Bria Coates, MD 

Unlike other respiratory viruses, the novel coronavirus SARS-CoV-2 causes severe illness and death in the elderly, but only rarely causes severe disease in children. Prior exposure to common cold coronaviruses may result in T cells which can initiate an immune response to SARS-CoV-2. These T cells may not mount a strong response against SARS-CoV-2 and may lead to disrupted antiviral responses. We will study whether children are less likely than adults to have these T cells in the blood and nasal mucosa and hence less likely to develop severe COVID-19. We will examine the age-related differences in the body’s response to SARS-CoV-2. Our research will help define protective responses to SARS-CoV-2, identify biomarkers that predict illness severity, and reveal new therapeutic targets. 

Impact of NOD-like receptor signaling in juvenile influenza A virus infection (2015-2016)

Influenza A virus (IAV) is a highly contagious virus that causes respiratory tract infections in up to 40 percent of children each year. Lung injury due to IAV infection is the result of damage from both the virus and the immune system's response to the virus. We have found that juvenile mice infected with IAV show continued activation of two inflammatory signaling pathways even after removal of the virus. This project will determine the contribution of these signaling pathways to the susceptibility of juvenile mice to IAV-induced acute lung injury. We will perform a preclinical trial to determine the effectiveness of three drugs in reducing the severity of IAV infection. Our results may support the use of medications to treat children with IAV-induced acute lung injury.