Abstract
Pixuna virus (PIXV) is an enzootic member of the Venezuelan Equine Encephalitis Virus complex and belongs to the New World cluster of alphaviruses. Herein we explore the role of the cellular cytoskeleton during PIXV replication. We first identified that PIXV undergoes an eclipse phase consisting of 4 h followed by 20 h of an exponential phase in Vero cells. The infected cells showed morphological changes due to structural modifications in actin microfilaments (MFs) and microtubules (MTs). Cytoskeleton-binding agents, that alter the architecture and dynamics of MFs and MTs, were used to study the role of cytoskeleton on PIXV replication. The virus production was significantly affected (p < 0.05) after treatment with paclitaxel or nocodazole due to changes in the MTs network. Interestingly, disassembly of MFs with cytochalasin D, at early stage of PIXV replication cycle, significantly increased the virus yields in the extracellular medium (p < 0.005). Furthermore, the stabilization of actin network with jasplakinolide had no effect on virus yields. Our results demonstrate that PIXV relies not only on intact MTs for the efficient production of virus, but also on a dynamic actin network during the early steps of viral replication.
Highlights
Pixuna virus (PIXV) is a New World alphavirus from the family Togaviridae and belongs to the Venezuelan Equine Encephalitis (VEE) complex[1]
The main goal of this study was to evaluate the interconnection between the host cell cytoskeleton and PIXV in the course of viral replication
The growth curve we obtained in Vero cells is consistent with the one we previously described in mouse embryonic fibroblasts[15]
Summary
Pixuna virus (PIXV) is a New World alphavirus from the family Togaviridae and belongs to the Venezuelan Equine Encephalitis (VEE) complex[1]. Many studies have previously demonstrated that viruses can use actin microfilaments (MFs) and microtubules (MTs) transport systems to accomplish several steps during their life cycle[7,8,9,10,11]. These steps include: (i) the transport of newly synthesized viral proteins and genomes to specific sites within the infected cell for virus assembly and (ii) the membrane extrusion (viral budding) that ends with the exit of new viral progeny from the infected cell[7,8,9,10,11]. Understanding the relationship of PIXV with the host cytoskeleton will provide a valuable insight into host cell-virus interactions, but may explain the pathogenic properties of VEE viruses
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