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. 2011 Jun 30;7(6):e1002109. doi: 10.1371/journal.ppat.1002109

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Rapid replication of HSV-2 in epithelial cells could drive a low level HSV-2 infection in neighboring DCs, imprinting on them a “mucosal-like” phenotype and inducing the ability to release RA. RA can profoundly affect resident and/or recruited lymphocytes and expand the pool of α₄β₇ ^highCD4⁺ T cells at the mucosal site of infection. These highly susceptible cells could contribute to increase HIV-1 replication rate and HIV-1 rapid access gut inductive sites, PPs and MLNs. Therefore, the RA-driven immunomodulatory effect and other HSV-2 driven changes – that need to be investigated - could partner to create an environment particularly susceptible to HIV-1 infection.