Michael Engle

TL;DR: Whereas the immune evasion capabilities and lifelong persistence of herpesviruses are commonly viewed as solely pathogenic, the data suggest that latency is a symbiotic relationship with immune benefits for the host.

TL;DR: In postexposure therapeutic trials in mice, a single dose of humanized E16 protected mice against WNV-induced mortality, and may therefore be a viable treatment option against W NV infection in humans.

TL;DR: It is concluded that antibodies and B cells play a critical early role in the defense against disseminated infection by WNV and Passive transfer of heat-inactivated serum from infected and immune wild-type mice protected μMT mice against morbidity and mortality.

TL;DR: It is demonstrated that in response to WNV infection, neurons secrete theChemokine CXCL10, which recruits effector T cells via the chemokine receptor CXCR3, which leads to a decrease in CX CR3+ CD8+ T-cell trafficking, an increase in viral burden in the brain, and enhanced morbidity and mortality.

TL;DR: The induction of a specific, neutralizing IgM response early in the course of WNV infection limits viremia and dissemination into the central nervous system, and protects against lethal infection.