Research on the immune response to Herpes Simplex Virus (HSV) has revealed significant insights into its interaction with the immune system, particularly in the context of HIV. One study demonstrated that HSV-2 infection leads to an influx of activated CD4+ T cells to sites of viral replication, which in turn promotes HIV latency reversal by upregulating MALAT1, a long non-coding RNA associated with HIV replication (ref: Pierce doi.org/10.1172/JCI164317/). This finding highlights the dual role of HSV-2 in modulating immune responses that may inadvertently facilitate HIV reactivation. Another study focused on the role of natural killer (NK) cells during HSV-2 genital infections, showing that granzyme B derived from NK cells contributes to epithelial ulceration, a hallmark of genital herpes (ref: Lim doi.org/10.1016/j.celrep.2023.112410/). This underscores the complex interplay between HSV-2 and the host immune response, where immune activation can lead to tissue damage. Additionally, a pilot study explored the effects of valaciclovir, an antiviral treatment, on neuroinflammation in schizophrenia, suggesting that herpes virus infections may contribute to cognitive impairments through inflammatory pathways (ref: Jonker doi.org/10.1017/S0033291723000430/). Overall, these studies illustrate the multifaceted nature of HSV-2's impact on immune responses and its potential implications for co-infections like HIV.