key: cord-0880427-xf6mscn6
authors: Lin, Yong; Yuan, Jun; Long, Quanxin; Hu, Jieli; Deng, Haijun; Zhao, Zhenyu; Chen, Juan; Lu, Mengji; Huang, Ailong
title: Patients with SARS-CoV-2 and HBV co-infection are at risk of greater liver injury
date: 2020-11-18
journal: Genes Dis
DOI: 10.1016/j.gendis.2020.11.005
sha: 2f6ac84e47b2192a53d66d905eb1e198cb0604b2
doc_id: 880427
cord_uid: xf6mscn6

To date, it remains unclear if severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) co-infection exacerbates liver injury in patients with chronic hepatitis B virus (HBV) infection. In this study, we present a retrospective study of 133 hospitalized confirmed mild coronavirus disease 2019 (COVID-19) cases, including 116 patients with COVID-19 with negative serum hepatitis B antigen and 17 HBV inactive carriers with COVID-19. We found that there were no significant differences for the discharge rate or duration of hospitalization between the two groups. However, inactive HBV carriers with SARS-CoV-2 co-infection are at a higher risk of abnormal liver function tests. The enhanced liver injury induced by SARS-CoV-2 and HBV co-infection was identified as the hepatocyte type rather than the cholangiocyte type. Moreover, the inflammatory response, including abnormal lactate dehydrogenase, D-dimer and interleukin-6 production, may contribute to this injury following SARS-CoV-2 co-infection. Collectively, SARS-CoV-2 and HBV co-infection exacerbates liver function of the patients with COVID-19.

Mann-Whitney U test was used to determine significant differences (Graph Pad Prism 7).

Categorical variables were presented as frequency and percentages and compared by the 86 chi-square test or Fisher exact test. Differences were considered as statistically significant 87 when a P-value <0.05. (Table 1 ). There were no differences in 97 age and sex distribution (P >0.05) between these two groups. Throughout the course of their Additionally, we further analyzed the levels of serum ALP and GGT, which are the 129 diagnostic biomarkers for cholangiocyte injury. 6 While the COVID-19 cases with HBV 130 co-infection had higher ratios of abnormal GGT than the COVID-19 cases without HBV 131 COVID-19 cases with HBV co-infection at 2-3 week after the onset of symptoms (Fig. 3A-B) , suggesting that related inflammatory factors would contribute to their liver injury to some 143 extent.

To investigate the possible mechanisms of immune mediated liver injury, we further Currently, there are limited data available regarding liver injury related to SARS-CoV-2 158 co-infection. 5-7,10,11 A recent study has revealed that the liver injury in the patients with 159 SARS-CoV-2/HBV co-infection was related to disease severity and worse prognosis. 8 Our 160 study showed that a greater proportion of inactive HBV carriers had abnormal alterations of 161 liver function parameters after SARS-CoV-2 co-infection, indicating a high risk of liver 162 injury as hepatocyte type. 6 The enhanced liver injury of inactive HBV carriers is likely 163 caused by inflammatory factors.

Our study reported liver injury in mild COVID-19 cases with or without HBV co-infection. between the two groups, respectively. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not 310 significant. ALP, alkaline phosphatase; GGT, gamma-glutamyltransferase. 

Therapeutic strategies for hepatitis B 243 virus infection: towards a cure

Systemic viral infections and collateral damage in the liver

COVID-19 Induced Hepatitis B Virus 286 Reactivation: A Novel Case From the United Arab Emirates

Hospital stays, median (IQR), days

Data are median (IQR) or n (%). HBeAg, hepatitis B e antigen

HBsAg, hepatitis B surface antigen

HBV, hepatitis B virus

* Two data are missed