B35-21 Breathless After a Cold: Post-RSV Dermatomyositis-Associated Interstitial Lung Disease

Abstract Introduction Reports of post-viral dermatomyositis with pulmonary involvement have been increasingly recognized. We present a case of post-respiratory syncytial virus (RSV) Anti-Melanoma Differentiation-Associated gene 5 (MDA5) positive dermatomyositis leading to rapidly progressive interstitial lung disease (RP-ILD). Case Description A 37 y/o male with no significant past medical history presented to the hospital with shortness of breath. He was positive for RSV and diagnosed with bilateral multifocal pneumonia. Patient was discharged on Augmentin. Four weeks later, he returned with similar complaints. CT Chest redemonstrated unchanged multifocal PNA pattern with basilar peribronchovascular predominance. Pulmonology was consulted, who performed bronchoscopy with a bronchoalveolar lavage showing macrophage predominance with low lymphocytes. Infectious and malignancy workup were unrevealing. Initially, there were concerns for organizing pneumonia versus an autoimmune disorder. Prednisone was started early on. Despite three months of 20mg/day of Prednisone, the patient became more hypoxic, limiting his ability to work. An extensive autoimmune workup revealed positive MDA5 antibodies on the extended myositis panel. On exam, Gottron’s papules were found bilaterally on his fingers. The patient underwent EBUS of multiple mediastinal lymph nodes, but no evidence of malignancy or lymphoma was found. The patient was started on Mycophenolate Mofetil and Prednisone taper. Discussion In recent years, there has been a surge in serum anti-MDA5-positive dermatomyositis RP-ILD cases preceded by an RNA virus infection (1). The pathogenesis of how the virus triggers this autoimmune response is still unclear. It is theorized that an unidentified viral trigger on the background of genetic predisposition culminates in an acquired type 1 interferonopathy (2). Clinical presentation can vary drastically, but the development of RP-ILD is the most severe complication. RNA viruses known to trigger this autoimmune reaction are SARS-CoV-2, Parvovirus, and Coxsackie virus (2). However, MDA5 is a known cytosolic RNA viral sensor, indicating the propensity for other RNA viruses to trigger dermatomyositis. We describe the first case of post-RSV dermatomyositis with RP-ILD per literature review. Treatment is largely based on observational studies and case reports. Early and aggressive combined immunosuppression has been reported to be successful (2). Further clinical research is needed to determine the most effective combined immunosuppression regimen. References 1. Lattarulo S, Centrone F, Chironna M. Anti-MDA5+ dermatomyositis following SARS-COV-2 infections: a systematic review. Front Immunol. 2025;16:1565803. Published 2025 Sep 2. doi:10.3389/fimmu.2025.1565803 2. Mehta P, Machado PM, Gupta L. Understanding and managing anti-MDA 5 dermatomyositis, including potential COVID-19 mimicry. Rheumatol Int. 2021;41(6):1021-1036. doi:10.1007/s00296-021-04819-1 This abstract is funded by: None