Immunological Response to Herpes Virus and Its Relationship with Interleukin 10

Abstract

A class of DNA viruses called herpesviruses is well-known for its capacity to create latent infections that last a lifetime and to elude the host's immune system. Natural killer (NK) cells, cytotoxic T lymphocytes, and antibody-mediated reactions are examples of both innate and adaptive immunity that are involved in the immune response to herpesvirus infection. Modulating host cytokine responses is one of the complex strategies that herpesviruses have evolved to circumvent these defences. The anti-inflammatory cytokine interleukin-10 (IL-10) is essential for controlling immunological responses and preventing tissue damage. To inhibit immune activation and increase viral persistence, a number of herpesviruses, including Epstein-Barr virus (EBV) and cytomegalovirus (CMV), encode viral homologs of IL-10 or cause the host to produce IL-10. This immunomodulatory effect aids in the development of latency and reactivation as well as the virus's ability to evade immune surveillance. Knowing how herpesviruses and IL-10.