Herpesviruses

Herpesviruses are a family of DNA viruses with extremely high prevalence rates. Once a human host is infected, the infection is life-long. While generally, immunocompetent hosts are able to keep the virus in a latent state and remain asymptomatic, several of these viruses can cause symptoms if they reactivate. They can also increase the risk of autoimmune disease and cancer.

Types
Viruses in this family include HSV-1 and HSV-2, Epstein-Barr virus (HHV4), which causes mononucleosis, Varicella zoster virus, which causes chickenpox and shingles. More than 90% of adults have been infected with at least one of these viruses.

Other herpesviruses include human cytomegalovirus, HHV-6, HHV-7, and Kaposi's sarcoma-associated herpesvirus.

Latency
They share in common that after the initial infection, these viruses usually remain latent for life.

Reactivation
Reactivation of these viruses have been associated with a number of diseases. HSV-1 has been implicated in Alzheimer's.

Several of these viruses have transactivating potential.

Chronic fatigue syndrome
It is unclear whether herpesviruses associated with Chronic fatigue syndrome play an etiological role or are "bystanders" – opportunistic reactivations under a state of immune dysregulation.

Studies related to Herpesviruses and ME/CFS

 * 2016, Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Disease "'In this review, we provide evidence from animal and human studies of the Epstein-Barr virus as a prototype, supporting the notion that herpesviruses dUTPases are a family of proteins with unique immunoregulatory functions that can alter the inflammatory microenvironment and thus exacerbate the immune pathology of herpesvirus-related diseases including myalgic encephalomyelitis/chronic fatigue syndrome, autoimmune diseases, and cancer...[we] approached the possibility that two or more herpesviruses may act synergistically and that virus-encoded proteins, rather than the viruses themselves, may act as drivers of or contribute to the pathophysiological alterations observed in a subset of patients with ME/CFS.'"