A team of researchers at Kyoto University in Japan reported that rapid lymphocyte expansion is a good predictive factor for increased HHV-6 reactivation, as well as reduced CMV antigenemia. Patients with aplastic anemia as a primary disease had a 5 fold increased risk of HHV-6 reactivation.
Japanese investigators found that those who were administered mycophenolate mofetil along with a calcineurin inhibitor developed a much higher rate of infection: 12% in cord blood and 6% in other transplants.
A new method to assess antiviral activity against DNA viruses has been developed, using automated format and qPCR to measure the accumulation of viral DNA. Of the FDA approved drugs, foscarnet showed the highest selectivity index for HHV-6B.
Chinese investigators found a high prevalence of HHV-6 and Epstein Barr virus in the brain tissues of children with Rasmussen’s encephalitis but in none of the controls. There was a significant association between viral presence and brain atrophy, raising a strong suspicion for the involvement of both viruses.
In a study led by Manfred Marschall German investigators analyzed the potency of novel pyrrolopyridine-class compounds and found one that is highly active against CMV and HHV-6A. It works at an early stage of viral protein production, and differs from ganciclovir in mechanism.
Swedish investigators set out to uncover the pathways that HHV-6B might utilize in triggering MTLE. They found that HHV-6B infection altered expression of MAPK genes, suggesting a possible pathogenic mechanisms of HHV-6B in mesial temporal lobe epilepsy.
NINDS investigators found that children with febrile seizures have elevated inflammatory cytokines compared to healthy controls and children with fever. One of those cytokines, Il-1β, correlated with HHV-6 saliva viral load.
HHV-6 was found more frequently in the Purkinje cells of bipolar and major depressive disorder patients compared to controls. Furthermore HHV-6A was associated with a reduced Purkinje cell size. HHV-6 was not found, however in patients with schizophrenia.
German investigators suggest that silencing of HHV-6A by the ND10 complex may explain why HHV-6A is more likely than other herpesviruses to establish a quiescent infection.
Investigators in Spain and Italy attempted to reduce the rate of acute GVHD in pediatric transplant patients by infusing manipulated stem cells. Not only was there no reduction in expected acute GVHD, the patients experienced an unusually high rate of HHV-6 disease.
Investigators from Japan looked at HHV-6 and HHV-7 DNA levels in saliva to see if they might be biomarkers for cancer-related fatigue (CRF) in multiple myeloma patients.
German investigators have identified a marker for what they believe is the earliest stage of viral reactivation, or “transactivation” marked by transcription of several viral small non-coding RNAs in the absence of detectable viral replication. The group believes that these viral small RNAs could be developed as biomarkers.
Investigators at Mt Sinai used “big data” models to determine that the genes involved with fighting Alzheimer’s are the same ones that fight virus. They found HHV-6A and HHV-7 to be more abundant in Alzheimer’s brains, and singled out HHV6-A as a key modulator of the genes involved in amyloidosis and neuronal death.
Researchers at Harvard studied how neurons responded to the presence of herpesviruses HSV1 and HHV-6, and found that they rapidly induce amyloid plaque production within 24 to 48 hours.
Large insurance data studies in Taiwan have found that seniors with shingles or serious HSV1 infections have a 2-3 fold increased risk of certain forms of dementia, and that antiviral treatment can reduce that risk by 90%.