A group led by Professor Niza Frenkel of Tel Aviv University in Israel has determined that HHV-6A limits its own replication to avoid detection and destruction, leading to a long life-cycle with limited propagation. This finding may reveal the mechanism behind persistent HHV-6A infections and help explain some disease associations.
Investigators from Uppsala University in Sweden found that HHV-6 IgG reactivity was significantly lower in Alzheimer’s Disease patients compared to controls. The authors suggest reduced immunity may be one reason why past studies have found increased levels of HHV-6 DNA in the brains of Alzheimer’s patients compared to controls.
A young woman on rituximab and two other immunomodulatory agents for the treatment of dermatomyositis developed encephalitis with severe anterograde amnesia. As the use of biologic treatments for refractory autoimmune disease has been increasing, physicians are advised to consider HHV-6 and offer prompt antiviral therapy to limit irreversible morbidity.
Investigators from the University of Ferrara, Italy have found evidence suggesting that high levels of U94 in ciHHV6 may predispose to the formation of marker chromosomes. A patient with diffuse large B-cell lymphoma positive for inherited chromosomally integrated HHV-6A and HHV-6A was also found in a marker chromosome, an abnormal piece of chromosome that is seen in some leukemia and lymphomas.
A group from Japan has found that the deformation of erythroblasts seen in transient erythroblastopenia of childhood, is caused by HHV-6. Erythroblasts are progenitor cells in the bone marrow, necessary for the production of red blood cells.
HHV-6 has been linked in numerous studies to multiple sclerosis. Now, investigators at the University of British Columbia have published new data suggesting that HHV-6A may be a key player in the development of multiple sclerosis. The investigators propose that the viral protein U24 may dysregulate myelination.
A group from Aarhus University propose that differing isoform patterns of CD46 correlate with the ability of some HHV-6B strains to enter T cells.
Latvian researchers studied autopsy material from the olfactory bulb in patients with HHV-6 encephalopathy vs. controls and reported surprising differences.
Investigators led by Bhupesh Prusty, PhD at University of Wurzbürg in Germany have identified two cases of possible germline inherited chromosomally integrated HHV-7.
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.
Investigators at Yale University warn that hypersensitivity-associated HHV-6 lymphadenopathy can have the same presentation as lymphoma.
The HHV-6 Foundation is pleased to announce the creation of a new $250,000 research fund to honor the work Dharam Ablashi, the co-discoverer of HHV-6. The gift was made possible by a generous donation from a patient family in appreciation of Dharam’s outstanding service to the field of HHV-6 research over four decades. The funds will be used to offer pilot grants of up to $25,000 each to investigators seeking to gather preliminary data before embarking on larger studies.
Australian investigators studied 143 young children with febrile seizures for signs of viral infection and found that HHV-6 was the fifth most common virus after rhinovirus (22%), enterovirus (20%), adenovirus (21%) and influenza (13%). Overall, a virus was found in 71% of cases. Virus found in complex seizures was associated with HHV-6 (42%) or influenza (41%).
Biopsies from patients with 5 types of lymphoproliferative disorders of the ocular adnexa, were found to contain HHV-6 DNA in 9 of 70 (12.9%) samples. While an overall detection rate of 12.9% is significant, HHV-6 was even more prevalent among those with benign lymphoproliferative disorders; HHV-6 was found in 22.7% of those with IgG4-related ophthalmic disease and 28.6% of those with orbital reactive lymphoid hyperplasia.
A group from Hebrew University of Jerusalem has discovered the mechanism by cells with actively replicating HHV-6 evade elimination by natural killer (NK) cells.