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- W4313373630 abstract "Abstract HSV-2 is one of the most significant factors fueling the global HIV epidemic and coinfection is associated with higher HIV plasma viral loads and increased rates of HIV transmission and HSV-2 recurrences. The mechanisms underlying this syndemic likely reflect local and systemic effects. To explore potential systemic effects, we characterized PBMC from a cohort of HIV-1+ women who were or were not HSV-2 seropositive (HSV-2+) and identified phenotypic changes in CD4 T cells including increased frequencies of activated cells and cells expressing co-receptors for HIV entry in HIV+/HSV-2+ vs. HIV+/HSV-2 seronegative (HSV-2−) women. Surprisingly, IL-32, a proinflammatory cytokine, was lower in CD4 T cells from HSV-2+ women. Addition of IL-32γ to CD4 T cells from HIV+ women blocked HIV reactivation following stimulation with phytohemagglutinin, suggesting that HSV-2 induces phenotypic changes in CD4 T cells to promote HIV reactivation. Subsequent RNAseq analysis of CD4 T cells infected ex vivo with HSV-2 also showed lower levels of IL-32, as well as elevated bcl6, itch, and irf4 transcripts along with decreased ccr7, psgl1, and s1pr1, suggesting a transcriptional landscape consistent with T follicular helper (TFH) cells. Flow cytometry studies using CD4 T cells isolated from PBMC from HIV− or HIV+ donors, as well as from tonsils, showed an increased frequency of TFH cells in HSV-2 infected CD4 T cells, suggesting preferential infection of this subpopulation, which is known to harbor latent HIV. HSV-2 infection of CD4 T cells isolated from HIV+ donors or latently infected T cell lines triggered HIV reactivation. These findings demonstrate that HSV-2 directly infects CD4 T cell subpopulations including TFH cells to promote HIV reactivation." @default.
- W4313373630 created "2023-01-06" @default.
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- W4313373630 date "2020-05-01" @default.
- W4313373630 modified "2023-09-27" @default.
- W4313373630 title "HSV-2 infects T follicular helper cells to promote HIV reactivation" @default.
- W4313373630 doi "https://doi.org/10.4049/jimmunol.204.supp.247.24" @default.
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