Persistent HHV-6 infection in the liver is hard to detect from plasma samples and liver biopsies may miss spotty infections. Bile fluid may be the best method for detecting herpesviruses that are impacting the liver.
A Mayo clinic review of long-term outcome of patients with HHV-6 encephalitis showed that over 60% showed persistent sequelae associated with severe bilateral hippocampal atrophy. Symptoms included anterograde amnesia, aphasia, headaches, confusion and persistent memory deficits.
In a prospective study, patients with HHV-6 infection took longer to recover neutrophils and platelets. They also spent significantly more time in the hospital with complications.
A new study reports a surprisingly low rate of HHV-6 reactivation in recipients of half-matched bone marrow grafts using a reduced-intensity conditioning regimen. The authors speculate that the corticosteroid used for prophylaxis may have suppressed cytokine production which in turn limited reactivation of HHV-6.
Although foscarnet is widely used for HHV-6 encephalitis, it has never been specifically approved for HHV-6. Japan’s Ministry of Health, Labor and Welfare was the first to approve foscarnet (Foscavir) for the treatment of HHV-6 encephalitis.
Investigators from University of Michigan have demonstrated that murine roseolovirus is a useful homolog for the study of HHV-6 reactivation in lung disease. In a large retrospective study of HCT patients, they also found early HHV-6 reactivation to increase the risk of both idiopathic pneumonia syndrome and non-relapse mortality.
An analysis of 165 central nervous system viral infections by the Center for International Blood and Bone Marrow Transplant Research found that most were positive for HHV-6. The outcome for patients with viral infection was poor with 50% mortality within 6 months and only 30% survival at 5 years.
Investigators from the Children’s Hospital of Mexico found that although CMV caused the biggest increase in risk for liver rejection, HHV-6 was the more important infection associated with rejection of kidney transplants. A single HHV-6 infection resulted in an increased risk of over 5 fold, while a coinfection of EBV, HHV-6 and HHV-7 increased the risk of kidney rejection by over 17 fold.
A team at Stanford reported that 48% of young children with “liver failure of unknown etiology” had high viral loads of HHV-6 in their liver tissues. As a result, Stanford has now instituted routine evaluation for HHV-6 in all children who present with liver failure.
Investigators at University of Washington studied multiple samples to develop an assay that can detect active infection in patients with chromosomally integrated HHV-6. Current quantitative PCR DNA testing cannot determine whether a ciHHV6 patient has active replication.
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.
Although depleting naïve T cells has been successful in preventing acute graft vs host disease in several studies, investigators from Spain reported an unexpectedly high incidence of HHV-6 encephalitis in a cohort of haploidentical transplant patients.
A Japanese study found that unexplained fever and biliary atresia are associated with HHV-6B infection in pediatric transplant patients. 100% of seronegative infants developed a primary infection.
A new meta-analysis published in Biology of Blood and Marrow Transplantation shows that transplant patients who reactivate with HHV-6 are 2-3 times more likely to develop acute GVHD.
German investigators conducted a broad scale analysis of CD8 T cell responses to HHV-6B, identifying novel epitopes with potential for immunotherapy or vaccines. The strongest responses were directed against an epitope from IE-2.