Event Title

The Role of Autophagy in HSV-Mediated Cell to Cell Fusion

Session Number

C11

Advisor(s)

Dinesh Jaishankar, University of Illinois at Chicago
Shrey Patel, University of Illinois at Chicago
Deepak Shukla, University of Illinois at Chicago

Location

B-131 Grainger

Start Date

28-4-2016 10:40 AM

End Date

28-4-2016 11:05 AM

Disciplines

Biology

Abstract

Herpes simplex virus type-1 (HSV-1) is a widely prevalent virus and 67% of the world’s population is latently infected by the virus. One of the ways through which HSV-1 can spread is cell-to- cell fusion of infected and uninfected cells mediated by viral envelop glycoproteins. So far, there has been no cure against HSV-1 infection or its spread. Previous studies in our lab suggest that autophagy, a constructive degradative process that promotes cellular homeostasis, has important roles in several steps of HSV-1 lifecycle. However, it is unclear whether autophagy can influence virus-mediated plasma membrane fusion. Therefore, the aim of this study was to determine if autophagy has an effect on cell-to-cell fusion. For our studies a virus-free cell fusion assay was used. In this surrogate assay, the membrane fusion was mediated by expressing four viral glycoproteins, called gB, gD and gH-gL, in cells that mimic a viral infection. Pharmacological inducers and inhibitors of autophagy were administered to vary the levels of autophagy in virus-like cells that tend to fuse with neighboring cells. Our results show that suppressing or inducing autophagy by pharmacological drugs heavily alters the ability of cells to fuse. The suppressor of autophagy reduced the amount of basal cell-to-cell fusion while the inducer increased the amount of cellto- cell fusion. Thus, our results suggest that autophagy has a significant role in HSV-1 membrane fusion and viral spread pathway.


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Apr 28th, 10:40 AM Apr 28th, 11:05 AM

The Role of Autophagy in HSV-Mediated Cell to Cell Fusion

B-131 Grainger

Herpes simplex virus type-1 (HSV-1) is a widely prevalent virus and 67% of the world’s population is latently infected by the virus. One of the ways through which HSV-1 can spread is cell-to- cell fusion of infected and uninfected cells mediated by viral envelop glycoproteins. So far, there has been no cure against HSV-1 infection or its spread. Previous studies in our lab suggest that autophagy, a constructive degradative process that promotes cellular homeostasis, has important roles in several steps of HSV-1 lifecycle. However, it is unclear whether autophagy can influence virus-mediated plasma membrane fusion. Therefore, the aim of this study was to determine if autophagy has an effect on cell-to-cell fusion. For our studies a virus-free cell fusion assay was used. In this surrogate assay, the membrane fusion was mediated by expressing four viral glycoproteins, called gB, gD and gH-gL, in cells that mimic a viral infection. Pharmacological inducers and inhibitors of autophagy were administered to vary the levels of autophagy in virus-like cells that tend to fuse with neighboring cells. Our results show that suppressing or inducing autophagy by pharmacological drugs heavily alters the ability of cells to fuse. The suppressor of autophagy reduced the amount of basal cell-to-cell fusion while the inducer increased the amount of cellto- cell fusion. Thus, our results suggest that autophagy has a significant role in HSV-1 membrane fusion and viral spread pathway.