Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation

Author:

Wang Desheng1,Gomes Marta T.2,Mo Yanfei1,Prohaska Clare C.2,Zhang Lu1,Chelvanambi Sarvesh23,Clauss Matthias A.2,Zhang Dongfang4ORCID,Machado Roberto F.2,Gao Mingqi1,Bai Yang12ORCID

Affiliation:

1. Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, China

2. Division of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN 46202, USA

3. Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA

4. Department of Pharmacognosy, School of Pharmacy, China Medical University, Shenyang 110122, China

Abstract

Pulmonary arterial hypertension (PAH) is a pulmonary vascular disease characterized by the progressive elevation of pulmonary arterial pressures. It is becoming increasingly apparent that inflammation contributes to the pathogenesis and progression of PAH. Several viruses are known to cause PAH, such as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), human endogenous retrovirus K(HERV-K), and human immunodeficiency virus (HIV), in part due to acute and chronic inflammation. In this review, we discuss the connections between HERV-K, HIV, SARS-CoV-2, and PAH, to stimulate research regarding new therapeutic options and provide new targets for the treatment of the disease.

Funder

National Nature Science Foundation of China

National Heart, Lung, and Blood Institute of the National Institutes of Health

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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