GENERAL DATA: Human herpesvirus 6 (HHV-6) infects 90% of the human population before the age of 4 years, recognized as a childhood disease (sixth disease) or with no clinical manifestation. HHV-6 DNA has partial homogly with cytomegalovirus DNA. Two variants, A and B, are known. The main target cells are CD4+ T cells and macrophages via a partially elucidated mechanism. Primary infection is followed by a latency period and episodes of reactivation. Truly protective targets of the immune response are unknown. POORLY UNDERSTOOD NATURAL HISTORY: In organ transplant or hematopoietic stem cell recipients, the natural history of HHV-6 infection is difficult to establish because of small sample size in certain series, the lack of controls both for patients and samples and differences in the sensitivity of diagnostic tests. Serology is non-specific and cannot be used to study reinfection. Different studies have relied on culture and isolation, detection of viral antigens with monoclonal antibodies and PCR using mononucleated cells, serum and plasma.
Pathogenicity: In heart transplant recipients, HHV-6 infection can cause hepatitis and pancreatic or upper digestive tract disorders. It has also been suggested that HHV-6 could cause complications in liver transplant recipients and be involved in rejection episodes after kidney transplantation. In bone marrow graft recipients, HHV-6 could cause early onset interstitial pneumopathy, myelosuppression phenomena and aggravated graft versus host reactions. Nevertheless, viral DNA has been found in certain healthy controls. OTHER POSSIBILITIES: HHV-6 could also be a co-factor worsening cytomegalovirus infections as has been suggested in liver, heart and bone marrow recipients. A few cases of HHV-6 encephalitis have been reported in the literature and would appear to be authentic in transplanted or grafted subjects. Ganciclovir is effective. However, the practical clinical impact of HHV-6 infection remains to be established.