A recent study has provided intriguing insights into the susceptibility of different age groups to respiratory viruses like SARS-CoV-2, the culprit behind COVID-19. Contrary to common assumptions, the research suggests that while older individuals face an elevated risk of contracting the virus, the lungs of young adults may actually be more vulnerable to its effects.
Published on a preprint website, the study, although yet to undergo peer review, sheds light on the contrasting susceptibility of lung tissue to viral replication. Dr. Vipin M. Vashishtha, a member of WHO's Vaccine Safety Net, emphasised that older individuals exhibit less susceptibility to both SARS-CoV-2 and influenza virus replication compared to their younger counterparts. "In contrast to SARS-CoV-2, flu viruses replicate more efficiently in human alveolar cells, leading to stronger innate immune responses," he said in a post on X.
The investigation, led by researchers from the University of Bern in Switzerland, delved into the influence of lung ageing on the replication efficiency of influenza A virus (IAV) and SARS-CoV-2. Utilising precision-cut lung slices (PCLS) technology, a staple in respiratory research, the team analysed samples from donors spanning different age groups.
Remarkably, their findings indicated that influenza viruses, specifically H1N1 and H5N1, replicated within the lung parenchyma with notable efficacy. In contrast, SARS-CoV-2, including both the wild-type strain and the delta variant, exhibited lower replication efficiency in the same environment.
Moreover, the study uncovered a significant distinction in the immune response triggered by each virus. While SARS-CoV-2 infection did not lead to detectable cell death, influenza virus infection induced considerable cytotoxicity and prompted early interferon responses.
These revelations challenge previous assumptions and suggest that age-related susceptibility to severe respiratory diseases like COVID-19 may not solely stem from local viral replication dynamics. Instead, dysregulated immune mechanisms in aged lung tissue might play a pivotal role in determining disease severity. "These findings suggest that aged lung tissue might not favour viral dissemination, pointing to a determinant role of dysregulated immune mechanisms in the development of severe disease," the researchers said.
