza H5N1: prospects from a spatial-based model

abstract:
  Beginning in 2003, highly pathogenic avian influenza (HPAI) H5N1 virus spread across Southeast Asia, causing unprecedented epidemics. Thailand was massively infected in 2004 and 2005 and continues today to experience sporadic outbreaks. While research findings suggest that the spread of HPAI H5N1 is influenced primarily by trade patterns, identifying the anthropogenic risk factors involved remains a challenge. In this study, we investigated which anthropogenic factors played a role in the risk of HPAI in Thailand using outbreak data from the “second wave” of the epidemic (3 July 2004 to 5 May 2005) in the country. We first performed a spatial analysis of the relative risk of HPAI H5N1 at the subdistrict level based on a hierarchical Bayesian model. We observed a strong spatial heterogeneity of the relative risk. We then tested a set of potential risk factors in a multivariable linear model. The results confirmed the role of free-grazing ducks and rice-cropping intensity but showed a weak association with fighting cock density. The results also revealed a set of anthropogenic factors significantly linked with the risk of HPAI. High risk was associated strongly with densely populated areas, short distances to a highway junction, and short distances to large cities. These findings highlight a new explanatory pattern for the risk of HPAI and indicate that, in addition to agro-environmental factors, anthropogenic factors play an important role in the spread of H5N1. To limit the spread of future outbreaks, efforts to control the movement of poultry products must be sustained.


id: cord-001714-jfawhnsq
title: Bridge hosts, a missing link for disease ecology in multi-host systems
author: Caron, Alexandre
date: 2015-07-21
txt: ./txt/cord-001714-jfawhnsq.txt
cache: ./cache/cord-001714-jfawhnsq.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4509689/
doi: 10.1186/s13567-015-0217-9
summary:
  We illustrate this framework using the example of the transmission of Avian Influenza Viruses across wild bird/poultry interfaces in Africa and discuss a range of other examples that demonstrate the usefulness of our definition for other multi-host systems. Lastly, we present an operational framework to identify potential bridge host populations, using as a case study the ecology of avian influenza viruses at the wild/domestic bird interface in Africa and also giving other multi-host systems examples. As a consequence, the information available on most wild bird species is scarce and has been obtained mostly from by-catch (i.e. captured non-targeted species) of studies investigating AIV in maintenance waterfowl, resulting in small sample sizes that are inadequate to provide epidemiological understanding of the host roles in AIV ecology in Africa [26] . The range of methods available to characterize host competence for AIV and contact patterns between maintenance, potential bridge and target host populations is drawn from the fields of epidemiology and avian ecology ( Table 2) .

abstract:
  In ecology, the grouping of species into functional groups has played a valuable role in simplifying ecological complexity. In epidemiology, further clarifications of epidemiological functions are needed: while host roles may be defined, they are often used loosely, partly because of a lack of clarity on the relationships between a host’s function and its epidemiological role. Here we focus on the definition of bridge hosts and their epidemiological consequences. Bridge hosts provide a link through which pathogens can be transmitted from maintenance host populations or communities to receptive populations that people want to protect (i.e., target hosts). A bridge host should (1) be competent for the pathogen or able to mechanically transmit it; and (2) come into direct contact or share habitat with both maintenance and target populations. Demonstration of bridging requires an operational framework that integrates ecological and epidemiological approaches. We illustrate this framework using the example of the transmission of Avian Influenza Viruses across wild bird/poultry interfaces in Africa and discuss a range of other examples that demonstrate the usefulness of our definition for other multi-host systems. Bridge hosts can be particularly important for understanding and managing infectious disease dynamics in multi-host systems at wildlife/domestic/human interfaces, including emerging infections. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-015-0217-9) contains supplementary material, which is available to authorized users.


id: cord-003216-5qioku84
title: Pathobiology of Avian avulavirus 1: special focus on waterfowl
author: Rehman, Zaib Ur.
date: 2018-09-19
txt: ./txt/cord-003216-5qioku84.txt
cache: ./cache/cord-003216-5qioku84.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6148804/
doi: 10.1186/s13567-018-0587-x
summary:
  Besides the strong innate immune responses, waterfowl are generally considered long-term carrier of APMV-1 and disease outbreaks have been reported since 1997 [12] [13] [14] , and were confirmed by follow up experimental studies. Host innate immune responses of ducks infected with Newcastle disease viruses of different pathogenicities Pathotypical and genotypical characterization of strains of Newcastle disease virus isolated from outbreaks in chicken and goose flocks in some regions of China during Histopathological alterations in immune organs of chickens and ducks after experimental infection with virulent 9a5b newcastle disease virus Experimental co-infections of domestic ducks with a virulent Newcastle disease virus and low or highly pathogenic avian influenza viruses Phylogenetic diversity among low-virulence newcastle disease viruses from waterfowl and shorebirds and comparison of genotype distributions to those of poultry-origin isolates Genomic characterizations of a Newcastle disease virus isolated from ducks in live bird markets in China

abstract:
  Avian avulaviruses serotype 1 (abbreviated as APMV-1 for the historical name avian paramyxovirus 1) are capable of infecting a wide spectrum of avian species with variable clinical symptoms and outcomes. Ease of transmission has allowed the virus to spread worldwide with varying degrees of virulence depending upon the virus strain and host species. The emergence of new virulent genotypes from global epizootics, and the year-to-year genomic changes in low and high virulence APMV-1 imply that distinct genotypes of APMV-1 are simultaneously evolving at different geographic locations across the globe. This vast genomic diversity may be favoured by large variety of avian species susceptibility to APMV-1 infection, and by the availability of highly mobile wild birds. It has long been considered that waterfowls are not sensitive to APMV-1 and are unable to show any clinical signs, however, outbreaks from the 90′s contradict these concepts. The APMV-1 isolates are increasingly reported from the waterfowl. Waterfowl have strong innate immune responses, which minimize the impact of virus infection, however, are unable to prevent the viral shedding. Numerous APMV-1 are carried by domestic waterfowl intermingling with terrestrial poultry. Therefore, commercial ducks and geese should be vaccinated against APMV-1 to minimize the virus shedding and for the prevention the transmission. Genetic diversity within APMV-1 demonstrates the need for continual monitoring of viral evolution and periodic updates of vaccine seed-strains to achieve efficient control and eradication of APMV-1 in waterfowls. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13567-018-0587-x) contains supplementary material, which is available to authorized users.


id: cord-003506-ztqjo13e
title: A balanced game: chicken macrophage response to ALV-J infection
author: Feng, Min
date: 2019-03-06
txt: ./txt/cord-003506-ztqjo13e.txt
cache: ./cache/cord-003506-ztqjo13e.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6404279/
doi: 10.1186/s13567-019-0638-y
summary:
  ALV-J infection induced strong innate immune responses in chicken MDM at 3 hpi, instead of 36 hpi, according to the analysis results of Gene Ontology and KEGG pathway. In our previous study, we found that primary chicken monocyte-derived macrophages (MDM) were susceptible to ALV-J and infection resulted in expression of immune-related genes [10] . In this study, RNA-seq analysis platform and gene overexpression verification were employed to analyze chicken MDM gene expression after ALV-J infection. According to published studies [21] [22] [23] , 94 and 23 differentially expressed interferon-stimulated genes (ISG) were identified in ALV-J-infected MDM at 3 hpi and 36 hpi, respectively (Additional file 6). Overexpression of CISH, EX-FABP and SOCS3 significantly increased the expression of ALV-J env gene at protein levels ( Figures 8A and B) and mRNA levels ( Figure 8C ) in chicken MDM cells at 3 hpi.

abstract:
  Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression in infected chickens. Macrophages play a central role in host defense against invading pathogens. In this study, we discovered an interesting phenomenon: ALV-J replication is weakened from 3 hours post-infection (hpi) to 36 hpi, which was verified using Western blotting and RT-PCR. To further investigate the interaction between ALV-J and macrophages, transcriptome analysis was performed to analyze the host genes’ function in chicken primary monocyte-derived macrophages (MDM). Compared to the uninfected control, 624 up-regulated differentially expressed genes (DEG) and 341 down-regulated DEG at 3 hpi, and 174 up-regulated DEG and 87 down-regulated DEG at 36 hpi were identified in chicken MDM, respectively. ALV-J infection induced strong innate immune responses in chicken MDM at 3 hpi, instead of 36 hpi, according to the analysis results of Gene Ontology and KEGG pathway. Importantly, the host factors, such as up-regulated MIP-3α, IL-1β, iNOS, K60, IRG1, CH25H, NFKBIZ, lysozyme and OASL were involved in the host defense response during the course of ALV-J infection. On the contrary, up-regulated EX-FABP, IL4I1, COX-2, NFKBIA, TNFAIP3 and the Jak STAT pathway inhibitors including CISH, SOCS1 and SOCS3 are beneficial to ALV-J survival in chicken macrophages. We speculated that ALV-J tropism for macrophages helps to establish a latent infection in chicken MDM from 6 to 36 hpi. The present study provides a comprehensive view of the interactions between macrophages and ALV-J. It suggests the mechanisms of defense of chicken macrophages against ALV-J invasion and how ALV-J escape the host innate immune responses. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13567-019-0638-y) contains supplementary material, which is available to authorized users.


id: cord-003888-lgutt1r9
author: Lauterbach, Sarah E.
date: 2019-09-18
txt: ./txt/cord-003888-lgutt1r9.txt
cache: ./cache/cord-003888-lgutt1r9.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6749708/
doi: 10.1186/s13567-019-0684-5
summary:
  title: Assessing exhibition swine as potential disseminators of infectious disease through the detection of five respiratory pathogens at agricultural exhibitions Influenza A virus remains a top threat to animal and human health, but other pathogens may be disseminated through the exhibition swine population. Influenza A virus (IAV) has been routinely detected in swine at agricultural exhibitions, where subclinical infection is common and can make recognition difficult [3] [4] [5] [6] . Continued disease surveillance is vital to understanding the epidemiology of IAV and other pathogens infecting swine at agricultural exhibitions in order to protect animal and public health. There were 18 cases of variant influenza infections associated with the IAVs detected in this population of exhibition swine, and IAV should remain a priority for infectious disease surveillance and mitigation in exhibition swine [22] . Characterization of an influenza A virus isolated from pigs during an outbreak of respiratory disease in swine and people during a county fair in the United States

title:
  Assessing exhibition swine as potential disseminators of infectious disease through the detection of five respiratory pathogens at agricultural exhibitions

abstract:
  Widespread geographic movement and extensive comingling of exhibition swine facilitates the spread and transmission of infectious pathogens. Nasal samples were collected from 2862 pigs at 102 exhibitions and tested for five pathogens. At least one pathogen was molecularly detected in pigs at 63 (61.8%) exhibitions. Influenza A virus was most prevalent and was detected in 498 (17.4%) samples. Influenza D virus was detected in two (0.07%) samples. More than one pathogen was detected in 165 (5.8%) samples. Influenza A virus remains a top threat to animal and human health, but other pathogens may be disseminated through the exhibition swine population.


id: cord-004400-li1sc47z
author: Ma, Jingjiao
date: 2020-02-24
txt: ./txt/cord-004400-li1sc47z.txt
cache: ./cache/cord-004400-li1sc47z.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7038556/
doi: 10.1186/s13567-020-00747-3
summary:
  However, the growth of the deacetylated mutant virus WSN-NS1-108R was significantly impaired compared with that of the other two viruses in MDCK and A549 cells at 36 and 48 hpi, which indicated that the acetylated K108 of NS1 is important for virus replication in vitro at the late stage of infection (Figures 2A and B) . To further explore how the K108R mutation attenuated the IFN-β antagonistic ability of the NS1 protein, we co-transfected NS1 expression plasmids, an IFN-β reporter plasmid and different type I interferon pathway components, including RIG-I CARD, TBK1, and the active form of IRF3, into 293T cells. This result indicated that the deacetylation-mimic K108R substitution retained NS1 protein in the cytoplasm of infected cells, suggesting that the acetylated K108 residue is important for the nuclear localization of the NS1 protein ( Figures 5A-C ).

