Contributions of CD8 T cells to the pathogenesis of mouse adenovirus type 1 respiratory infection

- CD8 T cells were not essential for control of peak MAV-1 replication in the lungs.
- Clearance of virus from the lungs was delayed in CD8 T cell-deficient mice.
- CD8 T cells were required for virus-induced weight loss and airway inflammation.
- IFN-γ or perforin deficiency did not affect viral replication or airway inflammation.

CD8 T cells are key components of the immune response to viruses, but their roles in the pathogenesis of adenovirus respiratory infection have not been characterized. We used mouse adenovirus type 1 (MAV-1) to define CD8 T cell contributions to the pathogenesis of adenovirus respiratory infection. CD8 T cell deficiency in β2 m-/- mice had no effect on peak viral replication in lungs, but clearance of virus was delayed in β2 m-/- mice. Virus-induced weight loss and increases in bronchoalveolar lavage fluid total protein, IFN-γ, TNF-α, IL-10, CCL2, and CCL5 concentrations were less in β2 m-/- mice than in controls. CD8 T cell depletion had similar effects on virus clearance, weight loss, and inflammation. Deficiency of IFN-γ or perforin had no effect on viral replication or inflammation, but perforin-deficient mice were partially protected from weight loss. CD8 T cells promote MAV-1-induced pulmonary inflammation via a mechanism that is independent of direct antiviral effects.