A retrovirus that infected chimpanzees 4 million years ago may be associated with human susceptibility to the human immunodeficiency virus (HIV).
Researchers at the Fred Hutchinson Cancer Research Center have been studying the Pan troglodytes endogenous retrovirus (PtERV1), an ancient virus that caused infections in primates but not in humans.
Viruses reproduce (replicate) by incorporating themselves into host DNA in the nucleus of infected cells. Viral DNA makes up about 8% of the human genome. The PtERV1 researchers examined DNA from primates and humans. The largest difference between chimpanzee and human genomes was the inclusion of Pan troglodyte endogenous retrovirus in chimpanzee DNA. The reason that PtERV1 was not found in human DNA is related to the difference in susceptibility to the virus between primates and humans: if humans were susceptible to PtERV1, the virus would have been found incorporated in the human genome as it is with primates.
Protection against Pan troglodytes endogenous retrovirus in humans is believed to be credited to an antiviral defense gene – TRIM5a. TRIM5a prevents viral replication by producing a protein that binds to the virus and destroys it. Although TRIM5a provides protection against this particular retrovirus, it does not appear to provide protection against other retroviruses that cause human infection. In fact, TRIM5a may make humans more susceptible to HIV-1. The researchers found that changes made to TRIM5a to provide a greater HIV defense inhibited the ability to prevent infection with the Pan troglodytes endogenous retrovirus. And changes that provided greater defense against PtERV1 resulted in increased susceptibility to HIV-1.
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Source:
Kaiser SM, HS Malik, M Emerman. Restriction of an extinct retrovirus by the human TRIM5a antiviral protein. Science 22 June 2007; 316:1756-8.