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Visualization of SARS-CoV-2 using Immuno RNA-Fluorescence In Situ Hybridization
Published on: December 23, 2020
Human cell receptors: potential drug targets to combat COVID-19
Pawan Kumar Raghav1, Keerthana Kalyanaraman2, Dinesh Kumar3
1, New Delhi, India. pwnrghv@gmail.com.
Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the coronavirus disease 2019 (COVID-19). The World Health Organization (WHO) has announced that COVID-19 is a pandemic having a higher spread rate rather than the mortality. Identification of a potential approach or therapy against COVID-19 is still under consideration. Therefore, it is essential to have an insight into SARS-CoV-2, its interacting partner, and domains for an effective treatment. The present study is divided into three main categories, including SARS-CoV-2 prominent receptor and its expression levels, other interacting partners, and their binding domains. The first section focuses primarily on coronaviruses' general aspects (SARS-CoV-2, SARS-CoV, and the Middle East Respiratory Syndrome Coronaviruses (MERS-CoV)) their structures, similarities, and mode of infections. The second section discusses the host receptors which includes the human targets of coronaviruses like dipeptidyl peptidase 4 (DPP4), CD147, CD209L, Angiotensin-Converting Enzyme 2 (ACE2), and other miscellaneous targets (type-II transmembrane serine proteases (TTSPs), furin, trypsin, cathepsins, thermolysin, elastase, phosphatidylinositol 3-phosphate 5-kinase, two-pore segment channel, and epithelium sodium channel C-α subunit). The human cell receptor, ACE2 plays an essential role in the Renin-Angiotensin system (RAS) pathway and COVID-19. Thus, this section also discusses the ACE2 expression and risk of COVID-19 infectivity in various organs and tissues such as the liver, lungs, intestine, heart, and reproductive system in the human body. Absence of ACE2 protein expression in immune cells could be used for limiting the SARS-CoV-2 infection. The third section covers the current available approaches for COVID-19 treatment. Overall, this review focuses on the critical role of human cell receptors involved in coronavirus pathogenesis, which would likely be used in designing target-specific drugs to combat COVID-19.
Insights
Understanding the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its host cell receptors, like Angiotensin-Converting Enzyme 2 (ACE2), is crucial for developing effective COVID-19 therapies. This review details viral interactions and potential drug targets.
Area of Science:
- Virology and Molecular Biology
- Immunology
- Drug Discovery
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a global pandemic.
- Understanding viral entry mechanisms and host interactions is critical for therapeutic development.
Purpose of the Study:
- To review the general aspects of coronaviruses (SARS-CoV-2, SARS-CoV, MERS-CoV).
- To identify and discuss host cell receptors and interacting partners of SARS-CoV-2, focusing on Angiotensin-Converting Enzyme 2 (ACE2).
- To explore potential therapeutic strategies against COVID-19 based on viral-host interactions.
Main Methods:
- Literature review of coronaviruses, their structures, and infection modes.
- Analysis of host cell receptors (e.g., ACE2, DPP4, CD147) and their binding domains.
- Discussion of ACE2 expression in various human organs and its role in COVID-19 infectivity.
Main Results:
- Detailed comparison of SARS-CoV-2, SARS-CoV, and MERS-CoV.
- Identification of multiple host receptors and protein targets involved in coronavirus entry.
- Highlighting the critical role of ACE2 in the Renin-Angiotensin system and its implications for COVID-19 pathogenesis and infectivity across different tissues.
Conclusions:
- Human cell receptors, particularly ACE2, are pivotal in coronavirus pathogenesis.
- Targeting these receptors and their interactions offers a promising avenue for developing specific antiviral drugs.
- Understanding ACE2 expression patterns may inform strategies to limit SARS-CoV-2 infection.
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