HHV-6 encephalitis as a trigger in children with POLG mitochondrial disorders? Two cases of fatal Alpers-Huttenlocher syndrome
HHV-6A major capsid protein identified in CSF of MS patients: a case of molecular mimicry?
Two papers published this month highlight the potential of the new 3rd generation PCR assays in the field of HHV-6 diagnostics.
New model of HHV-6A infection demonstrates persistent abortive infection and neuroinflammation via TLR9
Dr. Hollsberg’s team at Aarhus University in Denmark has identified the protein responsible for this crucial mechanism of cell-cycle specific interruption.
While elevated TNF-a detected at the early onset of disease is a strong indicator for the early recognition of HHV-6 reactivation, this finding also reflects important therapeutic information that could be used as an early diagnostic marker of DIHS/DRESS.
Branka Horvat, MD, PhD, Director of Research at the International Centre for Infectiology Research in Lyon, France (INSERM), and her doctoral student Josephine Reynaud have recently published an important paper on a new transgenic mouse model
Additional evidence that shortened telomeres can cause the release and possible activation of integrated HHV-6.
Dr. Yoshizo Asano and colleagues in Japan report that in measles immunosuppression, cells sensitized to HHV-6B immediate early and early antigen proteins may suppress replication cycles and virus formation, resulting in an “incomplete” subclinical state of reactivation.
We are pleased to announce that with the help of a few HHV-6 specialists, especially Prof. Louis Flamand from Canada, we have generated the monoclonal antibody DR-7.
An international group of experts summarize the significant differences between the two viruses.
A group led by Steven Zeichner has published evidence that suggests the replication of all human herpesviruses can be activated by apoptosis.
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.