Human herpesvirus 6 (HHV-6) is a member of the Roseolovirus genus of the Betaherpesvirinae and consists of three distinct but closely related species, human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7. These viruses cause ubiquitous human infection and have important differences in epidemiology and pathogenesis. They establish latency after primary infection, and viral reactivation has been associated with a variety of complications in immunocompromised patients, especially after allogeneic hematopoietic cell transplantation (HCT). HHV-6B is the primary species associated with disease and is the most common infectious cause of encephalitis after HCT.
An important biologic phenomenon unique to HHV-6 is its ability to integrate into human chromosomal telomeres. When this occurs in germ-line cells, vertical transmission of chromosomally integrated HHV-6 (ciHHV-6) results in offspring with at least 1 copy of HHV-6 DNA in every nucleated cell of their body. Population-based studies have estimated this to occur in about 1% of people, and this condition poses considerable diagnostic and therapeutic challenges. Whether individuals with inherited ciHHV-6 can develop HHV-6 reactivation with associated pathogenicity, or other indirect complications, is an area of evolving understanding.
Our research focuses on clinical and translational investigations relating to human herpesvirus 6 (HHV-6) infections in immunocompromised hosts, with a focus on disease associations, risk stratification, and improved diagnostic and therapeutic strategies. Specific areas of interest include understanding the role of HHV-6B reactivation on central nervous system dysfunction and pulmonary disease after transplant, as well as diagnostic strategies and clinical implications of ciHHV-6.