Function of myosin during entry and egress of equid herpesvirus type 1 in primary murine neurons.

Abstract

Equid herpesvirus type 1 (EHV-1) is a major pathogen of horses with a worldwide distribution, which can cause various clinical signs ranging from mild respiratory disease to neurological disorders. To initiate an effective infection, EHV-1 evolved a broad spectrum of mechanisms exploiting the host cell, including its actin filaments. An actin-myosin-driven transport has been described to precede cellular entry of different viruses. Therefore, in the present study we investigated the role of actin motor protein - myosin, during replication of two EHV-1 strains: Jan-E (wild-type EHV-1 strain isolated from aborted equine fetus) and Rac-H (attenuated strain highly adapted in cell cultures in vitro) in primary murine neurons. In order to investigate this, we used two inhibitors: blebbistatin (BLB; non-muscle myosin II inhibitor) and 2,3-butanedione monoxime (BDM; inhibitor of myosin ATPase). Our results demonstrated that limitation of Jan-E EHV-1 replication occurred in cells treated with myosin inhibitor, which confirmed the important role of actin motor proteins during the entry and egress of EHV-1 virions. Application of blebbistatin did not affect Rac-H EHV-1 replication, while BDM caused reduction of replication in murine neurons. Based on these results it can be assumed that EHV-1 virion movement was myosin-dependent.