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.
Low sodium levels associated with HHV-6 encephalitis
Retrospective analysis of transplant patients revealed that low serum sodium levels are associated with HHV-6 encephalitis, but not HHV-6 myelitis. Low sodium is a possible marker for HHV-6 encephalitis post-transplantation.
New cell culture system established to study HHV-6A/B chromosomal integration
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.
HHV-6A, infertility and miscarriage: a hypothesis
Growing evidence implicates HHV-6, especially HHV-6A, in some cases of female infertility, miscarriage, and other gestational problems affecting both the mother and child. The authors of the paper wonder if heparin, an anticoagulant with antiviral properties often used to treat infertility, might mitigate the detrimental effects of HHV-6 in the uterine environment.
HHV-6 reactivation and poor CD4+ cell reconstitution predict pediatric acute GVHD
Over a dozen studies have now found HHV-6 to predict aGVHD, but this is the first to correlate viral reactivation with poor CD4+ cell immune reconstitution.
Antibodies to herpesvirus dUTPase a potential biomarker for Gulf War Illness and CFS
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 telomeric hypomethylation, possibly facilitating integration
HHV-6B induces unique, region-specific DNA hypomethylation, and findings suggest that the epigenetic modification may facilitate HHV-6B integration.
Solo DR and non-telomeric chromosomal 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.
Neoplasia: could iciHHV-6A cause a benign HPV strain to turn deadly?
Human papillomavirus 4 is a benign strain not associated with cancer. However, in a woman with inherited chromosomally integrated HHV-6A, a high grade vaginal squamous lesion developed rapidly. The authors warn that there may be a synergistic effect between HPV4 and iciHHV6A.
HHV-6 U24 tightly linked to specific E3 ubiquitin ligases
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.
New mouse model for HHV-6 & 7
Investigators at Washington University have sequenced a murine herpesvirus and determined that it is closely related to HHV-6 & 7. Named Murine Rosesolovirus (MRV), the virus causes severe depletion of CD4+ T cells and thymic necrosis in young mice. The authors believe that MRV will be a useful mouse model to study the impact of HHV-6 & 7 in humans.
Opinion: call for ciHHV6 screening in transplantion
Two physicians from Texas propose that ciHHV6 status of donors and recipients be determined before solid organ transplantion, using a single pre-transplant qPCR test on whole blood, and that patients with ciHHV-6 or ciHHV-6 donors be carefully monitored for signs of active HHV-6 infection.
Multiple viral infections and HHV-6B increase risk of mortality in HSCT
A retrospective study of allogeneic hematopoietic stem cell transplant patients at University of Washington found that reactivation of several double stranded DNA viruses significantly increased the risk of overall mortality, as did an increased quantitative burden of viral exposure. HHV-6B conferred a significantly increased risk for overall mortality.
New data provides insight into how HHV-6A establishes persistent infections
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.
Decreased HHV-6 IgG in Alzheimer’s
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.