Abstract
Herpes simplex virus-1 (HSV-1) causes a wide range of infections from mild to life-threatening in the human population. There are effective treatments for HSV-1 infections that are limited due HSV-1 latency and development of resistance to current therapeutics. The goal of this study was to investigate the antioxidant and antiviral effects of embelin on HSV-1 in cultured Vero cells. Oxidative stress was verified by an extensive production of a reactive oxygen species (ROS) H2O2. Vero cells were infected with a recombinant strain of HSV-1 and antiviral assays, time course attachment, penetration, and post penetration assays, confocal microscopy, qPCR, and antioxidant assays were conducted. Our results lead to the conclusion that embelin is noncytotoxic at concentrations tested ranging from 20 to 70 µM. Treatment of HSV-1 virions with embelin resulted in 98.7–100% inhibition and affected the early stage of HSV-1 infection of Vero cells, by inhibiting the attachment and penetration of HSV-1 virions to host cells. Treatment of virions with concentrations of embelin ranging from 35 to 60 µM significantly reduced the production of H2O2. In conclusion, embelin reduces oxidative damage caused by HSV-1 infection and is an effective antiviral to reduce the infection of HSV-1 in cultured Vero cells. Further studies are needed to explore the possibility of embelin as a medicinal agent.
Highlights
Herpes simplex virus-1 (HSV-1), a member of the family Herpesviridae, subfamilyAlphaherpesvirinae, is an enveloped virus with a double-stranded DNA genome that causes a wide range of infections in humans from mild, uncomplicated mucocutaneous infections to life-threatening ones [1]
The goal of this study is to investigate the antiviral effects of the antioxidant embelin on HSV-1 in cultured Vero cells
Vero cells were treated with increasing concentrations of embelin, up to 70 μM concentration and 2% dimethyl sulfoxide (DMSO) [27] the maximum percentage of DMSO in this assay was
Summary
Herpes simplex virus-1 (HSV-1), a member of the family Herpesviridae, subfamilyAlphaherpesvirinae, is an enveloped virus with a double-stranded (ds) DNA genome that causes a wide range of infections in humans from mild, uncomplicated mucocutaneous infections to life-threatening ones [1]. Entry of the virus to initiate lytic infection involves multiple surface glycoproteins [glycoprotein B (gB), glycoprotein C (gC), glycoprotein D (gD), glycoprotein H (gH), and glycoprotein L (gL)] interacting with surface receptors on the host cell. A number of cell receptors interact with gD Some of these known receptors include the herpes virus entry mediator, nectin-1, and 3-O-sulfated heparan sulfate [8,9]. This induces a conformational change leading to the formation of a fusion complex composed of gB, gH, and gL. Following entry of the virus into the cytoplasm, the virus particles travel to the nucleus where the viral DNA enters through the nuclear pore complex, and the viral genome replicates and is transcribed [11].
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