Recently, the research team led by Professor Tang Xiaoxiao of the SKRLD published a review paper with the title of “Virus Infection Induced Pulmonary Fibrosis” online in the “Journal of Translational Medicine” of the Nature Publishing Group, the UK.

Pulmonary fibrosis is the end stage of a broad range of lung diseases characterized by proliferation of fibroblast cells and extracellular matrix aggregation, accompanied by inflammatory injury and tissue structural disruption, which seriously affects the respiratory function and shows the symptoms of dry cough and progressive breathing difficulty. Several researches indicate that the virus attack will cause the occurrence and development of pulmonary fibrosis. Since the outbreak of the Covid-19 pandemic, the virus-induced pulmonary fibrosis has received more attention. However, its clinical manifestation and specific mechanism are still not clear. Clinically, there are still not treatment strategies and basis for it. Therefore, studying the mechanisms and intervention strategy for pulmonary fibrosis induced by virus such as SARS-CoV-2 is of important significance for finding out the pattern of lesion development or recovery, guiding the clinical practice, reducing the incidence rate of symptoms such as pulmonary fibrosis in patients and increasing the survival rate of patients.

Fig. 1 The main channels of virus-induced pulmonary injury and fibrosis

In this paper, we first introduced two main channels for virus to induce pulmonary fibrosis (Fig. 1). Channel 1: The virus infection causes direct injury, activates the abnormal repair, and ultimately leads to pulmonary fibrosis. Channel 2: The virus infection causes immune-mediated injury, activates the immune cells such as Macrophage, Neutrophil, Eosinophil and Th2 cell, leading to the secretion of a lot of Pro-inflammatory and pro-fibrotic cytokine/factors. The combined action of virus and these factors causes continuous pulmonary injury and ultimately leads to pulmonary fibrosis. Second, this paper systematically states the clinical and experimental evidences of pulmonary fibrosis induced by ten kinds of virus, including Human T-cell leukemia virus, Human immunodeficiency virus, Cytomegalovirus, Epstein-Barr virus, Murine γ-herpesvirus 68, Influenza virus, Avian influenza virus, Middle East Respiratory Syndrome-CoV, Severe acute respiratory syndrome-CoV, Severe acute respiratory syndrome-CoV-2 and deeply analyzed the signaling path and molecular mechanism for the virus-induced pulmonary fibrosis (Fig. 2). In the part of summary and prospect, we further summarized the common or unique mechanism of pulmonary fibrosis induced by various viruses, and focused on the research status and potential treatment targets of pulmonary fibrosis induced by SARS-CoV-2, providing important theoretical basis for clinical treatment and drug research and development.

Fig. 2 Key signaling path and molecular mechanism of virus-induced pulmonary fibrosis

This paper has been funded by programs such as the National Overseas High-level Talent Introduction Program, the National Natural Science Foundation of China and Guangdong Provincial Department of Science and Technology Program for Tackling the Covid-19.

Information about the paper:https://link.springer.com/article/10.1186/s12967-021-03159-9