AI Article Synopsis
- The study reveals that the narrow host range of HIV-1 is influenced by specific restriction factors present in humans and monkeys.
- Interaction between HIV-1's capsid protein and host cyclophilin A (CypA) is crucial for the virus's ability to evade these restrictions in human cells but increases vulnerability in monkey cells.
- Sequence variations among HIV-1 isolates affect their sensitivity to restriction, with a specific mutation (H87Q) in the capsid playing a key role in HIV-1's immune evasion mechanism.
Article Abstract
The narrow host range of human immunodeficiency virus type 1 (HIV-1) is due in part to dominant acting restriction factors in humans (Ref1) and monkeys (Lv1). Here we show that gag encodes determinants of species-specific lentiviral infection, related in part to such restriction factors. Interaction between capsid and host cyclophilin A (CypA) protects HIV-1 from restriction in human cells but is essential for maximal restriction in simian cells. We show that sequence variation between HIV-1 isolates leads to variation in sensitivity to restriction factors in human and simian cells. We present further evidence for the importance of target cell CypA over CypA packaged in virions, specifically in the context of gp160 pseudotyped HIV-1 vectors. We also show that sensitivity to restriction is controlled by an H87Q mutation in the capsid, implicated in the immune control of HIV-1, possibly linking immune and innate control of HIV-1 infection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC523279 | PMC |
| http://dx.doi.org/10.1128/JVI.78.21.11816-11822.2004 | DOI Listing |
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