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The role of UL24 in herpes simplex virus infection of polarized epithelial cells

Dridi, Slimane et Pearson, Angela . The role of UL24 in herpes simplex virus infection of polarized epithelial cells In: 16th International Symposium on Microbial Ecology, Montréal, Canada, 12-15 juin 2016, Montréal, Qc, Canada.

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Herpes simplex virus 1 (HSV-1) infects human mucosal, including polarized, epithelia. During primary HSV-1 infection, the virus infects epithelial cells and sensory neurons of the mucosal epithelia and spreads into the trigeminal ganglia, an important site for HSV-1 latency and recurrent productive lytic infection. Our earlier studies showed that the viral UL24protein promotes viral spread between the epithelium and neurons of the trigeminal ganglia. Moreover, the protein affects the subcellular distribution of viral glycoproteins (VGP) implicated in membrane fusion. We propose that studying HSV infection of polarized cells may provide insights into the mechanisms involving UL24 that may not appear in the case of non-polarized cell infection. Caco-2 cells, a human colorectal adenocarcinoma cell line,were grown to confluency on inserts with 3 µm pores in 12-well plates. Measurements of transepithelial electrical resistance were performed to assess permeability and confirm polarization of the cells. The polarized cell cultures were infected either apically or basolaterally at a multiplicity of infection of 10 with the wild-type HSV-1 strain (KOS), the UL24-null virus (UL24X) or the UL24X-Rescue virus. At 24 hours post-infection (h.p.i), supernatants from the apical and basolateral chambers were collected separately and used for plaque assays in order to quantify the virus yields. In the absence of UL24, we observed up to a 10-fold reduction of viral titers as compared to KOS, which is similar to the reduction observed during infection of non-polarized cells. Interestingly, the 10-fold reduction during basolateral UL24X infection was observed mainly in the apical chamber. These data suggest that UL24 is implicated in the polarized sorting of HSV-1 particles. Several apical sorting signals for proteins have been identified including N-linked glycans. HSV envelope glycoproteins are N-glycosylated. To determine if N-glycosylation of VGP is involved in the role of UL24, HSV-infected polarized Caco-2 cells were treated with tunicamycin to inhibit N-glycosylation of the HSV envelope glycoproteins. We found that blocking N-glycosylation did not eliminate the reduction of viral titers observed during UL24X infection as compared to KOS. These data suggest that the reduction of viral titers in the apical chamber due to the loss of UL24 is independent of N-glycosylation. Taken together, our results suggest a possible role for UL24 in apical sorting of HSV-1, which does not involve N-glycosylation

Type de document: Document issu d'une conférence ou d'un atelier
Informations complémentaires: Affiche scientifique
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Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 25 juin 2018 16:53
Dernière modification: 19 oct. 2023 13:16
URI: https://espace.inrs.ca/id/eprint/5927

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