Does this help explain how HHV-6 causes CFS/AIDS/Autism etc.?
GP96 interacts with HHV-6 during viral entry and directs it for cellular degradation.
Abstract
CD46
and CD134 mediate attachment of Human Herpesvirus 6A (HHV-6A) and HHV-6B
to host cell, respectively. But many cell types interfere with viral
infection through rapid degradation of viral DNA. Hence, not all cells
expressing these receptors are permissive to HHV-6 DNA replication and
production of infective virions suggesting the involvement of additional
factors that influence HHV-6 propagation. Here, we used a proteomics
approach to identify other host cell proteins necessary for HHV-6
binding and entry. We found host cell chaperone protein GP96 to interact
with HHV-6A and HHV-6B and to interfere with virus propagation within
the host cell. In human peripheral blood mononuclear cells (PBMCs), GP96
is transported to the cell surface upon infection with HHV-6 and
interacts with HHV-6A and -6B through its C-terminal end. Suppression of
GP96 expression decreased initial viral binding but increased viral DNA
replication. Transient expression of human GP96 allowed HHV-6 entry
into CHO-K1 cells even in the absence of CD46. Thus, our results suggest
an important role for GP96 during HHV-6 infection, which possibly
supports the cellular degradation of the virus.
