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Tissue-resident memory T cells (TRM) were first described in 2009. While initially the major focus was on CD8 + TRM, there has recently been increased interest in defining the phenotype and the role of CD4 + TRM in diseases. Circulating CD4 + T cells seed CD4 + TRM, but there also appears to be an equilibrium between CD4 + TRM and blood CD4 + T cells. CD4 + TRM are more mobile than CD8 + TRM, usually localized deeper within the dermis/lamina propria and yet may exhibit synergy with CD8 + TRM in disease control. This has been demonstrated in herpes simplex infections in mice. In human recurrent herpes infections, both CD4 + and CD8 + TRM persisting between lesions may control asymptomatic shedding through interferon-gamma secretion, although this has been more clearly shown for CD8 + T cells. The exact role of the CD4 + /CD8 + TRM axis in the trigeminal ganglia and/or cornea in controlling recurrent herpetic keratitis is unknown. In HIV, CD4 + TRM have now been shown to be a major target for productive and latent infection in the cervix. In HSV and HIV co-infections, CD4 + TRM persisting in the dermis support HIV replication. Further understanding of the role of CD4 + TRM and their induction by vaccines may help control sexual transmission by both viruses.

The Role of Tissue Resident Memory CD4 T Cells in Herpes Simplex Viral and HIV Infection