Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 16, Pages 8621-8633Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00759-07
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Funding
- NIAID NIH HHS [R01 AI 46980, R01 AI046980, R37 AI 41945, R37 AI041945] Funding Source: Medline
- NIMHD NIH HHS [L60 MD003100] Funding Source: Medline
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The basis for the switch from CCR5 to CXCR4 coreceptor usage seen in similar to 50% of human immunodeficiency virus type 1 (HIV-1) subtype B-infected individuals as disease advances is not well understood. Among the reasons proposed are target cell limitation and better immune recognition of the CXCR4 (X4)-tropic compared to the CCR5 (115)-tropic virus. We document here X4 virus emergence in a rhesus macaque (RM) infected with R5-tropic simian/human immunodeficiency virus, demonstrating that coreceptor switch can happen in a nonhuman primate model of HIV/AIDS. The switch to CXCR4 usage in RM requires envelope sequence changes in the V3 loop that are similar to those found in humans, suggesting that the R5-to-X4 evolution pathways in the two hosts overlap. Interestingly, compared to the inoculating R5 virus, the emerging CXCR4-using virus is highly neutralization sensitive. This finding, coupled with the observation of X4 evolution and appearance in an animal with undetectable circulating virus-specific antibody and low cellular immune responses, lends further support to an inhibitory role of antiviral immunity in HIV-1 coreceptor switch.
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