Observational analysis shows ZAP resistance in HIV-2, indicating adaptations in U3 LTR and implications for interferon response in primary human T cells.
Key Points
HIV-2 exhibits greater resistance to ZAP than HIV-1 despite having more CpG dinucleotides.
ZAP-targeting regions identified in HIV-2 map to the nef/U3 region, enhancing its replication in primary human T cells.
SIVsmm strains infect human T cells but are more sensitive to interferon than HIV-2, suggesting barriers to their spread.
Findings highlight the potential for HIV-2 adaptations to circumvent ISG-mediated restrictions during human infection.