4.7 Review

Virus infection induced pulmonary fibrosis

Journal

JOURNAL OF TRANSLATIONAL MEDICINE
Volume 19, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12967-021-03159-9

Keywords

Virus infection; Pulmonary fibrosis; Mechanisms; SARS-CoV-2; Potential anti-fibrotic therapy

Funding

  1. National High-Level Talents Program
  2. National Natural Science Foundation of China [81770015]
  3. Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program [2017BT01S155]
  4. Open Project of State Key Laboratory of Respiratory Disease [SKLRD-OP-202109]
  5. Special Fund for Science and Technology Innovation of Guangdong Province [2020B1111330001]
  6. Guangzhou Institute of Respiratory Health Open Project (China Evergrande Group)Project [2020GIRHHMS16]

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Pulmonary fibrosis, the end stage of various lung diseases, may be triggered by virus infection, but the specific mechanisms are not fully understood. Studying the relationship between pulmonary fibrosis and various viruses, as well as the infection mechanisms, may provide insights into potential anti-fibrotic treatment targets.
Pulmonary fibrosis is the end stage of a broad range of heterogeneous interstitial lung diseases and more than 200 factors contribute to it. In recent years, the relationship between virus infection and pulmonary fibrosis is getting more and more attention, especially after the outbreak of SARS-CoV-2 in 2019, however, the mechanisms underlying the virus-induced pulmonary fibrosis are not fully understood. Here, we review the relationship between pulmonary fibrosis and several viruses such as Human T-cell leukemia virus (HTLV), Human immunodeficiency virus (HIV), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Murine gamma-herpesvirus 68 (MHV-68), Influenza virus, Avian influenza virus, Middle East Respiratory Syndrome (MERS)-CoV, Severe acute respiratory syndrome (SARS)-CoV and SARS-CoV-2 as well as the mechanisms underlying the virus infection induced pulmonary fibrosis. This may shed new light on the potential targets for anti-fibrotic therapy to treat pulmonary fibrosis induced by viruses including SARS-CoV-2.

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