title:
  Acetylation at K108 of the NS1 protein is important for the replication and virulence of influenza virus

abstract:
  Non-structural protein 1 (NS1) of influenza virus is a multifunctional protein that plays an important role in virus replication and virulence. In this study, an acetylation modification was identified at the K108 residue of the NS1 protein of H1N1 influenza virus. To further explore the function of the K108 acetylation modification of the NS1 protein, a deacetylation-mimic mutation (K108R) and a constant acetylation-mimic mutation (K108Q) were introduced into the NS1 protein in the background of A/WSN/1933 H1N1 (WSN), resulting in two mutant viruses (WSN-NS1-108R and WSN-NS1-108Q). In vitro and mouse studies showed that the deacetylation-mimic mutation K108R in the NS1 protein attenuated the replication and virulence of WSN-NS1-108R, while the constant acetylation-mimic mutant virus WSN-NS1-108Q showed similar replication and pathogenicity as the wild-type WSN virus (WSN-wt). The results indicated that acetylation at K108 of the NS1 protein has an important role in the replication and virulence of influenza virus. To further explore the potential mechanism, the type I interferon (IFN-I) antagonistic activity of the three NS1 proteins (NS1-108Q, NS1-108R, and NS1-wt) was compared in cells, which showed that the K108R mutation significantly attenuated the IFN-β antagonistic activity of the NS1 protein compared with NS1-wt and NS1-108Q. Both NS1-wt and NS1-108Q inhibited the IFN-β response activated by RIG-I CARD domain, MAVS, TBK1, and IRF3 more efficiently than the NS1-108R protein in cells. Taken together, the results indicated that acetylation at NS1 K108 is important for the IFN antagonistic activity of the NS1 protein and virulence of the influenza virus.


id: cord-010835-nnorilo6
author: Lu, Mingmin
date: 2020-05-13
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7222441/
doi: 10.1186/s13567-020-00790-0
title:
  Proteomic analysis revealed T cell hyporesponsiveness induced by Haemonchus contortus excretory and secretory proteins

abstract:
  Haemonchus contortus has evolved highly integrated and sophisticated mechanisms to promote coexistence with hosts. The excretory-secretory (ES) products generated by this parasite contribute to the regulation of the host immune response to facilitate immune evasion and induce chronicity, but the proteins responsible for this process and the exact cellular mechanisms have yet to be defined. In this study, we identified 114 H. contortus ES proteins (HcESPs) interacting with host T cells and 15 T cell binding receptors via co-immunoprecipitation and shotgun liquid chromatography-tandem mass spectrometry analysis. Based on bioinformatics analysis, we demonstrated that HcESPs could inhibit T cell viability, induce cell apoptosis, suppress T cell proliferation and cause cell cycle arrest. Furthermore, the stimulation of HcESPs exerted critical control effects on T cell cytokine production profiles, predominantly promoting the secretion of interleukin (IL)-10, IL-17A and transforming growth factor-β1 and inhibiting IL-2, IL-4 and interferon-γ production. Collectively, these findings may provide insights into the interaction between ES proteins and key host effector cells, enhancing our understanding of the molecular mechanism underlying parasite immune evasion and providing new clues for novel vaccine development.


id: cord-025152-3wqtu9ey
author: Lee, Ji Eun
date: 2020-05-24
txt: ./txt/cord-025152-3wqtu9ey.txt
cache: ./cache/cord-025152-3wqtu9ey.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7245620/
doi: 10.1186/s13567-020-00788-8
summary:
  title: Bacillus subtilis spores as adjuvants against avian influenza H9N2 induce antigen-specific antibody and T cell responses in White Leghorn chickens subtilis spores, as adjuvants, enhance not only H9N2 virus-specific IgG but also CD4(+) and CD8(+) T cell responses, with an increase in pro-inflammatory cytokine production. subtilis spore adjuvant in chickens produces a significant effect on antigen-specific antibody and T cell responses against avian influenza virus. B. subtilis spores not only enhance innate immunity that protects against respiratory infections [12] [13] [14] but also induce an increase in antigen-specific antibody and T cell responses when co-administered with a soluble antigen [15] [16] [17] . subtilis spores act as adjuvants in chickens, enhancing antigen-specific immune responses when immunized with the inactivated H9N2 avian influenza virus. subtilis spores could act as potential vaccine adjuvants that synergistically provide antigen-specific immune responses against the avian influenza virus H9N2 in White Leghorn chickens.

title:
  Bacillus subtilis spores as adjuvants against avian influenza H9N2 induce antigen-specific antibody and T cell responses in White Leghorn chickens

abstract:
  Low-pathogenicity avian influenza H9N2 remains an endemic disease worldwide despite continuous vaccination, indicating the need for an improved vaccine strategy. Bacillus subtilis (B. subtilis), a gram-positive and endospore-forming bacterium, is a non-pathogenic species that has been used in probiotic formulations for both animals and humans. The objective of the present study was to elucidate the effect of B. subtilis spores as adjuvants in chickens administered inactivated avian influenza virus H9N2. Herein, the adjuvanticity of B. subtilis spores in chickens was demonstrated by enhancement of H9N2 virus-specific IgG responses. B. subtilis spores enhanced the proportion of B cells and the innate cell population in splenocytes from chickens administered both inactivated H9N2 and B. subtilis spores (Spore + H9N2). Furthermore, the H9N2 and spore administration induced significantly increased expression of the pro-inflammatory cytokines IL-1β and IL-6 compared to that in the H9N2 only group. Additionally, total splenocytes from chickens immunized with inactivated H9N2 in the presence or absence of B. subtilis spores were re-stimulated with inactivated H9N2. The subsequent results showed that the extent of antigen-specific CD4(+) and CD8(+) T cell proliferation was higher in the Spore + H9N2 group than in the group administered only H9N2. Taken together, these data demonstrate that B. subtilis spores, as adjuvants, enhance not only H9N2 virus-specific IgG but also CD4(+) and CD8(+) T cell responses, with an increase in pro-inflammatory cytokine production. This approach to vaccination with inactivated H9N2 together with a B. subtilis spore adjuvant in chickens produces a significant effect on antigen-specific antibody and T cell responses against avian influenza virus.


id: cord-028887-eseo7lyh
title: Exploring heterologous prime-boost vaccination approaches to enhance influenza control in pigs
author: Li, Chong
date: 2020-07-09
txt: ./txt/cord-028887-eseo7lyh.txt
cache: ./cache/cord-028887-eseo7lyh.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7344353/
doi: 10.1186/s13567-020-00810-z
summary:
  We performed a vaccination-challenge study to evaluate the protective efficacy of using multivalent inactivated vaccine and/or a live attenuated IAV vaccine (LAIV) in pigs following multiple prime-boost vaccination protocols against a simultaneous H1N1 and H3N2 IAV infection. Based on the BALF samples collected from pigs receiving WIV, the least amount of virus post-contact was detected in the heterologous treatment group AUT/ COM (Table 3) . We also tested the frequency of virus-specific IFN-γ secreting cells in PBMC samples collected at 1 week after boost vaccination from pigs in selected groups (COM/COM, AUT/AUT, LAIV/ COM and LAIV/NONE) and obtained similar results between the WIV administration groups (COM/COM and AUT/AUT). We found the heterologous prime-boost vaccination protocols may have expanded the antibody response to both H1 and H3 challenge strains as demonstrated by the higher HI titers especially in pigs from AUT/COM and LAIV/COM treatment groups.

abstract:
  Influenza A viruses evolve rapidly to escape host immunity. In swine, this viral evolution has resulted in the emergence of multiple H1 and H3 influenza A virus (IAV) lineages in the United States (US) pig populations. The heterologous prime-boost vaccination strategy is a promising way to deal with diverse IAV infection in multiple animal models. However, whether or not this vaccination strategy is applicable to US swine to impart immunity against infection from North American strains of IAV is still unknown. We performed a vaccination-challenge study to evaluate the protective efficacy of using multivalent inactivated vaccine and/or a live attenuated IAV vaccine (LAIV) in pigs following multiple prime-boost vaccination protocols against a simultaneous H1N1 and H3N2 IAV infection. Our data show that pigs in the heterologous prime-boost vaccination group had more favorable outcomes consistent with a better response against virus challenge than non-vaccinated pigs. Additionally, delivering a multivalent heterologous inactivated vaccine boost to pigs following a single LAIV administration was also beneficial. We concluded the heterologous prime boost vaccination strategy may potentiate responses to suboptimal immunogens and holds the potential applicability to control IAV in the North American swine industry. However, more studies are needed to validate the application of this vaccination approach under field conditions.


id: cord-033692-txfuuu7d
author: Lim, Byeonghwi
date: 2020-10-13
txt: ./txt/cord-033692-txfuuu7d.txt
cache: ./cache/cord-033692-txfuuu7d.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7552595/
doi: 10.1186/s13567-020-00850-5
summary:
  In this study, we investigated the molecular mechanisms of PRRSV infection by integrating the differences in the expression of various genes in tissues responsible for respiration (lungs) and immunity (bronchial lymph nodes [BLNs] , and tonsils) using RNA-Seq data at serial time points. To validate the results of specific groups, GSEA based on the KEGG database were performed using log 2 -normalised TMM counts at each time point for each tissue to identify the maximum gene expression changes for each group, and the GSEA results were consistent with the KEGG enrichment analyses of DEGs. GSEA using the 3-dpi data for all tissues revealed many significant pathways related to viral infection, among which influenza A showed the highest NES ( Figure 5A ). Significant KEGG terms related to viral infections and immune signalling were identified through KEGG enrichment analyses performed for each up-and down-regulated genes (343 and 287 genes, respectively), based on the time point for each tissue with a maximum FC value in the GCN, which was constructed using serial DEGs ( Figure 4A ).

title:
  Integrated time-serial transcriptome networks reveal common innate and tissue-specific adaptive immune responses to PRRSV infection

abstract:
  Porcine reproductive and respiratory syndrome virus (PRRSV) infection is the most important viral disease causing severe economic losses in the swine industry. However, mechanisms underlying gene expression control in immunity-responsible tissues at different time points during PRRSV infection are poorly understood. We constructed an integrated gene co-expression network and identified tissue- and time-dependent biological mechanisms of PRRSV infection through bioinformatics analysis using three tissues (lungs, bronchial lymph nodes [BLNs], and tonsils) via RNA-Seq. Three groups with specific expression patterns (i.e., the 3-dpi, lung, and BLN groups) were discovered. The 3 dpi-specific group showed antiviral and innate-immune signalling similar to the case for influenza A infection. Moreover, we observed adaptive immune responses in the lung-specific group based on various cytokines, while the BLN-specific group showed down-regulated AMPK signalling related to viral replication. Our study may provide comprehensive insights into PRRSV infection, as well as useful information for vaccine development.


id: cord-259296-qsaewje2
title: Tomatidine inhibits porcine epidemic diarrhea virus replication by targeting 3CL protease
author: Wang, Pengcheng
date: 2020-11-11
txt: ./txt/cord-259296-qsaewje2.txt
cache: ./cache/cord-259296-qsaewje2.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-020-00865-y
doi: 10.1186/s13567-020-00865-y
summary:
  We screened an FDA-approved library of 911 natural products and found that tomatidine, a steroidal alkaloid extracted from the skin and leaves of tomatoes, demonstrates significant inhibition of PEDV replication in Vero and IPEC-J2 cells in vitro. After transfer, the membrane was incubated in blocking buffer (5% non-fat milk in PBST w/v) for 2 h at room temperature, washed three times with PBST, then probed with the following antibodies: anti-PEDV N-protein ( The detection of mRNA levels of TGEV, PRRSV, and SVA was performed as described previously [13, 19, 20] . When Vero cells were treated with increasing concentrations of tomatidine, the cleaved fragments clearly decreased in a dose-dependent manner ( Figure 6B ), indicating that tomatidine inhibited the activity of PEDV 3CL protease.

