Premium
The Effects of EGCG‐stearate on the Cellular Processes of HSV‐1 Infected Vero Cells
Author(s) -
Paschalis Valerie,
Vega Quinn
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.889.10
Subject(s) - vero cell , chemistry , stearate , virology , microbiology and biotechnology , biology , virus , organic chemistry
The Herpes Simplex Virus (HSV) is the cause of oral and genital herpes and infects one in six individuals globally. Epigallocatechin‐3‐gallate (EGCG) is the most common polyphenol derived from green tea, and has been shown to exhibit antioxidant, anticancer, and antiviral properties. Since antiviral medication can only reduce the number of outbreaks but cannot cure herpes, EGCG‐stearate, a lipid‐soluble derivative of EGCG, is of interest as a novel approach to herpes treatment due to its increased stability and antiviral activity. Studies have shown that when HSV is treated directly with EGCG, EGCG damages HSV envelope glycoproteins gD and gB, which are essential for HSV infectivity, resulting in a significant inhibitory effect.While it is known that EGCG has an effect on viral glycoproteins, there is less information regarding the molecular changes that occur in response to EGCG treatment. Receptor tyrosine kinases are ubiquitous on cell surfaces, and tyrosine phosphorylation is part of a major cell‐signaling pathway. The focus of this research is to explore the interaction of EGCG stearate with host African Green Monkey (Vero) cells' receptor tyrosine kinases, as well to test how EGCG‐stearate effects the interactions between the viral glycoproteins and host cell surface receptors during HSV‐1 infection. This study will lend insight into the molecular mechanisms by which EGCG‐stearate interacts with Vero cells infected with HSV‐1 by analyzing EGCG dependent changes in protein tyrosine kinase activity and MAPK family member activity through SDS‐PAGE, Western blotting, and reporter gene assays.