Lung inflammation drives Long Covid

Abstract

Although great strides have been made in understanding and mitigating acute manifestations of COVID-19, post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (PASC) or “Long Covid”—which includes long-term lung, neurological, and cardiovascular complications—remains a substantial burden to patients and the health care system. The mechanisms that underlie PASC are not clear, but aberrant immune responses have been implicated. On page 1054 of this issue, Wei et al. (1) report dysfunction in alveolar macrophages—lung-resident immune cells involved in tissue repair—as a contributing factor to persistent lung pathology after SARS-CoV-2 infection. Loss of peroxisomes (organelles involved in oxidative reactions and metabolism) from these macrophages after infection in mice (Mus musculus) resulted in impaired regeneration of lung tissue and persistent fibrosis—scar tissue harmful to lung function. These findings elucidate the etiology of post-viral lung disease and suggest avenues for therapeutic intervention.