abstract:
  Porcine epidemic diarrhea virus (PEDV) causes lethal diarrhea in suckling piglets, leading to severe economic losses worldwide. There is an urgent need to find new therapeutic methods to prevent and control PEDV. Not only is there a shortage of commercial anti-PEDV drugs, but available commercial vaccines fail to protect against highly virulent PEDV variants. We screened an FDA-approved library of 911 natural products and found that tomatidine, a steroidal alkaloid extracted from the skin and leaves of tomatoes, demonstrates significant inhibition of PEDV replication in Vero and IPEC-J2 cells in vitro. Molecular docking and molecular dynamics analysis predicted interactions between tomatidine and the active pocket of PEDV 3CL protease, which were confirmed by fluorescence spectroscopy and isothermal titration calorimetry (ITC). The inhibiting effect of tomatidine on 3CL protease was determined using cleavage visualization and FRET assay. Tomatidine-mediated blocking of 3CL protease activity in PEDV-infected cells was examined by western blot detection of the viral polyprotein in PEDV-infected cells. It indicates that tomatidine inhibits PEDV replication mainly by targeting 3CL protease. In addition, tomatidine also has antiviral activity against transmissible gastroenteritis virus (TGEV), porcine reproductive and respiratory syndrome virus (PRRSV), encephalo myocarditis virus (EMCV) and seneca virus A (SVA) in vitro. These results may be helpful in developing a new prophylactic and therapeutic strategy against PEDV and other swine disease infections.


id: cord-263785-0iift8zy
author: Zhang, Xiaorong
date: 2020-07-31
txt: ./txt/cord-263785-0iift8zy.txt
cache: ./cache/cord-263785-0iift8zy.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32736651/
doi: 10.1186/s13567-020-00819-4
summary:
  title: Evaluation of the reproductive system development and egg-laying performance of hens infected with TW I-type infectious bronchitis virus Our findings suggest that TW I-type IBV is deadly to chickens and could cause permanent damage to the oviduct, resulting in the poor laying performance of female survivors and decreasing the breeding value and welfare of the infected flock. In this study, the pathogenicity of TW I-type IBV was evaluated by examining clinical symptoms, mortality rates, virus shedding, lesions, and laying performance in terms of egg quantity and quality in infected chickens. The pathogenicity of TW I-type IBV in the early stage post-infection was evaluated via the clinical symptoms, pathological lesions, and virus shedding from trachea and cloaca. Abbreviations IBV: infectious bronchitis virus; SPF: specific-pathogen-free; dpi: days post infection; RT-qPCR: reverse transcription-quantitative polymerase chain reaction.

title:
  Evaluation of the reproductive system development and egg-laying performance of hens infected with TW I-type infectious bronchitis virus

abstract:
  The prevalence of TW I-type infectious bronchitis virus (IBV) has been increasing rapidly, and it has become the second most common genotype of IBV in China threatening the poultry industry. In this study, 1-day-old specific-pathogen-free (SPF) chickens infected with TW I-type IBV were continuously observed for 200 days. TW I-type IBV affected the respiratory, urinary, and female reproductive systems, resulting in a mortality rate of 10% as well as a decrease in egg quantity and an increase in inferior eggs. During the monitoring period, serious lesions occurred in the female reproductive system, such as yolk peritonitis, a shortened oviduct, and cysts of different sizes with effusion in the degenerated right oviduct. The infective viruses persisted in vivo for a long time, and due to the stress of laying, virus shedding was detected again after the onset of egg production. Our findings suggest that TW I-type IBV is deadly to chickens and could cause permanent damage to the oviduct, resulting in the poor laying performance of female survivors and decreasing the breeding value and welfare of the infected flock.


id: cord-264888-h560slug
author: Goossens, Evy
date: 2016-04-27
txt: ./txt/cord-264888-h560slug.txt
cache: ./cache/cord-264888-h560slug.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-016-0336-y
doi: 10.1186/s13567-016-0336-y
summary:
  title: The C-terminal domain of Clostridium perfringens alpha toxin as a vaccine candidate against bovine necrohemorrhagic enteritis Using an intestinal loop model in calves, we investigated the protection afforded by antisera raised against native alpha toxin or its non-toxic C-terminal fragment against C. The aim of this study was to evaluate whether the nontoxic C-terminal fragment of alpha toxin could be a candidate for effective vaccination of calves against bovine necrohemorrhagic enteritis. Incubation of cell-free supernatants of the wild-type strain JIR325 (concentrated tenfold using Vivaspin, Sartorius Stedim Biotech GmbH, Göttingen, Germany) on sheep blood agar at 37 °C overnight results in an inner, complete zone of hemolysis caused by perfringolysin O and a less complete outer zone caused by alpha toxin. perfringens strain by sera from calves immunized with the native alpha toxin (rCpa) or the non-toxic C-terminal fragment of the alpha toxin (Cpa 247-370 ). perfringens in the intestinal loop model was significantly reduced only by co-administration of antisera from animals vaccinated with the native alpha toxin.

title:
  The C-terminal domain of Clostridium perfringens alpha toxin as a vaccine candidate against bovine necrohemorrhagic enteritis

abstract:
  Bovine necrohemorrhagic enteritis is caused by Clostridium perfringens and leads to sudden death. Alpha toxin, together with perfringolysin O, has been identified as the principal toxin involved in the pathogenesis. We assessed the potential of alpha toxin as a vaccine antigen. Using an intestinal loop model in calves, we investigated the protection afforded by antisera raised against native alpha toxin or its non-toxic C-terminal fragment against C. perfringens-induced intestinal necrosis. Immunization of calves with either of the vaccine preparations induced a strong antibody response. The resulting antisera were able to neutralize the alpha toxin activity and the C. perfringens-induced endothelial cytotoxicity in vitro. The antisera raised against the native toxin had a stronger neutralizing activity than those against the C-terminal fragment. However, antibodies against alpha toxin alone were not sufficient to completely neutralize the C. perfringens-induced necrosis in the intestinal loop model. The development of a multivalent vaccine combining the C-terminal fragment of alpha toxin with other C. perfringens virulence factors might be necessary for complete protection against bovine necrohemorrhagic enteritis.


id: cord-266199-smlq11y9
title: Nanoparticle-based vaccine development and evaluation against viral infections in pigs
author: Dhakal, Santosh
date: 2019-11-06
txt: ./txt/cord-266199-smlq11y9.txt
cache: ./cache/cord-266199-smlq11y9.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/31694705/
doi: 10.1186/s13567-019-0712-5
summary:
  The economic burden caused by virus infections such as Porcine Reproductive and Respiratory Syndrome Virus, Swine influenza virus, Porcine Epidemic Diarrhea Virus, Porcine Circovirus 2, Foot and Mouth Disease Virus and many others are associated with severe morbidity, mortality, loss of production, trade restrictions and investments in control and prevention practices. Likewise, DCs targeted chitosan NPs loading plasmid DNA encoding nucleocapsid protein of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) induced better nucleocapsid protein-specific mucosal IgA antibody response compared to soluble unentrapped antigens after nasal immunization in mice [57] . In this review, only studies conducted in pigs related to the development and evaluation of NPs-based vaccine candidates by using virus-like particles (VLPs), biodegradable polymers, polysaccharides and liposomes against porcine viral infections are included (Table 3) . Chitosan-based NPs are used in pigs to deliver adjuvants such as bee venom and plasmid encoding porcine IL-2 and IL-4/IL-6 genes, which improved induction of better virus-specific immune responses of respective vaccines against PRRSV and PCV2 [103, 104] .

abstract:
  Virus infections possess persistent health challenges in swine industry leading to severe economic losses worldwide. The economic burden caused by virus infections such as Porcine Reproductive and Respiratory Syndrome Virus, Swine influenza virus, Porcine Epidemic Diarrhea Virus, Porcine Circovirus 2, Foot and Mouth Disease Virus and many others are associated with severe morbidity, mortality, loss of production, trade restrictions and investments in control and prevention practices. Pigs can also have a role in zoonotic transmission of some viral infections to humans. Inactivated and modified-live virus vaccines are available against porcine viral infections with variable efficacy under field conditions. Thus, improvements over existing vaccines are necessary to: (1) Increase the breadth of protection against evolving viral strains and subtypes; (2) Control of emerging and re-emerging viruses; (3) Eradicate viruses localized in different geographic areas; and (4) Differentiate infected from vaccinated animals to improve disease control programs. Nanoparticles (NPs) generated from virus-like particles, biodegradable and biocompatible polymers and liposomes offer many advantages as vaccine delivery platform due to their unique physicochemical properties. NPs help in efficient antigen internalization and processing by antigen presenting cells and activate them to elicit innate and adaptive immunity. Some of the NPs-based vaccines could be delivered through both parenteral and mucosal routes to trigger efficient mucosal and systemic immune responses and could be used to target specific immune cells such as mucosal microfold (M) cells and dendritic cells (DCs). In conclusion, NPs-based vaccines can serve as novel candidate vaccines against several porcine viral infections with the potential to enhance the broader protective efficacy under field conditions. This review highlights the recent developments in NPs-based vaccines against porcine viral pathogens and how the NPs-based vaccine delivery system induces innate and adaptive immune responses resulting in varied level of protective efficacy.


id: cord-269531-7gy4epzo
title: Proteomic analysis of purified turkey adenovirus 3 virions
author: Kumar, Pankaj
date: 2015-07-09
txt: ./txt/cord-269531-7gy4epzo.txt
cache: ./cache/cord-269531-7gy4epzo.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-015-0214-z
doi: 10.1186/s13567-015-0214-z
summary:
  To develop a better understanding of virus-host interactions, we performed a comprehensive proteomic analysis of proteinase K treated purified TAdV-3 virions isolated from spleens of infected turkeys, by utilizing one-dimensional liquid chromatography mass spectrometry. The LC-MS/MS analysis of proteinase K treated CsCl 2 density gradient purified TAdV-3 virions identified eleven virus-encoded proteins (hexon, pVI, pVII, penton base, pVIII, sialidase, IIIA, adenain, pX, IVa2 and DBP) previously reported to be in other adenoviruses (Table 3 and Figure 3A ) [16] . In addition, five host proteins namely, vitronectin, collagen alpha-3 (VI) chain, collagen alpha-2 (VI) chain, tyrosine protein phosphatase and turkey heterophil peptide 2 (THP-2) were only detected in proteinase K treated TAdV-3 virions. The proteomic analysis of proteinase K treated purified virions identified eleven cellular proteins incorporated in TAdV-3, which have been identified in other viruses (Table 4 ). In addition, proteomic analysis identified seven host proteins incorporated in TAdV-3 virions (Table 4) , which have not been identified so far in any other virus.

abstract:
  Turkey adenovirus 3 (TAdV-3) causes high mortality and significant economic losses to the turkey industry. However, little is known about the molecular determinants required for viral replication and pathogenesis. Moreover, TAdV-3 does not grow well in cell culture, thus detailed structural studies of the infectious particle is particularly challenging. To develop a better understanding of virus-host interactions, we performed a comprehensive proteomic analysis of proteinase K treated purified TAdV-3 virions isolated from spleens of infected turkeys, by utilizing one-dimensional liquid chromatography mass spectrometry. Our analysis resulted in the identification of 13 viral proteins associated with TAdV-3 virions including a novel uncharacterized TaV3gp04 protein. Further, we detected 18 host proteins in purified virions, many of which are involved in cell-to cell spread, cytoskeleton dynamics and virus replication. Notably, seven of these host proteins have not yet been reported to be present in any other purified virus. In addition, five of these proteins are known antiviral host restriction factors. The availability of reagents allowed us to identify two cellular proteins (collagen alpha-1 (VI) chain and haemoglobin) in the purified TAdV-3 preparations. These results represent the first comprehensive proteomic profile of TAdV-3 and may provide information for illustrating TAdV-3 replication and pathogenesis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-015-0214-z) contains supplementary material, which is available to authorized users.


