40,000 people die every year in the U.S. from influenza and secondary infections and anti-biotic resistant bacteria are implicated in many of these cases.
When we’re exposed to a virus, like the flu, special proteins called interferons are released by our cells. These interfere with the virus replication mechanism to help protect us against the infection.
However, 7 days after infection part of this response, known as type I interferon (IFN) signaling, can actually increase susceptibility to secondary infection by antibiotic-resistant bacteria.
In this paper, led by lab postdoc Kelly Shepardson, we delve into the complex dynamics of how this works at a cellular level. Our results reveal that IFN signaling pathways regulate susceptibility to post-influenza infections over time.
Critically, at just 3 days after flu infection (pre-clinical), defense against secondary infections is higher than normal, but then declines leading up to and at day 7 (clinical) of flu infection as previously found. This up-and-down protection is driven by two types of signals: IFN-beta at day 3 and IFN-alpha at day 7.
The implication of this research is that we can now start developing treatments that augment IFN-beta and/or inhibit IFN-alpha production around day 7 post-infection, in order to reduce susceptibility to deadly superinfections.