Abstract
Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) gains entry into the lung epithelial cells by binding to the surface protein angiotensin-converting enzyme 2. Severe SARS-CoV-2 infection, also known as coronavirus disease 2019 (COVID-19), can lead to death due to acute respiratory distress syndrome mediated by inflammatory immune cells and cytokines. In this review, we discuss the molecular and biochemical bases of the interaction between SARS-CoV-2 and human cells, and in doing so we highlight knowledge gaps currently precluding development of new effective therapies. In particular, discovery of novel treatment targets in COVID-19 will start from understanding pathologic changes based on a large number of autopsy lung tissue samples. Pathogenetic roles of potential molecular targets identified in human lung tissues must be validated in established animal models. Overall, this stepwise approach will enable appropriate selection of candidate therapeutic modalities targeting SARS-CoV2 and the host inflammatory response.
Abstract
A large number of autopsy samples and reliable preclinical animal models are required to understand the inflammatory process in #COVID19 https://bit.ly/3jWUVp4
Footnotes
Conflict of interest: R. Kumar reports grants from the American Heart Association and the ATS Foundation/Pulmonary Hypertension Association during the conduct of the study.
Conflict of interest: M.H. Lee has nothing to disclose.
Conflict of interest: C. Mickael has nothing to disclose.
Conflict of interest: B. Kassa has nothing to disclose.
Conflict of interest: Q. Pasha has nothing to disclose.
Conflict of interest: R. Tuder has nothing to disclose.
Conflict of interest: B. Graham reports grants from the National Institutes of Health during the conduct of the study.
Support statement: R. Kumar avails the American Heart Association Grant (19CDA34730030) and ATS Foundation/Pulmonary Hypertension Association Research Fellowship; B. Graham avails NIH grant R01HL135872; R. Tuder and B. Graham avail NIH grant P01HL014985; and C. Mickael, R. Tuder and B. Graham avail NIH grant P01HL152961. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received June 20, 2020.
- Accepted October 27, 2020.
- Copyright ©ERS 2020
This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.