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 new study reported that HHV-6A infects the lining of the uterus in 43% of women with unexplained infertility but cannot be found in uterine lining of fertile women. Furthermore, the cytokine and the natural killer cell profiles were very different in patients with the infection. HHV-6A was found only in uterine endothelial cells, and not in the blood.
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.
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.
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.
A fifth case of limbic encephalitis associated with GAD antibodies and HHV-6 infection has been reported, this time in an immunocompetent woman with chromosomally integrated HHV-6, epilepsy, and psychosis. The patient’s condition improved (with a drop in GAD antibody titers and stabilization of psychotic symptoms) in response to three weeks of antiviral therapy but relapsed when antiviral therapy was withdrawn.
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.
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 .
An interview with head researcher Nicola Royle, PhD: Should transplant patients & donors be screened?
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.
Bhupesh Prusty and Thomas Rudel of University of Wuerzburg, Germany, in collaboration with Dr. Yasuko Mori of Japan, have shed new light on the long-standing mystery of HHV-6 cell tropsim.
The December 2014 issue of Current Opinions in Virology features a “Special Section on Roseoloviruses.” Top experts in the field contributed a set of 14 reviews that span a wide range of critical topics encompassing the molecular biology and the