Figure 1. Model of cutaneous and mucosal immune responses to HSV-2 reactivation.

In recurrent infections, clusters of antiviral CD4⁺ and CD8⁺ T cells form in the dermis and submucosa, along with dendritic cells and macrophages. Interferon production from T cells helps resolve the viral insult. Naive B cells and ASCs are recruited to these dermal clusters. The latter secrete antibodies that may contribute to blockade of viral spread. During healing, MLCs form. As lesions heal over time, T cell density decreases (though T_RMs remain), and B cell populations are no longer, or rarely, observed. DEJ, dermal-epidermal junction.