M. W. Bańbura

TL;DR: It is demonstrated that some neurons may survive (limited) virus replication during primary infection, and these neurons (eight weeks p.i.) harbour EHV-1 and were still able to transmit infection to other cells.

TL;DR: The results allow us to suggest that the actin cytoskeleton participates in EHV-1 infection of primary murine neurons but is not essential, and that other components of the cytos skeleton and/or cellular mechanisms may be also involved during EHVs infection.

TL;DR: It is shown that the ubiquitous human pathogens HHV-1 andHHV-2 induce changes in the mitochondrial morphology and distribution in the early and late phases of productive infection in human keratinocytes (HaCaT cells).

TL;DR: It was shown that during acute EHV-1 infection the majority of infected neurons remained unchanged and survived for more than eight weeks in culture, suggesting some protective mechanisms induced by the virus.

TL;DR: It is shown that starting from the first stages of HHV-1 andHHV-2 infection, an interaction of viral particles with the mitochondrial network occurs, and changes observed in the organization of the mitochondria network and physiology of productively infected neurons provide appropriate conditions for HHV -1 and HHv-2 replication and are required for effective viral spread.