# Chitin and chitinases in SARS-CoV-2 infection > **NIH NIH R21** · WASHINGTON UNIVERSITY · 2024 · $233,250 ## Abstract ABSTRACT Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and resultant coronavirus disease 2019 (COVID-19) has caused a global health crisis, surpassing 100 million infections in the United States. SARS- CoV-2 infections range from asymptomatic to respiratory failure and death, and can result in an array of long- term effects collectively referred to as post-acute sequelae of SARS-CoV-2 infection (PASC). The pathobiological mechanisms and environmental factors underlying the intensity and duration of these effects remain unclear, but a range of chronic lung impairments that resemble complications associated with age-related pulmonary fibrosis have been documented in severe COVID-19, suggesting that environmental drivers implicated in pulmonary fibrosis may also influence the course of SARS-CoV-2 infection and PASC. We have identified the environmental constituent chitin as a candidate environmental driver of persistent SARS-CoV-2- induced disease, consistent with its previously described role in pulmonary fibrosis. Our preliminary studies show that chitin spontaneously accumulates in the lungs of SARS-CoV-2-infected mice, and is accompanied by alterations in the expression patterns of the major lung chitinase, AMCase, suggesting that chitin-chitinase interactions may contribute to SARS-CoV-2 pathogenesis. In comparison with wild-type (WT) controls, mice that genetically lack AMCase exhibit exacerbated lung pathology after infection with SARS-CoV-2, implicating chitin and chitinases in the pathologic sequelae that occur during the recovery phase. Thus, we hypothesize that environmental chitin can drive COVID-19 severity, epithelial dysregulation, and disease persistence, and that epithelial chitinases attenuate this process by degrading chitin. In this project, we leverage recently developed mouse models of SARS-CoV-2 infection and chitin exposure to delineate a host-environmental interaction that may contribute to persistent lung impairments following SARS-CoV-2 infection. We will test our hypothesis by addressing two Aims: (1) determine the influence of environmental chitin on the severity and persistence of lung pathology after SARS-CoV-2 infection, and (2) define the role of mammalian chitinases in SARS-CoV-2 infection and persistent lung disease. Understanding how environmental chitin influences long-lasting pathologic responses after SARS-CoV-2 infection may lead to the identification of new biomarkers and therapeutic targets associated with differential disease outcomes in COVID-19 and PASC. ## Key facts - **NIH application ID:** 10851030 - **Project number:** 5R21AI163640-02 - **Recipient organization:** WASHINGTON UNIVERSITY - **Principal Investigator:** Steven Van Dyken - **Activity code:** R21 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 2024 - **Award amount:** $233,250 - **Award type:** 5 - **Project period:** 2023-06-01 → 2025-05-31 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/10851030 ## Citation > US National Institutes of Health, RePORTER application 10851030, Chitin and chitinases in SARS-CoV-2 infection (5R21AI163640-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10851030. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*