id: cord-275443-9ib77yws
title: Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
author: Xie, Xing
date: 2015-03-19
txt: ./txt/cord-275443-9ib77yws.txt
cache: ./cache/cord-275443-9ib77yws.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-015-0146-7
doi: 10.1186/s13567-015-0146-7
summary:
  Considering that mAb D7 resulted in a significant reduction in viral titers in the lungs of mice infected with three different virus strains at 6 dpi, we chose that time point to determine the viral RNA loads in different tissues and fecal samples. To compare the above results with pathological findings in mice infected with three different virus strains, and treated with mAb D7 and irrelevant mAb IgG, we chose the heart, brain and lung from different treatment groups at 6 dpi to perform histopathological and immunohistochemical analysis. To gain a better understanding of the effect of CIV on the innate immune response and to ascertain whether passive immunization with monoclonal antibody affected the levels of cytokines, we examined the levels of IFN-γ and TNF-α in the lungs of mice in the virus-infected and mAb D7 groups.

abstract:
  Canine influenza virus (CIV) subtype H3N2 is a newly identified, highly contagious respiratory pathogen that causes cough, pneumonia and other respiratory symptoms in dogs. Data indicate that the virus is responsible for recent clinical cases of dog disease in China. However, therapeutic options for this disease are very limited. In this study, seven monoclonal antibodies (mAbs) against CIV JS/10 (an H3N2 subtype virus) were produced and characterized. Among them, mAb D7, which is specific for the HA2 glycopeptide (gp), induced the highest neutralization titers. The protection provided by mAb D7 was evaluated in BALB/c mice challenged with homologous or heterologous strains of H3N2 influenza virus, including two strains of CIV and one strain of swine influenza virus (SIV). The data show that mAb D7 protected the mice from infection with the three viral strains, especially the homologous strain, which was indicated by the recovery of body weight, reduction of viral load, and reduction of tissue damage. Moreover, the levels of IFN-γ and TNF-α in the lungs, as detected by ELISA, were reduced in the infected mice treated with the mAb D7 compared with those without mAb D7 treatment. Thus, our findings demonstrate, for the first time, that a mAb could reduce the release of IFN-γ and TNF-α associated with tissue damage by CIV infection and that the mAb might be of great therapeutic value for CIV infection. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-015-0146-7) contains supplementary material, which is available to authorized users.


id: cord-278479-vl296i1b
title: Experimental infection of hamsters with avian paramyxovirus serotypes 1 to 9
author: Samuel, Arthur S
date: 2011-02-23
txt: ./txt/cord-278479-vl296i1b.txt
cache: ./cache/cord-278479-vl296i1b.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/21345199/
doi: 10.1186/1297-9716-42-38
summary:
  In this study, groups of hamsters were infected with a prototype strain of each APMV serotype by the intranasal route and monitored for virus replication, clinical symptoms, histopathology, and seroconversion. Our results showed that each of the APMV serotypes replicated in hamsters without causing adverse clinical signs of illness, although histopathologic evidence of disease was observed in some cases, and also induced high neutralizing antibody titers. Necropsies were performed immediately postmortem and the following tissue samples were collected for immunohistochemistry (IHC), histopathology, and virus isolation: brain, nasal turbinates, lung, spleen, kidney and small intestine. Deparaffinized sections of the virus-infected and uninfected control tissue (brain, lungs, nasal turbinates, small intestine, kidney, and spleen) were immunostained using polyclonal antisera against the N protein of the homologous APMV serotypes. In animals infected with any of the other APMV serotypes, virus-specific antigens were detected on 3 dpi in the lungs and nasal turbinates (Figure 3 ).

abstract:
  Avian paramyxoviruses (APMVs) are frequently isolated from domestic and wild birds throughout the world and are separated into nine serotypes (APMV-1 to -9). Only in the case of APMV-1, the infection of non-avian species has been investigated. The APMVs presently are being considered as human vaccine vectors. In this study, we evaluated the replication and pathogenicity of all nine APMV serotypes in hamsters. The hamsters were inoculated intranasally with each virus and monitored for clinical disease, pathology, histopathology, virus replication, and seroconversion. On the basis of one or more of these criteria, each of the APMV serotypes was found to replicate in hamsters. The APMVs produced mild or inapparent clinical signs in hamsters except for APMV-9, which produced moderate disease. Gross lesions were observed over the pulmonary surface of hamsters infected with APMV-2 & -3, which showed petechial and ecchymotic hemorrhages, respectively. Replication of all of the APMVs except APMV-5 was confirmed in the nasal turbinates and lungs, indicating a tropism for the respiratory tract. Histologically, the infection resulted in lung lesions consistent with bronchointerstitial pneumonia of varying severity and nasal turbinates with blunting or loss of cilia of the epithelium lining the nasal septa. The majority of APMV-infected hamsters exhibited transient histological lesions that self resolved by 14 days post infection (dpi). All of the hamsters infected with the APMVs produced serotype-specific HI or neutralizing antibodies, confirming virus replication. Taken together, these results demonstrate that all nine known APMV serotypes are capable of replicating in hamsters with minimal disease and pathology.


id: cord-278635-vwdxr1bl
author: Świętoń, Edyta
date: 2020-08-28
txt: ./txt/cord-278635-vwdxr1bl.txt
cache: ./cache/cord-278635-vwdxr1bl.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-020-00833-6
doi: 10.1186/s13567-020-00833-6
summary:
  In the present study we compared the clinical outcome, mortality and transmission in chickens and turkeys infected with the same infectious doses of H7N7 low pathogenic avian influenza virus containing different levels of defective gene segments (95/95(DVG-high) and 95/95(DVG-low)). Virions containing highly deleted forms of genome segments (defective viral genes-DVGs) are able to replicate only in the presence and at the expense of fully infectious virus, hence the term "defective interfering particles" (DIPs) [4] . To evaluate the effect of DIPs on the course of infection with low pathogenic avian influenza virus (LPAIV), a comparison of pathogenicity of two virus stocks of H7N7 LPAIV with different levels of defective genomes was performed in turkeys and chickens. Infected birds received the same infectious dose of the virus but with different amount of DVGs. The semiquantitative analysis of defective particles was done by a combination of RT-PCR, real time RT-PCR and whole genome sequencing and indicated significantly higher amount of truncated gene segments in 95/95(DVG-high).

title:
  Low pathogenic avian influenza virus isolates with different levels of defective genome segments vary in pathogenicity and transmission efficiency

abstract:
  Defective interfering particles (DIPs) of influenza virus are generated through incorporation of highly truncated forms of genome segments, mostly those coding polymerase complex proteins (PB2, PB1, PA). Such particles are able to replicate only in the presence of a virus with the complete genome, thus DIPs may alter the infection outcome by suppressing production of standard virus particles, but also by stimulating the immune response. In the present study we compared the clinical outcome, mortality and transmission in chickens and turkeys infected with the same infectious doses of H7N7 low pathogenic avian influenza virus containing different levels of defective gene segments (95/95(DVG-high) and 95/95(DVG-low)). No clinical signs, mortality or transmission were noted in SPF chickens inoculated with neither virus stock. Turkeys infected with 95/95(DVG-high) showed only slight clinical signs with no mortality, and the virus was transmitted only to birds in direct contact. In contrast, more severe disease, mortality and transmission to direct and indirect contact birds was observed in turkeys infected with 95/95(DVG-low). Apathy, lower water and food intake, respiratory system disorders and a total mortality of 60% were noted. Shedding patterns in contact turkeys indicated more efficient within- and between-host spread of the virus than in 95/95(DVG-high) group. Sequencing of virus genomes showed no mutations that could account for the observed differences in pathogenicity. The results suggest that the abundance of DIPs in the inoculum was the factor responsible for the mild course of infection and disrupted virus transmission.


id: cord-287153-jbuuph6w
author: Lund, Morten
date: 2016-10-21
url: https://www.ncbi.nlm.nih.gov/pubmed/27769313/
doi: 10.1186/s13567-016-0389-y
title:
  Experimental Piscine orthoreovirus infection mediates protection against pancreas disease in Atlantic salmon (Salmo salar)

abstract:
  Viral diseases are among the main challenges in farming of Atlantic salmon (Salmo salar). The most prevalent viral diseases in Norwegian salmon aquaculture are heart and skeletal muscle inflammation (HSMI) caused by Piscine orthoreovirus (PRV), and pancreas disease (PD) caused by Salmonid alphavirus (SAV). Both PRV and SAV target heart and skeletal muscles, but SAV additionally targets exocrine pancreas. PRV and SAV are often present in the same locations and co-infections occur, but the effect of this crosstalk on disease development has not been investigated. In the present experiment, the effect of a primary PRV infection on subsequent SAV infection was studied. Atlantic salmon were infected with PRV by cohabitation, followed by addition of SAV shedder fish 4 or 10 weeks after the initial PRV infection. Histopathological evaluation, monitoring of viral RNA levels and host gene expression analysis were used to assess disease development. Significant reduction of SAV RNA levels and of PD specific histopathological changes were observed in the co-infected groups compared to fish infected by SAV only. A strong correlation was found between histopathological development and expression of disease related genes in heart. In conclusion, experimentally PRV infected salmon are less susceptible to secondary SAV infection and development of PD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-016-0389-y) contains supplementary material, which is available to authorized users.


id: cord-290593-vhmi2559
author: Lannes, Nils
date: 2012-08-30
txt: ./txt/cord-290593-vhmi2559.txt
cache: ./cache/cord-290593-vhmi2559.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/1297-9716-43-64
doi: 10.1186/1297-9716-43-64
summary:
  title: Interplay of foot-and-mouth disease virus, antibodies and plasmacytoid dendritic cells: virus opsonization under non-neutralizing conditions results in enhanced interferon-alpha responses Vaccine-induced immune protection correlates with the presence of high levels of neutralizing antibodies but also opsonising antibodies have been proposed as an important mechanism of the immune response contributing to virus clearance by macrophages and leading to the production of type-I interferon (IFN) by plasmacytoid dendritic cells (pDC). The present study demonstrates that the opsonising antibody titres mediating enhanced IFN-α responses in pDC were similar to neutralizing titres, when antigenically related viruses from the same serotype were employed. Considering the possible importance of opsonising antibodies and pDC in the protection against FMDV, the main aim of this study was to characterize the relationship between neutralizing and opsonising activities of polyclonal sera from immunized pigs. Plasmacytoid dendritic cell activation by foot-and-mouth disease virus requires immune complexes

title:
  Interplay of foot-and-mouth disease virus, antibodies and plasmacytoid dendritic cells: virus opsonization under non-neutralizing conditions results in enhanced interferon-alpha responses

abstract:
  Foot-and-mouth disease virus (FMDV) is a highly infectious member of the Picornaviridae inducing an acute disease of cloven-hoofed species. Vaccine-induced immune protection correlates with the presence of high levels of neutralizing antibodies but also opsonising antibodies have been proposed as an important mechanism of the immune response contributing to virus clearance by macrophages and leading to the production of type-I interferon (IFN) by plasmacytoid dendritic cells (pDC). The present study demonstrates that the opsonising antibody titres mediating enhanced IFN-α responses in pDC were similar to neutralizing titres, when antigenically related viruses from the same serotype were employed. However, sera cross-reacted also with non-neutralized isolates of multiple serotypes, when tested in this assay. Both uncomplexed virus and immune complexed virus stimulated pDC via Toll-like receptor 7. An additional finding of potential importance for strain-specific differences in virulence and/or immunogenicity was that pDC activation by FMDV strongly differed between viral isolates. Altogether, our results indicate that opsonising antibodies can have a broader reactivity than neutralizing antibodies and may contribute to antiviral responses induced against antigenically distant viruses.


