Transplant patients born with chromosomally integrated HHV-6 have elevated levels of C-reactive protein and tumor necrosis factor receptor 1, both markers associated with increased risk of acute graft-versus-host disease.
European guidelines recommend treating HHV-6 disease with either foscarnet or ganciclovir, in contrast to the Japanese guidelines that recommend foscarnet as first line treatment due to a lower mortality rate.
Investigators at the Fred Hutchinson Cancer Research Center and University of Washington in Seattle found that HHV-6B in lung fluid of bone marrow transplant recipients with pneumonia is associated with a 2-fold increased risk of death. Importantly, HHV-6B positive patients who were treated with an antiviral had a 60% lower risk of death.
A third of patients with acute liver failure were found to have a betaherpesvirus infection when tested for all herpesviruses. HHV-6 was the most common infection, followed by CMV and HHV-7. No other herpesviruses were found.
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 impact 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.
A rapid point-of-care test for patients with encephalitis and meningitis was heralded as a breakthrough, but because the test is not able to determine ciHHV-6 status or viral load, it now has physicians frustrated over how to interpret a positive result.
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.