Mila Ortigoza, MD, PhD

The flu virus has a remarkable ability to spread among people, but we still do not fully understand what makes an infected person contagious. To explore this, we developed a model using baby mice to study how both the virus and the host’s response to infection affect contagiousness. We discovered that flu infection in mice triggers a strong immune reaction called inflammation, which is the body's first line of defense against infection. Interestingly, highly contagious flu viruses provoke a stronger inflammatory response than less contagious ones. This response increases genetic and protein activity in the nose, leading to more phlegm production, which is a key cause of a “runny nose.” While inflammation is typically a sign of the body fighting an infection, our findings suggest that certain immune responses can unintentionally boost virus spread. This study highlights the virus’s clever ability to use the host’s defense system to maximize its transmission.

Funded in Memory of Richard Starr

Update: Our research has reached a major turning point with the submission of a landmark manuscript revealing a hidden driver of influenza transmission. We have identified a specific molecule in our own immune system, Interferon-gamma (IFN-γ), acts as a master switch for contagiousness. Using our specialized mouse model, we showed that highly transmissible flu strains hijack this immune response to trigger a "hyper-secretory" state: a flood of mucus and inflammation in the nose that literally flushes the virus out of the host and into the environment. This finding fundamentally rewrites the rules of virology: it shows that being contagious is not just a side effect of the virus growing, but a direct consequence of the body’s own attempt to clear the infection. By uncovering this mechanism, we are opening the door to new treatments that can stop the community's spread of respiratory viruses by "calming" these pro-shedding pathways without interfering with the body's ability to heal.