Immuno-metabolic changes in herpes virus infection

Recent evidences indicate that change in cellular metabolic pathways can alter immune response and function of the host; emphasizing the role of metabolome in health and diseases. Human Herpes simplex virus type-1 (HSV1) and type-2 (HSV-2) causes diseases from asymptomatic to highly prevalent oral and genital herpes, recurrent blisters or neurological complications. Immune responses against HSV are complex with delicate interplay between innate signaling pathways and adaptive immune responses. The innate response involves the induction of protective IFN-1; while Natural Killer (NK) cells and plasmacytoid Dendritic Cells (pDC) confer in vivo adaptive anti-HSV response along with humoral and cellular components in controlling infection and latency. Metabolic changes lead to up-/down-regulation of several cytokines and chemokines like IFN-gamma, IL-2, IL-4, IL-10 and MIP1 beta in HSV infection and recurrences. Recently, the viral protein ICP0 has been identified as an attenuator of TLR signaling, that inhibit innate responses to HSV. This review will summarize the role of metabolome in innate and adaptive effectors in infection, pathogenesis and immune control of HSV, highlighting the delicate interplay between the metabolic changes and immunity.