Variations in the CCR5 and CCL3L1 genes may affect immune system response to HIV and replication of the virus. Other genes may also play a role but more research is required to determine that, Agence France-Presse reported.
CCR5 controls a key receptor on the surface of the CD4 immune cell onto which HIV attaches, while CCL3L1 controls an immune system signalling molecule called a chemokine, which blocks HIV from attaching to the CCR5 receptor, the researchers said.
Viral load not so important?
In this study, the researchers analysed thousands of HIV-infected patients and healthy people and found that viral load accounted for only nine percent of the difference in how rapidly HIV-infected patients developed Aids.
"The genetic variations contribute nearly as much to the extent of inter-individual variability in Aids progression rates as does HIV-1 viral load," team leader Sunil Ahuja of the University of Texas Health Science Centre in San Antonio, told AFP.
"Even after accounting for the detrimental effects of a high viral burden, these genetic factors influence the pace of HIV-1 disease progression," said study first author Hemant Kulkarni, assistant professor of medicine at the Health Science Centre. – (HealthDayNews)
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HIV/Aids Centre
October 2007