The mechanisms of protective immunity against genital herpes infection

Abstract

Herpes simplex virus-2(HSV-2)is one of the most common sexually transmitted infections through genital epithelial cells followed by the establishment of latency in the sacral ganglia. So far, several pharmacological interventions are available to inhibit virus replication. However, HSV-2 has not been able to be completely cured by them. Furthermore, it’s been known that eonatal HSV-2 infection is seriously lethal without the treatment and HSV-2 infection in adults increases the susceptibility of high-risk HPV and HIV infection. Therefore, preventative vaccines or curative medicines are required for this disease. However, all of the current vaccine has been ineffective to prevent HSV-2 disease or infection despite inducing anti-HSV-2 immunity in the circulation. Towards developing vaccines to prevent HSV-2 transmission, a further understanding of the mechanism by which immune responses within peripheral tissues following HSV-2 infection are required. However, the immune mechanism of protection within the female genital mucosa and dorsal root ganglia(DRG)has been poorly understood. Until now, we have found that 1)genital tissue-resident immune response by establishing memory lymphocyte cluster (MLC)including HSV-2-specific T cell populations was required for preventing the spreading of HSV-2 from genital tissues to dorsal root ganglia(DRG)and 2)IFN-γ rapidly produced by circulating CD4⁺ memory T cells in DRG increased vascular permeability in blood-nerve barrier to allow the entry of anti-HSV antibody within neuronal tissues. Our results shed light on a previously unappreciated role of CD4⁺ memory T cells against genital herpes infection.