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Review
. 2025 Jul 24;14(15):5229.
doi: 10.3390/jcm14155229.

Hematologic and Immunologic Overlap Between COVID-19 and Idiopathic Pulmonary Fibrosis

Gabriela Mara  1   2 , Gheorghe Nini  2 , Stefan Marian Frenț  3 , Coralia Cotoraci  4
Affiliations
Review

Hematologic and Immunologic Overlap Between COVID-19 and Idiopathic Pulmonary Fibrosis

Gabriela Mara et al. J Clin Med. .

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing lung disease characterized by chronic inflammation, vascular remodeling, and immune dysregulation. COVID-19, caused by SARS-CoV-2, shares several systemic immunohematologic disturbances with IPF, including cytokine storms, endothelial injury, and prothrombotic states. Unlike general comparisons of viral infections and chronic lung disease, this review offers a focused analysis of the shared hematologic and immunologic mechanisms between COVID-19 and IPF. Our aim is to better understand how SARS-CoV-2 infection may worsen disease progression in IPF and identify converging pathophysiological pathways that may inform clinical management. We conducted a narrative synthesis of the peer-reviewed literature from PubMed, Scopus, and Web of Science, focusing on clinical, experimental, and pathological studies addressing immune and coagulation abnormalities in both COVID-19 and IPF. Both diseases exhibit significant overlap in inflammatory and fibrotic signaling, particularly via the TGF-β, IL-6, and TNF-α pathways. COVID-19 amplifies coagulation disturbances and endothelial dysfunction already present in IPF, promoting microvascular thrombosis and acute exacerbations. Myeloid cell overactivation, impaired lymphocyte responses, and fibroblast proliferation are central to this shared pathophysiology. These synergistic mechanisms may accelerate fibrosis and increase mortality risk in IPF patients infected with SARS-CoV-2. This review proposes an integrative framework for understanding the hematologic and immunologic convergence of COVID-19 and IPF. Such insights are essential for refining therapeutic targets, improving prognostic stratification, and guiding early interventions in this high-risk population.

Keywords: COVID-19; cytokine storm; endothelial dysfunction; fibrosis; idiopathic pulmonary fibrosis; immune dysregulation; thrombosis.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Mechanistic link between idiopathic pulmonary fibrosis and hematologic vulnerability.
Figure 2
Figure 2
Schematic representation of overlapping mechanisms in COVID-19 and IPF.
See this image and copyright information in PMC

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