id: cord-295661-v3q1spmm
title: Evaluation of mouse enteroids as a model for Lawsonia intracellularis infection
author: Resende, Talita Pilar
date: 2019-07-19
url: https://www.ncbi.nlm.nih.gov/pubmed/31324204/
doi: 10.1186/s13567-019-0672-9
abstract:
  Lawsonia intracellularis, an obligate intracellular bacterium, is an important enteric pathogen in pig herds and horse farms worldwide. The hallmark feature of L. intracellularis infection is the proliferation of epithelial cells in intestinal crypts. A major limitation to the study of L. intracellularis infection is the lack of an in vitro model that reproduces the changes observed in proliferative enteropathy. Here we investigated the suitability of mouse enteroids as a model to study L. intracellularis infection. Mouse enteroids were microinjected with L. intracellularis, filter-sterilized L. intracellularis culture supernatant, or sterile cell culture media (DMEM). L. intracellularis antigen was detected in mouse enteroids by immunohistochemistry and was located mostly in the basal region of the epithelium. There was no differential growth of enteroids among treatment groups, and cellular proliferation was not increased in L. intracellularis-infected enteroids in relation to non-infected enteroids based on immunofluorescence staining. L. intracellularis infection did not induce changes in gene expression of Ki-67 (proliferation marker), Sox9 (marker for transit amplifying cells) and Muc2 (marker for goblet cells). These results indicate that although L. intracellularis antigen is detectable in mouse enteroids, indicating susceptibility to infection, mouse enteroids fail to replicate the cellular proliferation and gene expression changes observed in proliferative enteropathy. Nevertheless, we have successfully demonstrated that mouse enteroids can be used to model days-long intracellular pathogen infection, serving as potential models for the study of other pathogens of interest in veterinary medicine.


id: cord-295704-3w6hivv8
author: Vidaña, Beatriz
date: 2016-11-08
txt: ./txt/cord-295704-3w6hivv8.txt
cache: ./cache/cord-295704-3w6hivv8.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/27825367/
doi: 10.1186/s13567-016-0395-0
summary:
  Severe cases after pH1N1 infection are consequence of interstitial pneumonia triggered by alveolar viral replication and an exacerbated host immune response, characterized by the up-regulation of pro-inflammatory cytokines and the influx of inflammatory leukocytes to the lungs. This study aims to clarify this question by studying the different induction of innate immune molecules by the distinct lung anatomic compartments (vascular, alveolar and bronchiolar) of ferrets intratracheally infected with a human pH1N1 viral isolate, by means of laser microdissection techniques. More severe lung lesions were observed at 24 h post infection (hpi) correlating with viral antigen detection in bronchiolar and alveolar epithelial cells. As the limitations of the technique did not allow us to completely individualize the target cells, we assessed the cytokine expression associated to the viral replication in the different lung compartments (vascular, alveolar and bronchiolar).

title:
  Involvement of the different lung compartments in the pathogenesis of pH1N1 influenza virus infection in ferrets

abstract:
  Severe cases after pH1N1 infection are consequence of interstitial pneumonia triggered by alveolar viral replication and an exacerbated host immune response, characterized by the up-regulation of pro-inflammatory cytokines and the influx of inflammatory leukocytes to the lungs. Different lung cell populations have been suggested as culprits in the unregulated innate immune responses observed in these cases. This study aims to clarify this question by studying the different induction of innate immune molecules by the distinct lung anatomic compartments (vascular, alveolar and bronchiolar) of ferrets intratracheally infected with a human pH1N1 viral isolate, by means of laser microdissection techniques. The obtained results were then analysed in relation to viral quantification in the different anatomic areas and the histopathological lesions observed. More severe lung lesions were observed at 24 h post infection (hpi) correlating with viral antigen detection in bronchiolar and alveolar epithelial cells. However, high levels of viral RNA were detected in all anatomic compartments throughout infection. Bronchiolar areas were the first source of IFN-α and most pro-inflammatory cytokines, through the activation of RIG-I. In contrast, vascular areas contributed with the highest induction of CCL2 and other pro-inflammatory cytokines, through the activation of TLR3. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-016-0395-0) contains supplementary material, which is available to authorized users.


id: cord-308298-5ntdb8yf
title: Porcine CD8α(dim/-)NKp46(high) NK cells are in a highly activated state
author: Mair, Kerstin H
date: 2013-03-01
txt: ./txt/cord-308298-5ntdb8yf.txt
cache: ./cache/cord-308298-5ntdb8yf.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/23452562/
doi: 10.1186/1297-9716-44-13
summary:
  Functional analyses revealed that splenic NKp46(high) NK cells produced much higher levels of Interferon-γ and Tumor Necrosis Factor-α upon stimulation with cytokines or phorbol-12-myristate-13-acetate/Ionomycin compared to the other two subsets. Splenic NKp46 high NK cells showed a significantly reduced level of CD8α expression compared to the other splenic NK-cell subsets in all animals analysed Sequences of primers (5''-3'') for target genes as well as primer positions on (+) strand, length of specific product in base pairs (bp) and product melting temperature in°C are indicated. Splenic NKp46 high NK cells showed an overall higher expression of this receptor compared to NKp46and NKp46 + NK-cell subsets from both spleen and blood. Splenic NKp46 high NK cells showed highly elevated expression of this activating receptor compared to the other two NKp46-defined subsets in spleen as well as in blood in all animals analysed, which could be demonstrated on protein as well as on mRNA level.

abstract:
  Natural Killer (NK) cells play a crucial role in the early phase of immune responses against various pathogens. In swine so far only little information about this lymphocyte population exists. Phenotypical analyses with newly developed monoclonal antibodies (mAbs) against porcine NKp46 recently revealed that in blood NKp46(-) and NKp46(+) cells with NK phenotype exist with comparable cytotoxic properties. In spleen a third NKp46-defined population with NK phenotype was observed that was characterised by a low to negative CD8α and increased NKp46 expression. In the current study it is shown that this NKp46(high) phenotype was correlated with an increased expression of CD16 and CD27 compared to the CD8α(+)NKp46(-) and NKp46(+) NK-cell subsets in spleen and blood. Additionally NKp46(high) NK cells expressed elevated levels of the chemokine receptor CXCR3 on mRNA level. Functional analyses revealed that splenic NKp46(high) NK cells produced much higher levels of Interferon-γ and Tumor Necrosis Factor-α upon stimulation with cytokines or phorbol-12-myristate-13-acetate/Ionomycin compared to the other two subsets. Furthermore, cross-linking of NKp46 by NKp46-specific mAbs led to a superior CD107a expression in the NKp46(high) NK cells, thus indicating a higher cytolytic capacity of this subset. Therefore porcine splenic NKp46(high) NK cells represent a highly activated subset of NK cells and may play a profound role in the immune surveillance of this organ.


id: cord-310194-f5jtufja
author: Benedictus, Lindert
date: 2014-12-17
txt: ./txt/cord-310194-f5jtufja.txt
cache: ./cache/cord-310194-f5jtufja.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-014-0129-0
doi: 10.1186/s13567-014-0129-0
summary:
  Since alloantigens (including MHC I and MHC class I associated B2M) and MHC class II are genetically determined and therefore heritable, we studied whether differences in these genes between dams and/or calves may explain why BNP only occurs in part of the calves born to PregSure© BVD vaccinated dams. We conclude that the development of BNP in calves is a heritable trait of the dam rather than the calf and that genetic differences between BNP and non-BNP dams are likely due to genes controlling the quantitative alloantibody response following vaccination. We conclude that the development of BNP in calves is a heritable trait of the dam rather than the calf and that genetic differences between BNP and non-BNP dams are likely due to genes controlling the quantitative alloantibody response following vaccination.

title:
  Bovine Neonatal Pancytopenia is a heritable trait of the dam rather than the calf and correlates with the magnitude of vaccine induced maternal alloantibodies not the MHC haplotype

abstract:
  Bovine Neonatal Pancytopenia (BNP), a bleeding syndrome of neonatal calves, is caused by alloantibodies absorbed from the colostrum of particular cows. A commercial BVD vaccine is the likely source of alloantigens eliciting BNP associated alloantibodies. We hypothesized that the rare occurrence of BNP in calves born to vaccinated dams could be associated with genetic differences within dams and calves. We found that the development of BNP within calves was a heritable trait for dams, not for calves and had a high heritability of 19%. To elucidate which genes play a role in the development of BNP we sequenced candidate genes and characterized BNP alloantibodies. Alloantigens present in the vaccine have to be presented to the dam’s immune system via MHC class II, however sequencing of DRB3 showed no differences in MHC class II haplotype between BNP and non-BNP dams. MHC class I, a highly polymorphic alloantigen, is an important target of BNP alloantibodies. Using a novel sequence based MHC class I typing method, we found no association of BNP with MHC class I haplotype distribution in dams or calves. Alloantibodies were detected in both vaccinated BNP and non-BNP dams and we found no differences in alloantibody characteristics between these groups, but alloantibody levels were significantly higher in BNP dams. We concluded that the development of BNP in calves is a heritable trait of the dam rather than the calf and genetic differences between BNP and non-BNP dams are likely due to genes controlling the quantitative alloantibody response following vaccination. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-014-0129-0) contains supplementary material, which is available to authorized users.


id: cord-312695-1uw8xcxw
author: Sugiarto, Sarah
date: 2016-08-05
txt: ./txt/cord-312695-1uw8xcxw.txt
cache: ./cache/cord-312695-1uw8xcxw.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-016-0361-x
doi: 10.1186/s13567-016-0361-x
summary:
  In the present study we investigated whether the passive transfer of antibodies from Mhf-recovered cats to naïve recipient cats provided protection against bacteremia and clinical disease following homologous challenge with Mhf; moreover, we characterized the immune response in the recipient cats. The present study aimed to investigate whether the passive transfer of antibodies from Mhf-recovered to naïve recipient cats induced partial or complete protection against bacteremia and clinical disease following homologous challenge with Mhf. Different parameters addressing the humoral and cellular immune response were monitored in passively immunized and control cats. Our study demonstrated that the passive transfer of antibodies from Mhf-recovered to naïve SPF cats does not prevent infection, high bacterial loads and the development of clinical signs following homologous challenge with Mhf. The passively immunized and control cats showed no differences in the onset and extent of bacteremia and anemia during the course of Mhf infection.

title:
  Passive immunization does not provide protection against experimental infection with Mycoplasma haemofelis

abstract:
  Mycoplasma haemofelis (Mhf) is the most pathogenic feline hemotropic mycoplasma. Cats infected with Mhf that clear bacteremia are protected from Mhf reinfection, but the mechanisms of protective immunity are unresolved. In the present study we investigated whether the passive transfer of antibodies from Mhf-recovered cats to naïve recipient cats provided protection against bacteremia and clinical disease following homologous challenge with Mhf; moreover, we characterized the immune response in the recipient cats. Ten specified pathogen-free (SPF) cats were transfused with pooled plasma from cats that had cleared Mhf bacteremia; five control cats received plasma from naïve SPF cats. After homologous challenge with Mhf, cats were monitored for 100 days using quantitative PCR, hematology, blood biochemistry, Coombs testing, flow cytometry, DnaK ELISA, and red blood cell (RBC) osmotic fragility (OF) measurement. Passively immunized cats were not protected against Mhf infection but, compared to control cats, showed significantly higher RBC OF and B lymphocyte (CD45R/B220(+)) counts and occasionally higher lymphocyte, monocyte and activated CD4(+) T lymphocyte (CD4(+)CD25(+)) counts; they also showed higher bilirubin, total protein and globulin levels compared to those of control cats. At times of peak bacteremia, a decrease in eosinophils and lymphocytes, as well as subsets thereof (B lymphocytes and CD5(+), CD4(+) and CD8(+) T lymphocytes), and an increase in monocytes were particularly significant in the passively immunized cats. In conclusion, passive immunization does not prevent bacteremia and clinical disease following homologous challenge with Mhf, but enhances RBC osmotic fragility and induces a pronounced immune response. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-016-0361-x) contains supplementary material, which is available to authorized users.


