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.
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.
Investigators at Johns Hopkins have determined that emetine, an older drug used to treat dysentery as well as to induce vomiting, is also effective against cytomegalovirus (CMV/HHV-5). Not only was emetine effective at an extremely low dose, it demonstrated a synergistic effect when combined with ganciclovir in a mouse model of CMV infection and it worked at a much earlier stage of viral replication than the drugs currently in use.
Chinese investigators from Nanjing Medical University report that HHV-6A infection of astrocytes are associated with differences in gene expression that are also found in several CNS diseases including Alzheimer’s, glioma and multiple sclerosis. The investigators used gene ontology analysis to determine the biological processes, cellular components, and molecular functions of the differentially expressed genes and signalling pathways.
A group from the National Institute of Neurological Disorders and Stroke, NIH, has reported finding Epstein-Barr Virus (EBV) and HHV-6 but no cytomegalovirus (CMV) in astrocytomas, a brain tumor comprising approximately one quarter of all gliomas diagnosed. The group used digital droplet PCR (ddPCR), a technique that is highly precise but less sensitive than nested PCR and immunohistochemistry, techniques that have been used in previous studies.
When the research team led by Benedikt Kaufer attempted to shed light on the mechanism behind HHV-6 integration, they were suprised to find telomeric repeats were critical to the integration process. Since the U94 gene shares homology and biological properties with the adenovirus Rep68 gene responsible for viral integration into human chromosomes, U94 was considered the most likely candidate to mediate HHV-6 integration.
It has long been a mystery why HHV-6 is preferentially reactivated in drug reaction with eosinophilia and systemic symptoms (DRESS), also known as drug induced hypersensitivity syndrome (DIHS). HHV-6 reactivation occurs in over 60% of severe cases and is part of the definition of DIHS in Japan. Investigators in Japan suspect that the explanation may lie with the CD134 receptor on activated CD4 cells.
An Italian study on immunocompetent children with suspected CNS infections found HHV-6 and HHV-7 DNA in 4.2% and 4.8% of 304 cerebrospinal fluid (CSF) samples, respectively. Although once considered rare in the immunocompetent, recent studies with more sensitive methods have found HHV-6 in the CSF of 4-17% of immunocompetent children with seizures or suspected CNS infections.
A group led by Ursula Gompels from the London School of Hygiene & Tropical Medicine, University of London, did next generation sequencing on three ciHHV6A cardiac patients and found superinfections of HHV-6A in two of the three. They characterized the first full genome sequence of ciHHV-6A and demonstrated the inherited ciHHV6 genome was similar but distinct from known exogenous (community acquired) strains of HHV-6A .
HHV-6A infection of mesothelial cells causes HLA molecule modulation. This study demonstrates, for the first time, that human mesothelial cells are susceptible to HHV-6A infection. They also show that the virus causes modulated HLA expression on the cell surface, inducing the de novo expression of HLA class II and HLA-G
Congratulations to Joshua Hill, MD, Acting Instructor at the University of Washington and Research Associate at the Fred Hutchinson Cancer Research Center, who has won a K23 grant from the National Institute of Allergy and Infectious Diseases to study HHV-6 in lower respiratory tract disease and chromosomally integrated HHV-6 after stem cell transplantation (SCT).
Investigators led by Eain Murphy of Cleveland Clinic have identified a viral microRNA (miRNA) for HHV-6A, named miR-U86, that targets the HHV-6A intermediate early gene U86.