A recent review explored the complex relationship between respiratory viruses—particularly Influenza A virus and SARS-CoV-2—and chronic lung diseases, such as pulmonary fibrosis.

With respiratory tract infections continuing to pose a major public health threat, understanding how these viruses contribute to chronic lung damage can help protect and treat patients with chronic lung disease. Influenza alone accounts for up to 1 billion infections yearly, and the COVID-19 pandemic demonstrated the need to understand viral-induced lung damage, especially in vulnerable populations such as the elderly.

Pulmonary fibrosis leads to severe breathing difficulties and can result from persistent lung infections. Both influenza A virus (IAV) and SARS-CoV-2 trigger lung inflammation and abnormal healing processes, exacerbating fibrosis. The review emphasized that older adults with pre-existing lung conditions are at heightened risk for this progression.

The researchers noted how the immune system plays a dual role with early immune responses essential in controlling viral infections, but prolonged immune activity often worsens lung damage. Viral infections activate macrophages, which can exacerbate the inflammation contributing to pulmonary fibrosis.

The review published in The American Journal of Pathology also highlighted several therapeutic strategies, including antiviral drugs, anti-inflammatory treatments, and novel immunomodulatory therapies that could potentially halt the progression of fibrosis in individuals with chronic lung disease. The timing of treatments—particularly interferon therapies—emerges as a critical factor in minimizing lung damage.

The researchers noted the pressing need for further research to uncover the molecular mechanisms linking viral infections to chronic lung diseases and fibrosis. This could inform new preventive and therapeutic approaches, including personalized medicine strategies, especially for elderly populations.

The authors declared no conflicts of interest.