Analysis of intensity and distribution of total chondroitin sulfate, CHST15 and ARSB immunohistochemistry in sections from SARS-CoV-2-infected lungs demonstrated marked increase in chondroitin sulfate and prominence of vascular-associated CHST15, in contrast to decline in ARSB.1 These findings were similar to those observed in diffuse alveolar damage from other causes and suggest that accumulation of chondroitin sulfate might be a significant component in refractory lung disease and pulmonary fibrosis. Here, CHST15 is linked to pulmonary fibrosis.