HHV-6 was found more frequently in the Purkinje cells of bipolar and major depressive disorder patients compared to controls. Furthermore HHV-6A was associated with a reduced Purkinje cell size. HHV-6 was not found, however in patients with schizophrenia.
German investigators suggest that silencing of HHV-6A by the ND10 complex may explain why HHV-6A is more likely than other herpesviruses to establish a quiescent infection.
Investigators in Spain and Italy attempted to reduce the rate of acute GVHD in pediatric transplant patients by infusing manipulated stem cells. Not only was there no reduction in expected acute GVHD, the patients experienced an unusually high rate of HHV-6 disease.
Investigators from Japan looked at HHV-6 and HHV-7 DNA levels in saliva to see if they might be biomarkers for cancer-related fatigue (CRF) in multiple myeloma patients.
German investigators have identified a marker for what they believe is the earliest stage of viral reactivation, or “transactivation” marked by transcription of several viral small non-coding RNAs in the absence of detectable viral replication. The group believes that these viral small RNAs could be developed as biomarkers.
Investigators at Mt Sinai used “big data” models to determine that the genes involved with fighting Alzheimer’s are the same ones that fight virus. They found HHV-6A and HHV-7 to be more abundant in Alzheimer’s brains, and singled out HHV6-A as a key modulator of the genes involved in amyloidosis and neuronal death.
Researchers at Harvard studied how neurons responded to the presence of herpesviruses HSV1 and HHV-6, and found that they rapidly induce amyloid plaque production within 24 to 48 hours.
Large insurance data studies in Taiwan have found that seniors with shingles or serious HSV1 infections have a 2-3 fold increased risk of certain forms of dementia, and that antiviral treatment can reduce that risk by 90%.
A large prospective study in Africa adds weight to argument that HHV-6B infection is an important cause of febrile status epilepticus.
Although depleting naïve T cells has been successful in preventing acute graft vs host disease in several studies, investigators from Spain reported an unexpectedly high incidence of HHV-6 encephalitis in a cohort of haploidentical transplant patients.
Inherited ciHHV-6 has been shown to activate under conditions of immunosuppression and and the pan-HDAC inhibitor TSA activates integrated ciHHV-6 in vitro. This is the first case report of HHV-6 activation in a ciHHV-6 patient who received a pan-HDAC inhibitor drug.
Investigators at the National Cancer Institute found that HHV-6+ lymph nodes can be identified in biopsies from both lymphadenopathy and malignancies. They warn that failing to identify HHV-6 in these biopsies can lead to misdiagnosis in lymphoma cases.
A Japanese study found that unexplained fever and biliary atresia are associated with HHV-6B infection in pediatric transplant patients. 100% of seronegative infants developed a primary infection.
Many institutions are now using a new multiplex qualitative assay to get rapid diagnosis in encephalitis cases in the clinic. Unfortunately, this system cannot identify cases of inherited chromosomal integration, which creates confusion.
A new meta-analysis published in Biology of Blood and Marrow Transplantation shows that transplant patients who reactivate with HHV-6 are 2-3 times more likely to develop acute GVHD.