ACE2 Expression is Increased in the Lungs of Patients with Comorbidities Associated with Severe COVID-19

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Abstract

Patients who died from COVID-19 often had comorbidities, such as hypertension, diabetes, and chronic obstructive lung disease. Although angiotensin-converting enzyme 2 (ACE2) is crucial for SARS-CoV2 to bind and enter host cells, no study has systematically assessed the ACE2 expression in the lungs of patients with these diseases. Here, we analyzed over 700 lung transcriptome samples of patients with comorbidities associated with severe COVID-19 and found that ACE2 was highly expressed in these patients, compared to control individuals. This finding suggests that patients with such comorbidities may have higher chances of developing severe COVID-19. Correlation and network analyses revealed many potential regulators of ACE2 in the human lung, including genes related to histone modifications, such as HAT1, HDAC2, and KDM5B. Our systems biology approach offers a possible explanation for increase of COVID-19 severity in patients with certain comorbidities.

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Author and article information

Journal

Journal ID (nlm-ta): J Infect Dis

Journal ID (iso-abbrev): J. Infect. Dis

Journal ID (publisher-id): jid

Title: The Journal of Infectious Diseases

Publisher: Oxford University Press (US )

ISSN (Print): 0022-1899

ISSN (Electronic): 1537-6613

Publication date (Electronic): 11 June 2020

Electronic Location Identifier: jiaa332

Affiliations

[1 ] Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil

[2 ] Department of Bioengineering, University of Washington, Seattle, WA, USA

[3 ] Neuroimmune Interactions Laboratory – Department of Immunology – Institute of Biomedical Sciences - University of Sao Paulo, Sao Paulo, Brazil

[4 ] Scientific Platform Pasteur USP, São Paulo, Brazil

Author notes

Corresponding author information: Helder I Nakaya, PhD, Av. Prof. Lúcio Martins Rodrigues, 370, block C, 4th floor, São Paulo – SP – Brazil, CEP: 05508-020, Phone: + 55 11 2648-1130, e-mail: hnakaya@ 123456usp.br

These authors contribute equally to this work.

Article

Publisher ID: jiaa332

DOI: 10.1093/infdis/jiaa332

PMC ID: 7377288

PubMed ID: 32526012

SO-VID: 682de000-3c33-4ab0-b6d4-0527ee7f1326

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This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.