Genes U12 and U51 encode homologues of human G-protein-coupled receptors, and are potential triggers of autoimmunity.
Failure to distinguish HHV-6A from HHV-6A/B, and questions about assay sensitivity, make results difficult to interpret.
Pattern consistent with clinical studies suggesting these viruses may be one trigger of systemic sclerosis.
Early infection interferes with normal thymocyte development and disrupts central tolerance resulting in autoimmune disease later in life. Only infection during this critical time period resulted in autoimmunity.
The review covers the role the U94 gene product plays in the virus’s life cycle, replication, and latency, as well as in the immune response.
HHV-6, like some other herpesviruses, dysregulates autophagy in multiple cell types, with important biological consequences.
Japanese investigators found no cases of iciHHV6 among 846 patients with several chronic autoimmune diseases
While HHV-6B is well known to cause limbic encephalitis in transplant patients, it does not appear to play a role in other forms of limbic encephalitis.
A group led by Elisabetta Caselli at University of Ferrara discovered HHV-6A in the skin and elevated levels of HHV6-B in the peripheral blood of systemic sclerosis patients
Investigators from the La Jolla Institute of Immunology used high-resolution confocal microscopy to detect high levels of HHV-6 protein in the pancreatic islet cells from donors with type 1 diabetes.
Chinese investigators found a high prevalence of HHV-6 and Epstein Barr virus in the brain tissues of children with Rasmussen’s encephalitis but in none of the controls. There was a significant association between viral presence and brain atrophy, raising a strong suspicion for the involvement of both viruses.
Swedish investigators have found HHV-6 protein in the pancreatic islet cells of both type 1 diabetes patients and controls. The viral load was higher in the islet cells than in surrounding tissues. Unfortunately, they did not provide data on the difference between patients and controls in the viral load.
Antibodies to HHV-6 and VZV dUTPases were significantly elevated in Gulf War Illness patients compared to controls, and EBV dUTPase antibodies were elevated in Chronic Fatigue Syndrome patients.
Investigators by at the University of Ferrara report intriguing alterations in intracellular regulation of HHV-6A-infected thyrocytes and T cells. HHV-6A, but not HHV-6B nor HHV-7, altered expression of several microRNAs in a pattern that is considered a marker for patients with autoimmune thyroid disease.
A fifth case of limbic encephalitis associated with GAD antibodies and HHV-6 infection has been reported, this time in an immunocompetent woman with chromosomally integrated HHV-6, epilepsy, and psychosis. The patient’s condition improved (with a drop in GAD antibody titers and stabilization of psychotic symptoms) in response to three weeks of antiviral therapy but relapsed when antiviral therapy was withdrawn.
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