The fractalkine receptor, cx3cr1, contributes to influenza virus replication
Gresko, Anthony Keith
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Influenza A virus (IAV) places a high disease burden on the human population worldwide, especially in infants and the elderly. Due to the ability of IAV to mutate from year to year, it continues to present difficulties in generating effective methods of control, both with vaccination or antiviral therapies. Investigation of host cell interactions through genome-wide screens has provided new targets for therapeutic approaches in disease intervention. The chemokine receptor, CX3CR1, has become increasingly identified as a common host protein involved in viral infections. To begin to address the impact of CX3CR1 on IAV infection, RNA interference (RNAi) studies were performed to investigate the mechanism of CX3CR1 interaction with IAV. RNAi was used for efficient CX3CR1 gene knockdown in vitro followed by IAV infection. Knockdown of CX3CR1 resulted in significantly lower viral titers across multiple IAV strains. Using gene knockout mice, we determined that CX3CR1 was important for IAV replication in vivo at early stages of infection. Immunohistochemistry studies showed production of IAV proteins in CX3CR1 silenced cells but a decrease in total infected cells. These findings suggest that CX3CR1 is involved in the late stages of IAV replication and could provide a new therapeutic target for IAV disease intervention.