A new study in mice modeling Long COVID has identified persistent subchronic lung and brain injury following SARS-CoV-2 infection, even after the virus is cleared.
Researchers tracked mice after infection with mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). While both viruses caused severe acute illness and weight loss, surviving mice regained weight but showed ongoing tissue damage. Both infections led to prolonged lung inflammation and fibrosis over 28 days. However, influenza-infected mice showed signs of epithelial repair, while SARS-CoV-2 infected mice displayed sustained inflammatory and coagulation pathways, suggesting continued barrier dysfunction.
This divergence suggests that post-viral breathlessness may not follow a single pathway. The SARS-CoV-2 trajectory points to persistent inflammation and remodeling, potentially explaining prolonged dyspnea in some patients.
Furthermore, MA30 infection uniquely increased microhemorrhage frequency and drove persistent neuroinflammation without detectable brain infection. Brain profiling in MA30 mice indicated vascular dysfunction and extracellular matrix remodeling. These findings imply that Long COVID neurological symptoms may stem from inflammatory and microvascular mechanisms rather than direct brain invasion, underscoring the need to monitor cognitive and neuropsychiatric complaints post-SARS-CoV-2 infection.