Could treatment of HHV-6A co-infections slow AIDS progression?
Japanese group identifies several cytokine and chemokine responses associated with HHV-6B encephalopathy.
HHV-6A and HHV-6B each express distinct chemokines that are uniquely capable of activating key inflammatory cytokines.
CD134, a member of the TNF receptor superfamily, has now been shown as a specific entry receptor for HHV-6B.
A laboratory at the University of Wurzburg has published evidence that Chlamydia trachomatis may induce the activation of ciHHV-6.
A group from France has reported new findings which may help explain the mystery behind the increased rates of HHV-6 reactivation and encephalitis observed among umbilical cord blood transplant (CBT) patients.
A new study has reported that the use of Bortezomib, known commercially as Velcade, may increase the risk of HHV-6 reactivation in myeloma patients undergoing stem cell transplantation.
Findings indicate that HHV-6 infection leads to decreased glutathione production, increased oxidative stress, and induces chlamydial persistence during co-infection
A new study from the University of Munchen in Munich, Germany, has identified a subset of CD8+ T cells that specifically recognize HHV-6B and not HHV-6A.
The International Committee for Taxonomy of Viruses has made it official. HHV-6A and HHV-6B are two distinct viruses, each with their own characteristics and disease associations.
In a recent publication, investigators from the University of Massachusetts reported the first fine characterization of the CD4+ T cell response to HHV-6.
The trigger for neurological disease in a subset of patients with MS?