About this Research Topic
Herpesviruses are a large group of double-stranded DNA viruses, which have evolved strategies to persist and disseminate widely throughout the human population. Unlike RNA viruses which have the ability to alter their antigenic expression profile to evade host immune responses, herpesviruses can establish life-long latency in the infected host. Herpesviruses are divided into alpha, beta and gamma herpesviruses sub-families. The human members of the alpha-herpesvirinae subfamily is comprised of herpes simplex virus-1 and 2 (HSV-1 and HSV-2) and of varicella-zoster virus (VZV). These viruses are considered neurotropic, as they can (i) infect nerve endings; (ii) traffic via neuronal axons and (iii) establish latency in neuronal nuclei. On the other hand, the members of the beta-herpesvirinae subfamily such as human cytomegalovirus (HCMV), human herpesviruses 6 and 7 (HHV-6 and HHV-7) are known to establish latent infections in immune cell types such as monocytes and T cells. Epstein-Barr Virus (EBV) is a member of gamma-herpesvirinae subfamily that establishes latency in B lymphocytes. Additionally, HHV-8 also known as Kaposi’s Sarcoma-Associated Herpes virus (KSHV) is a γ-herpes virus which establishes latency in monocytes, dendritic cells, B lymphocytes and endothelial cells of the host.
Although members of the herpesviridae family share few properties, they differ significantly in terms of the expression of viral genes during the latent infection period, incidence of viral reactivation, the molecular mechanisms by which they evade the host immunity to establish latency, and the pathogenesis associated with viral reactivation. A better understanding of the virological and immunological events associated with herpesviruses infection should help in the development of prophylactic and therapeutic approaches to better manage these viral infections in patients worldwide.
In this Research Topic, we welcome the submission of Original Research, Review and Mini-Review articles focused on understanding the cellular and molecular mechanisms involved in (i) immunity and pathogenesis to viral infection, (ii) viral infection and replication, (iii) establishment of latency and (iv) viral reactivation by the members of herpesviridae family.
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