key: cord-0008524-6fti2z37
authors: Parris, G.E.
title: The timing is right: Evolution of AIDS-causing HIV strains is consistent with history of chloroquine use
date: 2006-06-27
journal: Med Hypotheses
DOI: 10.1016/j.mehy.2006.05.013
sha: f2e5748282861e00711d26a8c172640babe86cd6
doc_id: 8524
cord_uid: 6fti2z37

nan

deaminase activity [7] , after systemic administration of recombinant Clostridium spores and then 5-FC, detection of cytosine deaminase activity with MRS indicate the existence of tumor(s) that contain Clostridia. With this method we can detect a wide range of tumors, as colonization of Clostridia in tumors is unspecific. Also, nitroreductase or b-lactamase producing Clostridia, with suitable fluorinated prodrugs, might be used in such a system. The timing is right: Evolution of AIDS-causing HIV strains is consistent with history of chloroquine use Dear Sir, Consistent with my hypothesis [1] , chloroquine has been shown to act against both HIV/AIDS [2] and coronavirus/SARS [3] . Anti-viral activity creates an ecological stress that will cause evolution toward resistance in these non-targeted viruses just as in the case of the targeted malaria organism [4] . Exposure to chloroquine has undoubtedly caused evolution of these viruses. Korber et al. [5] projected that the common ancestor of the disease-causing strains of HIV likely existed in humans for an undetermined time (presumably without casing disease) and began its evolution into disease-causing strains circa 1931 (1915-1941, 95% confidence interval). Although the absolute timing has been disputed, Korber's figures [5] suggest that the evolution of HIV was in two spurts (i.e., not random over time and not one unique event). The major families (HIV-1A, B/D, C, J, H and F) all appear to have been founded near the beginning of the evolution. There was then a lull in evolution (i.e., mutations continued to occur at about 10 À3 per bp per year [5] , but there was no selection of new strains). After the lull, almost all the families (A, B, C, D and F) split into numerous sub-strains starting at about the same time (circa 1955) and continuing. 4-Aminoquinoline anti-malarials were first synthesized in 1934. The pattern as well as the timing of selected HIV strains [5] are consistent with the testing of 4-aminoquinoline anti-malarials in the Congo (1935) (1936) (1937) (1938) (1939) (1940) , suspension of use (1940) (1941) (1942) (1943) (1944) (1945) (1946) (1947) (1948) (1949) (1950) (1951) (1952) (1953) (1954) (1955) , followed by widespread and continuous use of chloroquine . The WHO launched a world-wide malaria eradication program in 1955. In sub-Saharan Africa, eradication of mosquitoes with DDT was considered impractical, but chloroquine was used at high levels [4] .

Can engineered bacteria help control cancer?

Use of bacteria in anti-cancer therapies

Clostridium spores for tumor-specific drug delivery

Clostridia in cancer therapy

19 F: A versatile reporter for non-invasive physiology and pharmacology using magnetic resonance

Noninvasive quantitation of cytosine deaminase transgene expression in human tumor xenografts with in vivo magnetic resonance spectroscopy

Random mutagenesis and selection of Escherichia coli cytosine deaminase for cancer gene therapy

Hypothesis links emergence of chloroquine-resistant malaria and other intracellular pathogens and suggests a new strategy for treatment of diseases caused by intracellular parasites

Effects of chloroquine on viral infections: an old drug against today's diseases?

Chloroquine is a potent inhibitor of SARS coronavirus infection and spread

History and importance of antimalarial drug resistance

Timing the ancestor of the HIV-1 pandemic strains

E-mail address: antimony_121@hotmail.com