id: cord-315072-b28yikvj
author: Giotis, Efstathios S.
date: 2016-08-05
txt: ./txt/cord-315072-b28yikvj.txt
cache: ./cache/cord-315072-b28yikvj.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/27494935/
doi: 10.1186/s13567-016-0363-8
summary:
  title: Chicken interferome: avian interferon-stimulated genes identified by microarray and RNA-seq of primary chick embryo fibroblasts treated with a chicken type I interferon (IFN-α) To generate a chicken ISG database we have compared data from three transcriptomic technology platforms: (i) the classical 3′-biased GeneChip Chicken Genome Array (32K; Affymetrix, High Wycombe, UK), (ii) the Chicken Gene 1.0 Sense Target (ST) whole transcriptome Array (Affymetrix) and (iii) Illumina (Little Chesterford, UK) RNA-seq. One of the most highly-expressed contigs was one which, when analysed by BLAST, proved to represent a homologue of STAT2, which is missing from the current ENSEMBL annotated reference chicken genome In (B) PYURF shows 24-fold suppression by IFN but the sequence surrounding PYURF shows 87-fold induction from the right-hand end of the unannotated, antisense LOC422513 and considerably higher upregulation from the left-hand end (due to its lower uninduced levels), consistent with these representing homologues of IFN-inducible human genes HERC6 and HERC5. Technologies identifying significant IRGs are listed as "1" RNA-seq (using Kal''s Z test); "2" Affymetrix 32K GeneChip Chicken Genome Array and "3" Chicken Gene 1.0 ST Array'' .

title:
  Chicken interferome: avian interferon-stimulated genes identified by microarray and RNA-seq of primary chick embryo fibroblasts treated with a chicken type I interferon (IFN-α)

abstract:
  Viruses that infect birds pose major threats—to the global supply of chicken, the major, universally-acceptable meat, and as zoonotic agents (e.g. avian influenza viruses H5N1 and H7N9). Controlling these viruses in birds as well as understanding their emergence into, and transmission amongst, humans will require considerable ingenuity and understanding of how different species defend themselves. The type I interferon-coordinated response constitutes the major antiviral innate defence. Although interferon was discovered in chicken cells, details of the response, particularly the identity of hundreds of stimulated genes, are far better described in mammals. Viruses induce interferon-stimulated genes but they also regulate the expression of many hundreds of cellular metabolic and structural genes to facilitate their replication. This study focusses on the potentially anti-viral genes by identifying those induced just by interferon in primary chick embryo fibroblasts. Three transcriptomic technologies were exploited: RNA-seq, a classical 3′-biased chicken microarray and a high density, “sense target”, whole transcriptome chicken microarray, with each recognising 120–150 regulated genes (curated for duplication and incorrect assignment of some microarray probesets). Overall, the results are considered robust because 128 of the compiled, curated list of 193 regulated genes were detected by two, or more, of the technologies. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-016-0363-8) contains supplementary material, which is available to authorized users.


id: cord-316908-8ti75mru
author: Wei, Xiaona
date: 2020-02-10
url: https://www.ncbi.nlm.nih.gov/pubmed/32041637/
doi: 10.1186/s13567-020-0739-7
title:
  PEDV enters cells through clathrin-, caveolae-, and lipid raft-mediated endocytosis and traffics via the endo-/lysosome pathway

abstract:
  With the emergence of highly pathogenic variant strains, porcine epidemic diarrhea virus (PEDV) has led to significant economic loss in the global swine industry. Many studies have described how coronaviruses enter cells, but information on PEDV invasion strategies remains insufficient. Given that the differences in gene sequences and pathogenicity between classical and mutant strains of PEDV may lead to diverse invasion mechanisms, this study focused on the cellular entry pathways and cellular transport of the PEDV GI and GII subtype strains in Vero cells and IPEC-J2 cells. We first characterized the kinetics of PEDV entry into cells and found that the highest invasion rate of PEDV was approximately 33% in the IPEC-J2 cells and approximately 100% in the Vero cells. To clarify the specific endocytic pathways, systematic research methods were used and showed that PEDV enters cells via the clathrin- and caveolae-mediated endocytosis pathways, in which dynamin II, clathrin heavy chain, Eps15, cholesterol, and caveolin-1 were indispensably involved. In addition, lipid raft extraction assay showed that PEDV can also enter cells through lipid raft-mediated endocytosis. To investigate the trafficking of internalized PEDV, we found that PEDV entry into cells relied on low pH and internalized virions reached lysosomes through the early endosome–late endosome–lysosome pathway. The results concretely revealed the entry mechanisms of PEDV and provided an insightful theoretical basis for the further understanding of PEDV pathogenesis and guidance for new targets of antiviral drugs.


id: cord-319685-dw0qsl4s
author: Porter, Emily
date: 2014-04-25
url: https://www.ncbi.nlm.nih.gov/pubmed/24767677/
doi: 10.1186/1297-9716-45-49
title:
  Amino acid changes in the spike protein of feline coronavirus correlate with systemic spread of virus from the intestine and not with feline infectious peritonitis

abstract:
  Recent evidence suggests that a mutation in the spike protein gene of feline coronavirus (FCoV), which results in an amino acid change from methionine to leucine at position 1058, may be associated with feline infectious peritonitis (FIP). Tissue and faecal samples collected post mortem from cats diagnosed with or without FIP were subjected to RNA extraction and quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) to detect FCoV RNA. In cats with FIP, 95% of tissue, and 81% of faecal samples were PCR-positive, as opposed to 22% of tissue, and 60% of faecal samples in cats without FIP. Relative FCoV copy numbers were significantly higher in the cats with FIP, both in tissues (P < 0.001) and faeces (P = 0.02). PCR-positive samples underwent pyrosequencing encompassing position 1058 of the FCoV spike protein. This identified a methionine codon at position 1058, consistent with the shedding of an enteric form of FCoV, in 77% of the faecal samples from cats with FIP, and in 100% of the samples from cats without FIP. In contrast, 91% of the tissue samples from cats with FIP and 89% from cats without FIP had a leucine codon at position 1058, consistent with a systemic form of FCoV. These results suggest that the methionine to leucine substitution at position 1058 in the FCoV spike protein is indicative of systemic spread of FCoV from the intestine, rather than a virus with the potential to cause FIP.


id: cord-324950-ux7shvji
title: Coinfections and their molecular consequences in the porcine respiratory tract
author: Saade, Georges
date: 2020-06-16
txt: ./txt/cord-324950-ux7shvji.txt
cache: ./cache/cord-324950-ux7shvji.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-020-00807-8
doi: 10.1186/s13567-020-00807-8
summary:
  In pigs, the term "Porcine Respiratory Disease Complex" (PRDC) is often used to describe coinfections involving viruses such as swine Influenza A Virus (swIAV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), and Porcine CircoVirus type 2 (PCV2) as well as bacteria like Actinobacillus pleuropneumoniae, Mycoplasma hyopneumoniae and Bordetella bronchiseptica. The outcome of any coinfection or superinfection can be affected by the interactions taking place between the infectious agents, the nature of the cell/host, adverse environmental and management conditions, intestinal and respiratory microbiomes, and the triggered immune response-innate and adaptive-developed afterwards [2, 3] . It is well-known that viral infections can induce an ideal environment for a bacterial superinfection through different mechanisms such as the destruction of the epithelial barrier, the over-expression of the receptors involved in the bacterial adhesion to the cells, and the alteration of the host immune response [1, 2, 94, 95] .

abstract:
  Understudied, coinfections are more frequent in pig farms than single infections. In pigs, the term “Porcine Respiratory Disease Complex” (PRDC) is often used to describe coinfections involving viruses such as swine Influenza A Virus (swIAV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), and Porcine CircoVirus type 2 (PCV2) as well as bacteria like Actinobacillus pleuropneumoniae, Mycoplasma hyopneumoniae and Bordetella bronchiseptica. The clinical outcome of the various coinfection or superinfection situations is usually assessed in the studies while in most of cases there is no clear elucidation of the fine mechanisms shaping the complex interactions occurring between microorganisms. In this comprehensive review, we aimed at identifying the studies dealing with coinfections or superinfections in the pig respiratory tract and at presenting the interactions between pathogens and, when possible, the mechanisms controlling them. Coinfections and superinfections involving viruses and bacteria were considered while research articles including protozoan and fungi were excluded. We discuss the main limitations complicating the interpretation of coinfection/superinfection studies, and the high potential perspectives in this fascinating research field, which is expecting to gain more and more interest in the next years for the obvious benefit of animal health.


id: cord-326723-jiauk4fq
author: Risalde, María A
date: 2013-03-18
txt: ./txt/cord-326723-jiauk4fq.txt
cache: ./cache/cord-326723-jiauk4fq.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/23506546/
doi: 10.1186/1297-9716-44-20
summary:
  The aim of this study was to clarify the mechanisms responsible for vascular changes occurring in the lungs of calves infected with bovine viral diarrhea virus (BVDV) and challenged later with bovine herpesvirus type 1 (BHV-1), evaluating the role of MΦs in the development of pathological lesions in this organ. Therefore, the aim of this study was to clarify the mechanisms responsible for ultrastructural and histopathological changes occurring in the lungs of calves pre-infected with BVDV and challenged later with BHV-1, as well as to analyze the role of MΦs in the appearance of the lesions. According to this, in the course of certain acute viral infections, platelets may be activated in vivo, leading to their degranulation, Figure 6 Pro-inflammatory cytokines in the lungs of calves with and without pre-existing BVDV challenged with BHV-1.1.

title:
  Pathogenic mechanisms implicated in the intravascular coagulation in the lungs of BVDV-infected calves challenged with BHV-1

abstract:
  Resistance to respiratory disease in cattle requires host defense mechanisms that protect against pathogens which have evolved sophisticated strategies to evade them, including an altered function of pulmonary macrophages (MΦs) or the induction of inflammatory responses that cause lung injury and sepsis. The aim of this study was to clarify the mechanisms responsible for vascular changes occurring in the lungs of calves infected with bovine viral diarrhea virus (BVDV) and challenged later with bovine herpesvirus type 1 (BHV-1), evaluating the role of MΦs in the development of pathological lesions in this organ. For this purpose, pulmonary lesions were compared between co-infected calves and healthy animals inoculated only with BHV-1 through immunohistochemical (MAC387, TNFα, IL-1α, iNOS, COX-2 and Factor-VIII) and ultrastructural studies. Both groups of calves presented important vascular alterations produced by fibrin microthrombi and platelet aggregations within the blood vessels. These findings were earlier and more severe in the co-infected group, indicating that the concomitance of BVDV and BHV-1 in the lungs disrupts the pulmonary homeostasis by facilitating the establishment of an inflammatory and procoagulant environment modulated by inflammatory mediators released by pulmonary MΦs. In this regard, the co-infected calves, in spite of presenting a greater number of IMΦs than single-infected group, show a significant decrease in iNOS expression coinciding with the presence of more coagulation lesions. Moreover, animals pre-inoculated with BVDV displayed an alteration in the response of pro-inflammatory cytokines (TNFα and IL-1), which play a key role in activating the immune response, as well as in the local cell-mediated response.


id: cord-330554-xg49foch
title: Suppression of feline coronavirus replication in vitro by cyclosporin A
author: Tanaka, Yoshikazu
date: 2012-04-30
txt: ./txt/cord-330554-xg49foch.txt
cache: ./cache/cord-330554-xg49foch.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/1297-9716-43-41
doi: 10.1186/1297-9716-43-41
summary:
  Cyclosporin A (CsA), an immunosuppressive agent that targets the nuclear factor pathway of activated T-cells (NF-AT) to bind cellular cyclophilins (CyP), dose-dependently inhibited FIPV replication in vitro. Cyclophilin B (CyPB) is another target of CsA that promotes hepatitis C virus (HCV) replication by regulating the RNA-binding ability of the HCV NS5B protein. Here, we show that CsA inhibits intracellular replication of the FIPV genome and viral protein expression in vitro independently of the NF-AT pathway. After adsorption for 1 h at 37°C, the medium containing the virus was removed, and the cells were rinsed three times with phosphate-buffered saline [PBS (−)] and incubated with or without various concentrations of CsA (Sigma-Aldrich), cyclosporin H (CsH; Cosmobio, Tokyo, Japan) and FK506 (Sigma-Aldrich) for 20 h. Quantitative RT-PCR showed that 0.63 -10 μM CsA dose-dependently suppressed FIPV RNA replication, whereas FK506 did not exert significant inhibitory effects, except at 10 μM FK506 (approximately 30 % reduction compared to 0 μM FK506, P < 0.05; Figure 3A ).

