Wily HIV fools immune system by recombining

July 22nd, 2008 - 2:36 pm ICT by IANS  


Washington, July 22 (IANS) When a second strain of wily HIV virus infects someone after the first, they swap genetic information, creating a third, recombinant strain, successfully outwitting the immune system. A study has shown how and where viral strains swap DNA may be determined by the immune response against the original infecting strain.

“The implication that recombination events are selected by immune responses identifies a new mechanism for the virus to escape the patient’s immune system,” said Hendrik Streeck, a co-author of the paper.

“This finding also has worldwide implications for the development of more complex strains of HIV,” added Streeck. He is from the Partners AIDS Research Centre at Massachusetts General Hospital (PARC/MGH).

Part of the immune system’s response against HIV is carried out by HIV-specific CD8 T cells or cytotoxic T lymphocytes (CTLs), which can identify and kill virus-infected cells.

Previous research has shown that the effectiveness of CTL response varies depending on which version of an immune system molecule called HLA Class I an individual has inherited.

The current study was undertaken to investigate why an HIV-positive research participant known to have a powerfully protective Class I allele called HLA-B27 began to experience rapid increases in viral levels much sooner than would have been expected.

An examination of blood samples from this individual revealed that his immune response against HIV had predictably controlled the virus for about a year and a half after he was first diagnosed.

The effective CTL response was primarily directed against a short segment of the Gag protein typically targeted in HLA-B27 patients.

Analysis after the abrupt increase in viral levels showed that the patient had become infected with a second strain of HIV, and two months later it was found that the two strains had exchanged portions of their Gag sequences initially targeted by his CTLs, allowing the virus to escape from that immune response.

The patient’s viral loads stabilized for a while but rose again months later, because of a second HIV mutation that more effectively evades control by HLA-B27 had developed.

These findings will appear in the Journal of Experimental Medicine.

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