LITERATURE REVIEW ON CORRELATION OF ACE2, TMPRSS2, AND FURIN RELATED TO SARS COV-2

Covid-19 caused by SARS CoV 2 has been pandemic for almost three years. SARS CoV 2 infection in host cells mediated by its surface glycoprotein named Spike protein. The Spike protein, that are settled in inactive form must be cleaved by host proteases to be activated. Proteins that are predict...

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Bibliographic Details
Main Author: Al Jannah, Shofi
Format: Final Project
Language:Indonesia
Online Access:https://digilib.itb.ac.id/gdl/view/69036
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Institution: Institut Teknologi Bandung
Language: Indonesia
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Summary:Covid-19 caused by SARS CoV 2 has been pandemic for almost three years. SARS CoV 2 infection in host cells mediated by its surface glycoprotein named Spike protein. The Spike protein, that are settled in inactive form must be cleaved by host proteases to be activated. Proteins that are predicted to act as important protease in SARS CoV 2 infections are ACE2, TMPRSS2 and Furin. Some research has found polymorphism in ACE2, TMPRSSS2 and Furin that thought to have an influence on SARS CoV 2 infection. Therefore, this study aims to uncovered the role of ACE2, TMPRSS2 and Furin and the effect each polymorphism on SARS CoV 2 varian infection. This study included some journal publish in 2020-2022 from Google scholar and PubMed website. In the present study, ACE2 is the main receptor for SAR CoV 2, meanwhile binding SARS CoV 2 to ACE2 need furin protease as spike activator. Furin activates spike proteins during the biosynthesis of new viral particles which occur in the Golgi membran. Furin activating the Spike by priming the S1/S2 cleavage site. Therefore, RBD can bind to ACE2 efficiently. TMPRSS2 will cleave the S2’ site right after the RBD binds to ACE2 which sequently trigger viral-cell fusion. ACE2, TMPRSS2 and Furin polymorphisms were found to occur in regulatory site and introns, causing an increase or decrease in the expression of each protein. The simultaneous increase in ACE2, TMPRSS2, and Furin was able to make SARS CoV 2 infection in such an optimal conditions, results in an increased risk of infection with SARS CoV 2. However, a decrease in the level of one of the proteins needs to be investigated further. This study is expected to assist the development of drug targeted ACE2, TMRSS2, and Furin, also examine the polymorphisms exist in each protein. Furthermore, the study conducted hopefully can be used as the reference for personalizes medicine especially for individuals with ACE2, TMPRSS2, and Furin Polymorphism.