In vitro studies confirm that the two viruses infect different cell types, and generate different cytopathic effects, cytokine and growth factor responses.
Prevalence of HHV-6A and HHV-6B was evenly divided in HIV+ patients in Western Africa, with over 6.3% positive for HHV-6 A and 5.0% for HHV-6B. HHV-6A was more common among those with a low viral HIV viral load.
Sequencing of over 8,000 individuals were used to determined the prevalence of 94 different viruses. HHV-7 was the most common virus, with HHV-6B and HHV-6A 4th and 5th respectively.
A team in Japan has reports that ciHHV-6A prevalence is influenced by a “founder effect” and is likely derived from a common ancestor. All of the individuals in the small study were found to have HHV-6A integrated into the telomeric region of chromosome 22, a common site of integration.
A new study on HHV-6B shedding in saliva during and after exanthema subitum found that peak detection rates and viral loads occurred during the convalescent period, between 3 to 7 months post-illness. Detection rates were lower in adults than in children suggesting that siblings may be more likely to transmit the virus than parents.
A new study led by Soren Gantt, MD from the University of British Columbia and Lawrence Corey, MD of the University of Washington revealed risk factors for transmission and symptoms of primary human herpesvirus infections among Ugandan infants.
A group from University College London and the University of Zambia has reported that 20.5% of hospitalized infants were positive for HHV-6B, second only to CMV (24.3%). In contrast to previous studies, HHV-6A was found in only 0.3% of patients.
An international group of experts summarize the significant differences between the two viruses.