Abstract
Herpes simplex type 1 (HSV-1) is a neurotropic virus that infects many types of cells. Previous studies have demonstrated that oligodendrocytic cells are highly susceptible to HSV-1 infection. Here we analysed HSV-1 infection of a human oligodendrocytic cell line, HOG, and oligodendrocyte precursor cells (OPCs) cultured under growth or differentiation conditions. In addition to cell susceptibility, the role of the major cell receptors for viral entry was assessed. Our results revealed that OPCs and HOG cells cultured under differentiation conditions became more susceptible to HSV-1. On the other hand, viral infection induced morphological changes corresponding to differentiated cells, suggesting that HSV-1 might be inducing cell differentiation. We also observed colocalization of HVEM and nectin-1 with viral particles, suggesting that these two major HSV-1 receptors are functional in HOG cells. Finally, electron microscopy assays indicated that HSV-1 may be also entering OLs by macropinocytosis depending on their differentiation stage. In addition, vesicles containing intracellular enveloped virions observed in differentiated cells point to an endocytic mechanism of virus entry. All these data are indicative of diverse entry pathways dependent on the maturation stage of OLs.
Highlights
Several infectious agents, ranging from mycobacteria to retroviruses, have been proposed to be associated with demyelinating diseases such as Multiple Sclerosis (MS), in which oligodendrocytes (OLs), the myelin-forming cells in the central nervous system (CNS), may be the initial target for the pathogenic onset [1,2,3]
Plaque assay showed a significantly larger number of plaques in cells cultured in differentiation medium (DM) compared to cells cultured in growth medium (GM) when cells are infected with the same viral dose (Figure 1A)
As previously observed [55], we detected an increase of proteolipid protein (PLP) levels in HOG cells cultured in DM (Figure 2A)
Summary
Several infectious agents, ranging from mycobacteria to retroviruses, have been proposed to be associated with demyelinating diseases such as Multiple Sclerosis (MS), in which oligodendrocytes (OLs), the myelin-forming cells in the central nervous system (CNS), may be the initial target for the pathogenic onset [1,2,3]. HSV-1 may be involved in cognitive alterations in bipolar or schizophrenia dysfunctions [15]. Herpesviruses usually infect their hosts for life, after the initial infection of epithelial cells, the virions spread to neurons and establish latent infections in sensory ganglia [16]. The entry of HSV into various cell types follows a complex process [19,20]
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