In 2012, the Centers for Disease Control and Prevention (CDC) established the Achieving Public Health Impact through Research (APHIR) contract mechanism. APHIR provides CDC's Centers, Institute, and Offices (CIOs) a mechanism that supports multiyear, high impact public health research. Awarded projects supported research on a wide range of topics (e.g., cancer surveillance, HIV education programs, development of biological assays, and evaluation of traumatic brain injury prevention programs) and achieved diverse outcomes (e.g., contribution to the body of knowledge in their field, changes in practice and health service delivery, and capacity building). This article describes how existing impact frameworks and a variety of methods and tools (key informant interviews, online survey, bibliometric analysis, Altmetric and document reviews) were used to identify the outcomes achieved by awarded projects. The approach discussed in this paper can be used to evaluate projects that involve a diversity of activities and outcomes.

BACKGROUND: Emergence of drug-resistant strains of influenza viruses, including avian H5N1 with pandemic potential, 1918 and 2009 A/H1N1 pandemic viruses to currently used antiviral agents, neuraminidase inhibitors and M2 Ion channel blockers, underscores the importance of developing novel antiviral strategies. Activation of innate immune pathogen sensor Retinoic Acid Inducible Gene-I (RIG-I) has recently been shown to induce antiviral state. RESULTS: In the present investigation, using real time RT-PCR, immunofluorescence, immunoblot, and plaque assay we show that 5'PPP-containing single stranded RNA (5PPP-RNA), a ligand for the intracytoplasmic RNA sensor, RIG-I can be used as a prophylactic agent against known drug-resistant avian H5N1 and pandemic influenza viruses. 5'PPP-RNA treatment of human lung epithelial cells inhibited replication of drug-resistant avian H5N1 as well as 1918 and 2009 pandemic influenza viruses in a RIG-I and type 1 interferon dependant manner. Additionally, 5'PPP-RNA treatment also inhibited 2009 H1N1 viral replication in vivo in mice. CONCLUSIONS: Our findings suggest that 5PPP-RNA mediated activation of RIG-I can suppress replication of influenza viruses irrespective of their genetic make-up, pathogenicity, and drug-sensitivity status.