HIV-2 evades restriction by ZAP through adaptations in the U3 LTR region despite increased CpG levels.

ABSTRACT: Simian immunodeficiency viruses infecting sooty mangabeys (SIVsmm) gave rise to nine groups of human immunodeficiency virus type 2 (HIV-2). Two of these (A and B) spread substantially with an estimated 1-2 million individuals affected. The evolutionary adaptations that facilitated HIV-2's spread in humans are still poorly understood. Here, we report that diverse SIVsmm strains efficiently infect primary human T cells. However, they are more sensitive to interferon than HIV-2, indicating that interferon-stimulated genes (ISGs) pose a barrier to the successful spread of SIVsmm in humans. One of the best-known antiviral ISGs is the zinc finger antiviral protein (ZAP), which targets CpG dinucleotides in RNA. To evade ZAP-mediated restriction, many viruses, including HIV-1, suppress their CpG c

SUBMITTER: Kmiec D 

PROVIDER: S-EPMC12397911 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature