Is there a cure for human herpesvirus 6?
2399146#4
Ganciclovir has also been used with some success in treating "Human herpesvirus 6" infections.
Ganciclovir
4160656#36
Human herpesvirus 6 lives primarily on humans and, while variants of the virus can cause mild to fatal illnesses, can live commensally on its host. It has been demonstrated that HHV-6 fosters the progression of HIV-1 upon coinfection in T cells. HHV-6 upregulates the expression of the primary HIV receptor CD4, thus expanding the range of HIV susceptible cells. Several studies also have shown that HHV-6 infection increases production of inflammatory cytokines that enhance in vitro expression of HIV-1, such as TNF-alpha, IL-1 beta, and IL-8. A more recent in vivo study shows HHV-6A coinfection to dramatically accelerate the progression from HIV to AIDS in pigtailed macaques.
Human herpesvirus 6
4160656#84
Finding a treatment can be difficult when HHV-6 reactivation occurs following transplant surgery because transplant medications include immunosuppressants.
Human herpesvirus 6
4160656#37
HHV-6 has also been demonstrated to transactivate Epstein–Barr virus.
Human herpesvirus 6
4160656#15
During maturation of HHV-6 virions, human cell membranes are used to form viral lipid envelopes (as is characteristic of all enveloped viruses). During this process HHV-6 utilizes lipid rafts, which are membranous microdomains enriched by cholesterol, sphingolipids, and glycosylphosphatidylinositol-anchored proteins. Early researchers suspected that HHV-6 virions mature in the nucleus; some even incorrectly published this, as they generalized and applied to HHV-6 what was known about other viruses. However, researched published in 2009 suggests that the HHV-6 virus utilizes trans-Golgi-network-derived vesicles for assembly.
Human herpesvirus 6
5735705#2
Human cytomegalovirus (HCMV, HHV-5) "seems to have a large impact on immune parameters in later life and may contribute to increased morbidity and eventual mortality." Human herpesvirus 6A (HHV-6A) has been described as more neurovirulent, and as such is more frequently found in patients with neuroinflammatory diseases such as multiple sclerosis. Both human herpesvirus 6B (HHV-6B) and human herpesvirus 7 (HHV-7), as well as other viruses, can cause a skin condition in infants known as exanthema subitum, roseola infantum (rose rash of infants) or the sixth disease.
Betaherpesvirinae
4160656#41
Transmission is believed to occur most frequently through the shedding of viral particles into saliva. Both HHV-6B and HHV-7 are found in human saliva, the former being at a lower frequency. Studies report varying rates of prevalence of HHV-6 in saliva (between 3–90%), and have also described the salivary glands as an in vivo reservoir for HHV-6. The virus infects the salivary glands, establishes latency, and periodically reactivates to spread infection to other hosts.
Human herpesvirus 6
4160656#33
A number of genes expressed by HHV-6 are unique to its inactive latency stage. These genes involve maintaining the genome and avoiding destruction of the host cell. For instance, the U94 protein is believed to repress genes that are involved in cellular lysis (apoptosis) and also may aid in telomeric integration. Once stored in human telomeres, the virus is reactivated intermittently.
Human herpesvirus 6
4160656#71
The role of HHV-6 during pregnancy leading to inflammation in the amniotic cavity has been studied.
Human herpesvirus 6
4160656#83
There are no pharmaceuticals approved specifically for treating HHV-6 infection, although the usage of "Cytomegalovirus" treatments (valganciclovir, ganciclovir, cidofovir, and foscarnet) have shown some success. These drugs are given with the intent of inhibiting proper DNA polymerization by competing with deoxy triphosphate nucleotides or specifically inactivating viral DNA polymerases.
Human herpesvirus 6