Modeling Ability of Herpes Simplex Virus 1 to Induce Cell-to-Cell Fusion

Session Number

C10

Advisor(s)

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

Location

B-110

Start Date

28-4-2016 8:00 AM

End Date

28-4-2016 8:25 AM

Abstract

Herpes simplex virus type-1 is estimated to be present in around 90% of humans. Although most cases of HSV-1 are latent, the virus still poses a threat, especially to patients with a weak immune system. Once the virus enters a cell and replicates itself using cell machinery, HSV-1 can induce cell-to-cell fusion and form syncytia. The four glycoproteins responsible for syncytia are the same as the 4 necessary for viral entry: gB, gD, and the gH-gL heterodimer. These syncytia are harmful to the body, and they provide some refuge for the virus, protecting it from immune functions. We used CHO-K1 cells, though they are not human, because of their quick reproduction and receptiveness to transfection, a crucial process for this experiment. After transfecting the cells with the viral glycoproteins and a few other essential plasmids, using a Split Luciferase Assay, the presence of syncytia was quantitatively measured. The equation for the curve that best fit the data is y = 14.941e0.3308x where x represents time and y represents Luciferase activity. The experiment was run without glycoprotein gB, and the data was found to be negligible, reaffirming the finding that the four aforementioned glycoproteins are all crucial to syncytia formation.


Share

COinS
 
Apr 28th, 8:00 AM Apr 28th, 8:25 AM

Modeling Ability of Herpes Simplex Virus 1 to Induce Cell-to-Cell Fusion

B-110

Herpes simplex virus type-1 is estimated to be present in around 90% of humans. Although most cases of HSV-1 are latent, the virus still poses a threat, especially to patients with a weak immune system. Once the virus enters a cell and replicates itself using cell machinery, HSV-1 can induce cell-to-cell fusion and form syncytia. The four glycoproteins responsible for syncytia are the same as the 4 necessary for viral entry: gB, gD, and the gH-gL heterodimer. These syncytia are harmful to the body, and they provide some refuge for the virus, protecting it from immune functions. We used CHO-K1 cells, though they are not human, because of their quick reproduction and receptiveness to transfection, a crucial process for this experiment. After transfecting the cells with the viral glycoproteins and a few other essential plasmids, using a Split Luciferase Assay, the presence of syncytia was quantitatively measured. The equation for the curve that best fit the data is y = 14.941e0.3308x where x represents time and y represents Luciferase activity. The experiment was run without glycoprotein gB, and the data was found to be negligible, reaffirming the finding that the four aforementioned glycoproteins are all crucial to syncytia formation.