Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

Abstract

Human herpesvirus 6 (HHV-6) is a betaherpesvirus that is closely related to human cytomegalovirus. It was discovered in 1986, and HHV-6 literature has expanded considerably in the past 10 years. We here present an up-to-date and complete overview of the recent developments concerning HHV-6 biological features, clinical associations, and therapeutic approaches. HHV-6 gene expression regulation and gene products have been systematically characterized, and the multiple interactions between HHV-6 and the host immune system have been explored. Moreover, the discovery of the cellular receptor for HHV-6, CD46, has shed a new light on HHV-6 cell tropism. Furthermore, the in vitro interactions between HHV-6 and other viruses, particularly human immunodeficiency virus, and their relevance for the in vivo situation are discussed, as well as the transactivating capacities of several HHV-6 proteins. The insight into the clinical spectrum of HHV-6 is still evolving and, apart from being recognized as a major pathogen in transplant recipients (as exemplified by the rising number of prospective clinical studies), its role in central nervous system disease has become increasingly apparent. Finally, we present an overview of therapeutic options for HHV-6 therapy (including modes of action and resistance mechanisms)

Human herpes virus 6 infection is a hallmark of cord blood transplant in adults and may participate to delayed engraftment: a comparison with matched unrelated donors as stem cell source

“…21 Human herpes virus 6 was discovered in 1986 and two subtypes can be found, type A and type B. HHV6-B is extremely widespread in the population and infects almost all children within the first few years of life establishing latency after primary infection. 22 As expected, none of the cord blood used in this study showed HHV6 positivity 23 and all HHV6 infections were because of the type B virus. 22 Thus, we postulate that HHV6 originates from the reactivation of endogenous HHV6.…”

“…22 As expected, none of the cord blood used in this study showed HHV6 positivity 23 and all HHV6 infections were because of the type B virus. 22 Thus, we postulate that HHV6 originates from the reactivation of endogenous HHV6. Compared with MUD, in which the results were in the range of most reported studies, 22,24,25 CBT showed a significant by higher incidence and an higher median viral load of HHV6 infections and for a longer period of time after transplant.…”

“…22 Thus, we postulate that HHV6 originates from the reactivation of endogenous HHV6. Compared with MUD, in which the results were in the range of most reported studies, 22,24,25 CBT showed a significant by higher incidence and an higher median viral load of HHV6 infections and for a longer period of time after transplant. It was described earlier in three studies but with a short follow-up post transplant.…”

Human herpes virus 6 reactivation: important predictor for poor outcome after myeloablative, but not non-myeloablative allo-SCT

“…To date, only broad-spectrum and relatively toxic antiherpes virus drugs (for example, (val)ganciclovir and foscarnet-sodium) are used in the treatment of HHV6 disease or -reactivation. 8,9 With the progress in molecular diagnostics, better monitoring allows for further elucidation of the role of HHV6 reactivation and therapeutic protocols after HSCT. Therefore, we studied the predictors for HHV6 reactivation and the association of HHV6 reactivation with clinical outcome in adult allogeneic-HSCT recipients.…”

Quantitative HHV-6B antigenemia test for the monitoring of transplant patients

“…Human herpesvirus-6 (HHV-6) is a ubiquitous virus which is widespread throughout the world [1]. Two major subgroups of HHV-6 have been identified, variants A and B, of which variant B is the most common.…”