abstract:
  The feline infectious peritonitis virus (FIPV) is a member of the feline coronavirus family that causes FIP, which is incurable and fatal in cats. Cyclosporin A (CsA), an immunosuppressive agent that targets the nuclear factor pathway of activated T-cells (NF-AT) to bind cellular cyclophilins (CyP), dose-dependently inhibited FIPV replication in vitro. FK506 (an immunosuppressor of the pathway that binds cellular FK506-binding protein (FKBP) but not CyP) did not affect FIPV replication. Neither cell growth nor viability changed in the presence of either CsA or FK506, and these factors did not affect the NF-AT pathway in fcwf-4 cells. Therefore, CsA does not seem to exert inhibitory effects via the NF-AT pathway. In conclusion, CsA inhibited FIPV replication in vitro and further studies are needed to verify the practical value of CsA as an anti-FIPV treatment in vivo.


id: cord-331001-7pyuy1os
author: Miyazaki, Ayako
date: 2011-11-09
txt: ./txt/cord-331001-7pyuy1os.txt
cache: ./cache/cord-331001-7pyuy1os.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/1297-9716-42-112
doi: 10.1186/1297-9716-42-112
summary:
  title: Genetic diversity of group A rotaviruses associated with repeated outbreaks of diarrhea in a farrow-to-finish farm: identification of a porcine rotavirus strain bearing a novel VP7 genotype, G26 Although a number of G and P genotypes have been identified in porcine GARs, few attempts have been made to study the molecular epidemiology of these viruses associated with diarrhea outbreaks within a farm over an extended period of time. Based on the sequence and phylogenic analysis of GAR strains detected among the four outbreaks, at least five combinations of G and P genotypes (G/P combinations) were identified: G9P [23] at the first outbreak, G9P[13]/ [22] and G9P [23] at the second, G3P [7] at the third, and G26P [7] , G9P [23] , and G5P [13] / [22] at the fourth ( Table 2) . Genetic diversity of group A rotaviruses associated with repeated outbreaks of diarrhea in a farrow-tofinish farm: identification of a porcine rotavirus strain bearing a novel VP7 genotype, G26

title:
  Genetic diversity of group A rotaviruses associated with repeated outbreaks of diarrhea in a farrow-to-finish farm: identification of a porcine rotavirus strain bearing a novel VP7 genotype, G26

abstract:
  Group A rotaviruses (GARs) are one of the most common causes of diarrhea in suckling pigs. Although a number of G and P genotypes have been identified in porcine GARs, few attempts have been made to study the molecular epidemiology of these viruses associated with diarrhea outbreaks within a farm over an extended period of time. Here, we investigated the molecular characteristics of GARs that caused four outbreaks of diarrhea among suckling pigs in a farrow-to-finish farm over the course of a year. G and P genotyping of GARs detected at each outbreak demonstrated genetic diversity in this farm as follows: G9P[23] was detected at the first outbreak, G9P[13]/[22] and G9P[23] at the second, G3P[7] at the third, and G9P[23], G5P[13]/[22], and P[7] combined with an untypeable G genotype at the fourth. Sequence analysis of the detected GARs revealed that such genetic diversity could have resulted not only from the introduction of new GAR strains, but also from gene reassortment between GAR strains within the farm. Further, the GAR strain carrying the untypeable G genotype was shown to be a novel porcine GAR bearing a new G26 genotype, as confirmed by the Rotavirus Classification Working Group.


id: cord-332881-mkm4ygh6
author: Kirchhoff, Jana
date: 2014-02-18
url: https://www.ncbi.nlm.nih.gov/pubmed/24548739/
doi: 10.1186/1297-9716-45-20
title:
  Three viruses of the bovine respiratory disease complex apply different strategies to initiate infection

abstract:
  Bovine respiratory disease complex (BRDC) is the major cause of serious respiratory tract infections in calves. The disease is multifactorial, with either stress or reduced immunity allowing several pathogens to emerge. We investigated the susceptibility of bovine airway epithelial cells (BAEC) to infection by the three major viruses associated with the BRDC: bovine respiratory syncytial virus (BRSV), bovine herpesvirus type 1 (BHV-1) and bovine parainfluenza virus type 3 (BPIV3). For this purpose, two culture systems for well-differentiated BAEC were used: the air-liquid interface (ALI) system, where filter-grown BAEC differentiate into a pseudostratified respiratory epithelium and precision-cut lung slices (PCLS) where BAEC are maintained in the original tissue organisation. Comparative infection studies demonstrated that entry and release of BPIV3 occurred specifically via the apical membrane with ciliated cells being the major target cells. By contrast, airway epithelial cells were largely resistant to infection by BHV-1. When the epithelial barrier was abolished by opening tight junctions or by injuring the cell monolayer, BHV-1 infected mainly basal cells. Respiratory epithelial cells were also refractory to infection by BRSV. However, this virus infected neither differentiated epithelial cells nor basal cells when the integrity of the epithelial barrier was destroyed. In contrast to cells of the airway epithelium, subepithelial cells were susceptible to infection by BRSV. Altogether, these results indicate that the three viruses of the same disease complex follow different strategies to interact with the airway epithelium. Possible entry mechanisms are discussed.


id: cord-334968-gonx5taq
author: Pignatelli, Jaime
date: 2013-12-23
txt: ./txt/cord-334968-gonx5taq.txt
cache: ./cache/cord-334968-gonx5taq.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/24364900/
doi: 10.1186/1297-9716-44-126
summary:
  In the first case, the two PToV-HE lineages were detected even within the same animal at two sequential sampling time points, indicating that both PToV strains carrying different HE proteins coexisted on the same farm infecting the same piglets, and suggesting that the immune response generated against one PToV strain did not protect the animals against the infection by the other strain. Hence, in order to examine the potential existence of antigenic differences between the two lineages of PToV-HE proteins, piglet serum samples were analyzed with an HI assay to detect the presence of specific antibodies against the receptor binding domain that prevents the RBC hemagglutination. In addition, to study the antibody response against the whole protein by a different approach, soluble c-myc tagged HE52.7 and HE52.11 proteins were generated by rVV methodology to obtain highly purified coating antigens that were used in ELISA to test the same field serum samples.

title:
  Lineage specific antigenic differences in porcine torovirus hemagglutinin-esterase (PToV-HE) protein

abstract:
  Hemagglutinin-esterases (HE) are viral envelope proteins present in some members from the toro-, corona- and orthomyxovirus families, all related with enteric and/or respiratory tract infections. HE proteins mediate reversible binding to sialic acid receptor determinants, very abundant glycan residues in the enteric and respiratory tracts. The role of the HE protein during the torovirus infection cycle remains unknown, although it is believed to be important in the natural infection process. The phylogenetic analysis of HE coding sequences from porcine torovirus (PToV) field strains revealed the existence of two distinct HE lineages. In a previous study, PToV virus strains with HE proteins from the two lineages were found coexisting in a pig herd, and they were even obtained from the same animal at two consecutive sampling time points. In this work, we report antigenic differences between the two HE lineages, and discuss the possible implications that the coexistence of viruses belonging to both lineages might have on the spread and sustainment of PToV infection in the farms.


id: cord-335215-h9p4kmss
author: Follet, Jérôme
date: 2011-12-02
txt: ./txt/cord-335215-h9p4kmss.txt
cache: ./cache/cord-335215-h9p4kmss.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/1297-9716-42-116
doi: 10.1186/1297-9716-42-116
summary:
  These studies on dairy calves reported a within herd prevalence of Cryptosporidium without identifying species or the relation to the host''s age. parvum at the age of 5 weeks were excluded because Cryptosporidium species could not be identified in all of the following samples collected in these animals. The present study based on 18S rDNA and gp60 gene analysis is the first in France to include molecular characterization to describe the prevalence and the host age related susceptibility to different Cryptosporidium species after a follow up of the same animal. This observation shows that prevalence of Cryptosporidium infection decreases with increasing age of the cattle in France as in many other countries [17, 19, [33] [34] [35] [36] [37] [38] . parvum, a prevalent zoonotic species, in 5-week-old calves was in agreement with the report of Atwill et al., who considered that the contribution of cattle to human cryptosporidiosis is limited to calves under 2 months of age [53] .

title:
  Cryptosporidium infection in a veal calf cohort in France: molecular characterization of species in a longitudinal study

abstract:
  Feces from 142 animals were collected on 15 farms in the region of Brittany, France. Each sample was directly collected from the rectum of the animal and identified with the ear tag number. Animals were sampled three times, at 5, 15 and 22 weeks of age. After DNA extraction from stool samples, nested PCR was performed to amplify partial 18S-rDNA and 60 kDa glycoprotein genes of Cryptosporidium. The parasite was detected on all farms. One hundred out of 142 calves (70.4%) were found to be parasitized by Cryptosporidium. Amplified fragments were sequenced for Cryptosporidium species identification and revealed the presence of C. parvum (43.8%), C. ryanae (28.5%), and C. bovis (27%). One animal was infected with Cryptosporidium ubiquitum. The prevalence of these species was related to the age of the animal. C. parvum caused 86.7% of Cryptosporidium infections in 5-week-old calves but only 1.7% in 15-week-old animals. The analysis of the results showed that animals could be infected successively by C. parvum, C. ryanae, and C. bovis for the study period. C. parvum gp60 genotyping identifies 6 IIa subtypes of which 74.5% were represented by IIaA15G2R1. This work confirms previous studies in other countries showing that zoonotic C. parvum is the dominant species seen in young calves.


id: cord-341305-zf97tcwe
author: Ge, Shikun
date: 2020-09-03
txt: ./txt/cord-341305-zf97tcwe.txt
cache: ./cache/cord-341305-zf97tcwe.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1186/s13567-020-00832-7
doi: 10.1186/s13567-020-00832-7
summary:
  The CPV-VLP and CPV-VP2 protein showed similar reaction values to the purified scFv in the ELISA test, and the results of ELISA analysis using IgY-scFv toward CPV clinical samples were consistent with commercial immunochromatographic assay (ICA) and PCR detection, the scFv did not show cross reactivity with canine distemper virus (CDV) and canine coronavirus (CCV). This study revealed the feasibility of a novel functional antibody fragment development strategy by generating diversified avian IgY-scFv libraries towards the pathogenic target of interest for both detection and therapeutic purposes in veterinary medicine. Functional antibody fragments (i.e.: scFv, Fab) generated by phage-display technology have been not yet routinely evaluated and applied in the veterinary medicine despite it has been well confirmed that such engineered antibodies offer a series of advantages over polyclonal and full-length monoclonal antibodies.

title:
  Canine Parvovirus is diagnosed and neutralized by chicken IgY-scFv generated against the virus capsid protein

abstract:
  Canine parvovirus (CPV) can cause acute and highly contagious bloody enteritis in dog. To obtain antibodies against CPV, hens were immunized with virus-like particles (VLP) of CPV-VP2. The IgY single chain fragment variables (scFv) were generated by T7 phage display system and expressed in E. coli system. The titer of the primary scFv library reached to 1.5 × 10(6) pfu/mL, and 95% of the phages contained the target fragments. The CPV-VLP and CPV-VP2 protein showed similar reaction values to the purified scFv in the ELISA test, and the results of ELISA analysis using IgY-scFv toward CPV clinical samples were consistent with commercial immunochromatographic assay (ICA) and PCR detection, the scFv did not show cross reactivity with canine distemper virus (CDV) and canine coronavirus (CCV). IgY-scFv was successfully expressed in CRFK cells, and in the virus suppression assay, 55% of CPV infections were eliminated within 24 h. Docking results demonstrated that the number of amino acids of the binding sides between scFv and VP2 were AA37 and AA40, respectively. This study revealed the feasibility of a novel functional antibody fragment development strategy by generating diversified avian IgY-scFv libraries towards the pathogenic target of interest for both detection and therapeutic purposes in veterinary medicine.


