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 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.
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.
A group from the University Medical Center in the Netherlands has shown that new gene editing technology can be used to impair viral replication and clear latent herpesvirus infections. The group used a CRISPR-Cas system to target viral genetic elements that completely eliminated CMV and HSV1 replication. They were also able to clear latent EBV from transformed human tumor cells.
A group led by Yasuko Mori in Japan has analyzed the crystal structure of HHV-6B U14, an important accomplishment for the understanding of HHV-6. Human herpesvirus 6B encodes numerous tegument proteins that make up the viral matrix. One of these tegument proteins is U14. In addition to being necessary for viral propagation, it is able to regulate host cell responses by interacting with host factors such as tumor suppressor p53.
Nicola Royle’s laboratory at the University of Leicester in the UK has reported that a ciHHV-6A patient with an HHV-8-negative primary effusion-like lymphoma had fully integrated genomes in the blood, but lost the integration in the tumor. Did the release of HHV-6A genomes play a role in tumor formation?
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 .
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.
Dr. Louis Flamand’s laboratory in Quebec, Canada, has published an article with evidence that points toward a detailed mechanism for inhibition of IL-2 gene expression by HHV-6.
A group from Japan has conducted a retrospective study of 130 patients who underwent stem cell transplantation in an attempt to identify a risk factor for the development of encephalopathy.
HHV-6 encephalitis as a trigger in children with POLG mitochondrial disorders? Two cases of fatal Alpers-Huttenlocher syndrome
We are pleased to announce that with the help of a few HHV-6 specialists, especially Prof. Louis Flamand from Canada, we have generated the monoclonal antibody DR-7.
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