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Published in Clinical & Translational Immunology, the study looked at how age impacts the composition of immune cells in the lung and how these changes influence the ability of the tissue to respond following exposure to influenza or SARS-CoV-2.

Researchers took lung tissue from organ donors of various ages, infected the tissue with either influenza virus or SARS-CoV-2 and looked at how the tissue responded to the infection.

University of Melbourne Dr Linda Wakim, Laboratory Head at the Doherty Institute, and senior author on the paper, explained that following infection with the flu, adult tissue produced a lot of inflammatory factors known to be able to limit virus replication.

“Interestingly, infection in the lungs of elderly donors did not result in this same rapid and robust antiviral response,” Dr Wakim said.

“We were able to link this lag in antiviral response in the elderly to an age-associated decay of a specific immune cell in the lung, termed CD8+ tissue resident memory T cells, an immune cell designed to kill virus-infected cells.”

They speculated that this loss of the local memory T cell pool may, in part, explain the increased vulnerability of the elderly to respiratory infections.

Dr Wakim explained that a better understanding of age-associated changes that occur in the lung immune response will allow for the development of strategies that boost or preserve these immune cells.

“This will enhance local antiviral immune responses, and in turn improve the capacity of the elderly to combat respiratory infections,” Dr Wakim said.

When they infected the tissue with SARs-CoV-2, neither the adult nor the elderly tissue could generate a rapid antiviral response.

This characteristic of the SARs-COV-2 virus, of not initially triggering a robust antiviral response, has already been described by other studies.