id: cord-343421-k1dqe4lk
author: Hoelzer, Karin
date: 2018-07-31
url: https://doi.org/10.1186/s13567-018-0561-7
doi: 10.1186/s13567-018-0561-7
title:
  Vaccines as alternatives to antibiotics for food producing animals. Part 2: new approaches and potential solutions

abstract:
  Vaccines and other alternative products are central to the future success of animal agriculture because they can help minimize the need for antibiotics by preventing and controlling infectious diseases in animal populations. To assess scientific advancements related to alternatives to antibiotics and provide actionable strategies to support their development, the United States Department of Agriculture, with support from the World Organisation for Animal Health, organized the second International Symposium on Alternatives to Antibiotics. It focused on six key areas: vaccines; microbial-derived products; non-nutritive phytochemicals; immune-related products; chemicals, enzymes, and innovative drugs; and regulatory pathways to enable the development and licensure of alternatives to antibiotics. This article, the second part in a two-part series, highlights new approaches and potential solutions for the development of vaccines as alternatives to antibiotics in food producing animals; opportunities, challenges and needs for the development of such vaccines are discussed in the first part of this series. As discussed in part 1 of this manuscript, many current vaccines fall short of ideal vaccines in one or more respects. Promising breakthroughs to overcome these limitations include new biotechnology techniques, new oral vaccine approaches, novel adjuvants, new delivery strategies based on bacterial spores, and live recombinant vectors; they also include new vaccination strategies in-ovo, and strategies that simultaneously protect against multiple pathogens. However, translating this research into commercial vaccines that effectively reduce the need for antibiotics will require close collaboration among stakeholders, for instance through public–private partnerships. Targeted research and development investments and concerted efforts by all affected are needed to realize the potential of vaccines to improve animal health, safeguard agricultural productivity, and reduce antibiotic consumption and resulting resistance risks.


id: cord-344845-52rehsd5
author: Opriessnig, Tanja
date: 2017-10-26
txt: ./txt/cord-344845-52rehsd5.txt
cache: ./cache/cord-344845-52rehsd5.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/29073936/
doi: 10.1186/s13567-017-0472-z
summary:
  title: Evaluation of the efficacy of a commercial inactivated genogroup 2b-based porcine epidemic diarrhea virus (PEDV) vaccine and experimental live genogroup 1b exposure against 2b challenge The aim of this study was to compare the ability of G1b-based live virus exposure against use of a commercial G2b–based inactivated vaccine to protect growing pigs against G2b challenge. Under the study conditions a commercial inactivated G2b-based vaccine protected pigs against G2b challenge, as evidenced by reduction of PEDV RNA in feces for 3–4 logs during peak shedding and a shorter viral shedding duration. The oral, but not the intramuscular, experimental G1b-based live virus exposure induced a high anti-PEDV IgA response prior to challenge, which apparently did not impact PEDV shedding compared to POS-CONTROL pigs. Anti-PEDV IgA antibodies in serum samples were first detected in 8/8 EXP-ORAL-1b pigs at dpv 14 ( Figure 3 ).

title:
  Evaluation of the efficacy of a commercial inactivated genogroup 2b-based porcine epidemic diarrhea virus (PEDV) vaccine and experimental live genogroup 1b exposure against 2b challenge

abstract:
  Porcine epidemic diarrhea virus strains from the G1b cluster are considered less pathogenic compared to the G2b cluster. The aim of this study was to compare the ability of G1b-based live virus exposure against use of a commercial G2b–based inactivated vaccine to protect growing pigs against G2b challenge. Thirty-nine PEDV naïve pigs were randomly divided into five groups: EXP-IM-1b (intramuscular G1b exposure; G2b challenge), EXP-ORAL-1b (oral G1b exposure; G2b challenge), VAC-IM-2b (intramuscular commercial inactivated G2b vaccination; G2b challenge), POS-CONTROL (sham-vaccination; G2b challenge) and NEG-CONTROL (sham-vaccination; sham-challenge). Pigs were vaccinated/exposed at 3 weeks of age (day post-vaccination 0, dpv 0), VAC-IM-2b pigs were revaccinated at dpv 14, and the pigs were challenged at dpv 28. Among all groups, VAC-IM-2b pigs had significantly higher anti-PEDV IgG levels on dpv 21 and 28 while EXP-ORAL-1b pigs had significantly higher anti-PEDV IgA levels on dpv 14, 21, 28 and 35. EXP-ORAL-1b also had detectable IgA in feces. Intramuscular PEDV exposure did not result in a detectable antibody response in EXP-IM-1b pigs. The fecal PEDV RNA levels in VAC-IM-2b pigs were significantly lower 5–7 days after challenge compared to the POS-CONTROL group. Under the study conditions a commercial inactivated G2b-based vaccine protected pigs against G2b challenge, as evidenced by reduction of PEDV RNA in feces for 3–4 logs during peak shedding and a shorter viral shedding duration. The oral, but not the intramuscular, experimental G1b-based live virus exposure induced a high anti-PEDV IgA response prior to challenge, which apparently did not impact PEDV shedding compared to POS-CONTROL pigs.


id: cord-350626-ov9fy10b
author: Nazki, Salik
date: 2020-05-13
url: https://doi.org/10.1186/s13567-020-00789-7
doi: 10.1186/s13567-020-00789-7
title:
  Evaluation of local and systemic immune responses in pigs experimentally challenged with porcine reproductive and respiratory syndrome virus

abstract:
  The host-associated defence system responsible for the clearance of porcine reproductive and respiratory syndrome virus (PRRSV) from infected pigs is currently poorly understood. To better understand the dynamics of host–pathogen interactions, seventy-five of 100 pigs infected with PRRSV-JA142 and 25 control pigs were euthanized at 3, 10, 21, 28 and 35 days post-challenge (dpc). Blood, lung, bronchoalveolar lavage (BAL) and bronchial lymph node (BLN) samples were collected to evaluate the cellular immune responses. The humoral responses were evaluated by measuring the levels of anti-PRRSV IgG and serum virus-neutralizing (SVN) antibodies. Consequently, the highest viral loads in the sera and lungs of the infected pigs were detected between 3 and 10 dpc, and these resulted in moderate to mild interstitial pneumonia, which resolved accompanied by the clearance of most of the virus by 28 dpc. At peak viremia, the frequencies of alveolar macrophages in infected pigs were significantly decreased, whereas the monocyte-derived DC/macrophage and conventional DC frequencies were increased, and these effects coincided with the early induction of local T-cell responses and the presence of proinflammatory cytokines/chemokines in the lungs, BAL, and BLN as early as 10 dpc. Conversely, the systemic T-cell responses measured in the peripheral blood mononuclear cells were delayed and significantly induced only after the peak viremic stage between 3 and 10 dpc. Taken together, our results suggest that activation of immune responses in the lung could be the key elements for restraining PRRSV through the early induction of T-cell responses at the sites of virus replication.


id: cord-351881-qea4b0i5
author: Eck, Melanie
date: 2016-02-19
txt: ./txt/cord-351881-qea4b0i5.txt
cache: ./cache/cord-351881-qea4b0i5.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/26895704/
doi: 10.1186/s13567-016-0318-0
summary:
  title: Virus replicon particles expressing porcine reproductive and respiratory syndrome virus proteins elicit immune priming but do not confer protection from viremia in pigs However, none of the PRRSV antigens expressed from VRP, with the exception of the N protein, did induce any detectable antibody response in pigs before challenge infection with PRRSV. These data show that the VSV replicon vector can induce immune responses to heterologous proteins in pigs, but that the PRRSV envelope proteins expressed from VSV VRP are poorly immunogenic. Again, before challenge infection, vaccination with VRP expressing the structural proteins of PRRSV did not induce any detectable antibody response against GP5, GP4 and GP3 as measured by ELISA (not shown). Following challenge infection, GP5-specific antibody responses were detected on day 7 pi in 2 out of 4 pigs, and all pigs vaccinated with VRP expressing the PRRSV proteins seroconverted to GP5 at day 11 pi (Table 3 ).

title:
  Virus replicon particles expressing porcine reproductive and respiratory syndrome virus proteins elicit immune priming but do not confer protection from viremia in pigs

abstract:
  Porcine reproductive and respiratory syndrome virus (PRRSV) is the causative agent of one of the most devastating and economically significant viral disease of pigs worldwide. The vaccines currently available on the market elicit only limited protection. Recombinant vesicular stomatitis virus (VSV) replicon particles (VRP) have been used successfully to induce protection against influenza A virus (IAV) in chickens and bluetongue virus in sheep. In this study, VSV VRP expressing the PRRSV envelope proteins GP5, M, GP4, GP3, GP2 and the nucleocapsid protein N, individually or in combination, were generated and evaluated as a potential vector vaccine against PRRSV infection. High level expression of the recombinant PRRSV proteins was demonstrated in cell culture. However, none of the PRRSV antigens expressed from VRP, with the exception of the N protein, did induce any detectable antibody response in pigs before challenge infection with PRRSV. After challenge however, the antibody responses against GP5, GP4 and GP3 appeared in average 2 weeks earlier than in pigs vaccinated with the empty control VRP. No reduction of viremia was observed in the vaccinated group compared with the control group. When pigs were co-vaccinated with VRP expressing IAV antigens and VRP expressing PRRSV glycoproteins, only antibody responses to the IAV antigens were detectable. These data show that the VSV replicon vector can induce immune responses to heterologous proteins in pigs, but that the PRRSV envelope proteins expressed from VSV VRP are poorly immunogenic. Nevertheless, they prime the immune system for significantly earlier B-cell responses following PRRSV challenge infection.


id: cord-354114-frdsct44
title: Pathogenic characteristics of persistent feline enteric coronavirus infection in cats
author: Vogel, Liesbeth
date: 2010-07-23
txt: ./txt/cord-354114-frdsct44.txt
cache: ./cache/cord-354114-frdsct44.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/20663472/
doi: 10.1051/vetres/2010043
summary:
  FECV is associated with asymptomatic persistent enteric infections, while FIPV causes feline infectious peritonitis (FIP), a usually fatal systemic disease in domestic cats and some wild Felidae. Faecal virus, i.e. genomic RNA, was detected during persistent FECV infection only in the large intestine, downstream of the appendix, and could occasionally be observed also in the blood. The cats were monitored for clinical signs, body weight, faecal virus shedding and serum antibody titres for 70 days post inoculation. In all animals, the amount of virus in the faeces subsequently increased within two days to peak levels of 10 6 -10 8 genomes/lL faeces, after which shedding remained high for an extended period until day 16 and day 23 post inoculation in FECV UCD and FECV RM infected cats, respectively. In order to determine in which part(s) of the gut virus was present during viral persistence, we screened the contents of the entire intestines of two FECV UCD infected cats.

abstract:
  Feline coronaviruses (FCoV) comprise two biotypes: feline enteric coronaviruses (FECV) and feline infectious peritonitis viruses (FIPV). FECV is associated with asymptomatic persistent enteric infections, while FIPV causes feline infectious peritonitis (FIP), a usually fatal systemic disease in domestic cats and some wild Felidae. FIPV arises from FECV by mutation. FCoV also occur in two serotypes, I and II, of which the serotype I viruses are by far the most prevalent in the field. Yet, most of our knowledge about FCoV infections relates to serotype II viruses, particularly about the FIPV, mainly because type I viruses grow poorly in cell culture. Hence, the aim of the present work was the detailed study of the epidemiologically most relevant viruses, the avirulent serotype I viruses. Kittens were inoculated oronasally with different doses of two independent FECV field strains, UCD and RM. Persistent infection could be reproducibly established. The patterns of clinical symptoms, faecal virus shedding and seroconversion were monitored for up to 10 weeks revealing subtle but reproducible differences between the two viruses. Faecal virus, i.e. genomic RNA, was detected during persistent FECV infection only in the large intestine, downstream of the appendix, and could occasionally be observed also in the blood. The implications of our results, particularly our insights into the persistently infected state, are discussed.


