Tea catechin as antiviral agent via apoptosis agonist and triple inhibitor mechanism against HIV-1 infection: A bioinformatics approach

Abstract

Context: Human immunodeficiency virus (HIV) antiretrovirals that target the binding of viral enzyme are chosen as the lead solution in the treatment of HIV-1 infection, such as non-catalytic site integrase inhibitor (NCINI), nevirapine, and darunavir. There are natural compounds from specific plants that can be effective in treating HIV-1 infection such as tea catechin. Tea catechin administration causes a decrease in viral load and inhibition of entry mechanisms and an increased effect of apoptosis in infected cells. Aims: To identify the triple inhibitor mechanism in tea catechins against the three HIV-1 enzymes and apoptosis agonists through in silico approach as an innovation in handling HIV-1 infection. Methods: The 3D structure of tea catechin compounds from the database was examined, and then all target compounds were analyzed for drug-likeness, molecular docking, pathway prediction, and molecular interactions to determine the potential of tea catechin compounds as antiviral HIV-1 in silico. Results: Tea catechin compounds have the potential to serve as antiviral against HIV-1 through apoptosis agonist and triple inhibitor mechanisms. Apoptosis occurs due to the interaction of tea catechins with pro-apoptotic proteins in cells, and the epigallocatechin gallate (EGCG) compound is a class of tea catechins with the same binding position as control. Conclusions: The binding of the EGCG molecule complex results in low binding energy. Therefore, it allows EGCG acts as a triple inhibitor in HIV-1 infection.