Impacts of vitamin A deficiency on mucosal immunity to respiratory syncytial virus infection

Abstract

Abstract Human respiratory syncytial virus (RSV) is a leading cause of severe acute lower respiratory tract disease in infants and young children worldwide. Vitamin A (VA) deficiency (VAD) is one of the most prevalent nutrition-related health problems globally. Acute childhood infections have been linked to an increased risk of VAD, while conversely, VAD leads to increased susceptibility to severe respiratory infections. To date, however, the impact of VAD on RSV infection specifically, or on adaptive immune responses in the respiratory tract, remains unexplored. Here, we used the BALB/c mouse model to determine the impact of VAD on RSV infection and lung virus-specific CD8 T cell immunity. Groups of VA sufficient (VAS) and VAD mice were infected with RSV strain A2. On day 8 after infection, antigen-specific CD8 T cell responses were evaluated using tetramer and intracellular cytokine staining and ELISA assays for IFNγ secretion in cell supernatants. Although no changes in morbidity and mortality were observed between groups, CD8 T cells from VAD animals showed significantly impaired production of IFNγ, suggesting changes in the Th1 balance of the lungs in the context of VAD. Future experiments will focus on changes in the innate and adaptive immune systems in the lungs during VAD and downstream effects on the response to RSV infection.