Sars-Cov-2 Infections Triggers Reduction In Circulating Monocytes That Leads To Persistent Post-COVID Pulmonary Fibrosis


A new study led by researchers from the Department of Medicine, University of Virginia, Charlottesville-USA has found that as a result of SARS-CoV-2 infections causing a reduction in circulating monocytes, the condition of persistent Post-COVID pulmonary fibrosis arises.

The study findings were published on a preprint server and are currently being peer reviewed.

Over 607 million cases of COVID-19 have been documented worldwide, and up to 30% of patients experience persistent symptoms months after illness1–4. Pulmonary fibrosis is common in COVID-19 patients following hospitalization in the intensive care unit (ICU) and mechanical ventilation. 27% of computed tomography (CT)-scanned patients have evidence of fibrosis during hospitalization, which increases to 33% six months after illness5,6.

The mechanisms that govern the resolution or persistence of pulmonary fibrosis associated with severe COVID-19 are largely unknown. There is a need to define the development of pulmonary fibrosis after infection with SARS-CoV-2 and to determine whether COVID-associated pulmonary fibrosis (COVID PF) is similar to progressive pulmonary fibrosis7.

Recent evidence indicates that abnormal immune function plays a significant role in COVID-19 severity8–11. For example, SARS-CoV-2 causes a robust inflammatory response within the lung that can lead to the development of acute respiratory distress syndrome (ARDS), tissue damage, and long-term respiratory dysfunction12–15.

A growing number of studies have begun to characterize COVID PF16–20, but further research is critically needed to identify biomarkers that predict poor outcomes within COVID PF and inform treatment plans. Peripheral immune cells are an ideal diagnostic tool as post-COVID-19 sequelae often manifests as a systemic disorder.

Furthermore, profiling peripheral blood mononuclear cells (PBMCs) has yielded insights into immune dysregulation and markers that predict disease outcomes in patients with idiopathic pulmonary fibrosis (IPF), the most common fibrotic lung disease21–25, setting a precedent that similar methodologies could be applied to COVID PF.

Here, we identify a cohort of COVID-19 patients who had restrictive lung physiology and early CT scan changes consistent with fibrosis more than one month after acute SARS-CoV-2 infection symptoms had resolved. At six-month outpatient follow-up visit, the cohort diverges into two groups: Patients whose physiologic restriction and early fibrotic changes resolved, which we termed “Early-Resolvers” (ER COVID-PF), and those with persistent restriction and pulmonary fibrosis, whom we termed “Late Resolvers” (LR COVID-PF) (Figure 1A).

The objective of our study was to first define immune features that discriminated LR COVID-PF from ER COVID-PF patients by performing single-cell RNA Sequencing and multiplex immunostaining analysis of PBMCs, and to second compare the resultant cellular and molecular signatures with IPF.


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