Investigators in the UK led by geneticist Nicola Royle, PhD, at the University of Leicester have reported that individuals with inherited HHV-6 (slightly less than 1% of the population) may be at risk for viral reactivation from a virus they inherited from a parent. The British team showed that the telomere (part of the chromosome) with integrated virus tends to be unstable and often shorter than other telomeres in these individuals, increasing the likelihood of chromosomal instability. To their surprise, the team detected extra-chromosomal viral DNA and occasionally circular molecules of HHV-6 that appear to be fully functional, indicating that the viral genome had become excised from the telomere. This may represent the first step towards viral reactivation.  READ MORE

A new study from Italy indicates that HHV-6 reactivation is selectively increased among patients suffering from autoimmune connective tissue diseases (ACTD).  HHV-6 DNA was detected in the serum at a significantly higher rate than controls.  By contrast, the rate of EBV viremia was similar in ACTD patients and controls groups, while CMV, HHV-8, and parvovirus B19 viremia was not detected in any subject. Furthermore, the authors used a highly sensitive assay in their investigation, and identified the median viral load for these patients at under 100 copies/ml, a value that would fall below the current level of detection at most clinical laboratories. The group also found a significant association between HHV-6 reactivation and the active disease state for lupus erythematosus (P = 0.021).  READ MORE

A French group suggests HHV-6 is a cause of confluent necrosis, the most common form of pathology found in liver transplant patients. In the study, liver tissue samples from 26 patients with graft hepatitis of unknown origin were investigated for the presence of HHV-6 DNA. Confluent periportal necrosis was observed in 4 of the 10 HHV-6+ patients, and found to be significantly associated with high viral load. Of note, mild hepatitis was also observed in 4 patients with low intragraft HHV-6 levels, as well as in 2 patients with elevated viral loads (both of these patients were highly immunosuppressed). Interestingly, a clear distinction was observed among patients in the cohort that went on to develop graft hepatitis in the absence of HHV-6.  All cases of HHV-6-negative graft hepatitis disclosed lobular necrotico-inflammatory activity without periportal necrosis.  For this reason, the authors conclude that the presence of confluent periportal necrosis suggests HHV-6-induced graft hepatitis.  READ MORE

Virologist Ursula Gompels from the London School of Hygiene and Tropical Medicine has reported that HHV-6A and HHV-6B each express distinct chemokines that are uniquely capable of activating key inflammatory cytokines.  These inflammatory monocytic cells have also been identified as playing a role in a number of important inflammatory conditions such as multiple sclerosis, artherosclerosis, diabetic nephropathy, cognitive decline in the elderly and Alzehiemer’s Disease.  READ MORE