After years of very little interest by the scientific community, there has suddenly been a lot of interest in HHV-6A, which along with HHV-7, appears to be central to the progression of Alzheimer’s disease.
Using a novel serological assay that can differentiate HHV-6A from HHV-6B, investigators found HHV-6A immediate early antibodies to be associated with an increased risk of non-Hodgkin lymphoma.
German investigators conducted a broad scale analysis of CD8 T cell responses to HHV-6B, identifying novel epitopes with potential for immunotherapy or vaccines. The strongest responses were directed against an epitope from IE-2.
A gigantic sequencing effort by investigators at University of Washington has provided a wealth of new information about the HHV-6B genome, including important flaws of the reference strains currently in use.
A broadscale investigation of the ovarian cancer oncobiome using a microarray system PathoChip found HHV-6A sequences at or near genes associated with tumorigenesis in ovarian cancer tissue samples.
Italian investigators showed that HHV-6A and -6B infection of natural killer cells have a remarkable effect on the expression of miRNAs and transcription factors, which in turn control natural killer cell development, maturation and function.
A team at University of Pittsburgh analyzed a large database of deep sequencing data from tumor and control tissues to look for viral sequences in 22 different cancers. They were surprised to find several herpesviruses in gastrointestinal cancers but not in control tissues.
Italian investigators found that HHV-6 latency-associated gene U94, inserted in a HSV1 vector, inhibited the development of breast cancer, cervical cancer, and lung metastasis. It also impaired tumor driven angiogenesis.
Most herpesviruses maintain latency by forming circular episomes in the nucleus of the cell. Investigators in Germany have provided further evidence that HHV-6A relies on their telomeres, not circular episomes, to maintain a persistent latent infection by integrating into the host chromosome.
A group led by Louis Flamand, PhD in Canada has developed a culture system that can be used to determine how the virus enters latency by integrating into the chromosome, and which drugs cause it to activate.
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.
HHV-6B induces unique, region-specific DNA hypomethylation, and findings suggest that the epigenetic modification may facilitate HHV-6B integration.
A new study shows that HHV-6A direct repeats can survive alone in an integrated state without the rest of the viral genome. The study also identified non-telomeric integration of HHV-6A in both in vitro cultured cells as well as one iciHHV-6A patient.
The group that recently discovered a ligand for U24 has expanded upon their previous experiments to further elucidate the viral protein’s interactions and functions as they pertain to MS.
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.