Antiviral therapeutic approaches for human rhinovirus infections

Casanova, Victor; Sousa, Filipa H; Stevens, Craig; Barlow, Peter G

Modulation or targeting of host molecules responsible for facilitating infection and viral replication may also provide a valuable therapeutic avenue for the therapeutic treatment of RV. One area of interest has focused upon the innate antiviral response, which results in broad range protection from infection, and was attributed to interferons [99] . Purification and further study of interferons found that they were devoid of inherent antiviral activity, but stimulated the production of other antiviral molecules [100, 101] , which led coining of the phrase 'antiviral state'. Upon recognition of pathogens by cellular sensors including TLRs and RLRs, the type I IFNs (IFN-α and IFN-β) and type III IFNs (IFN-λ) are some of the earliest immune mediators to be produced (reviewed in [102] ). Their subsequent binding to the interferon receptor induces expression of several interferon-stimulated genes, resulting in powerful antiviral and immunomodulatory effects to limit infection [103] . Features of this induced antiviral state include resistance to viral replication, induction of apoptotic cell death and increased expression of major histocompatibility complex class I in infected cells. Interferons also have an impact on immune cells, activating dendritic cells (DCs) and macrophages, and stimulating NK cells to enhance their cytolytic activity [104] . This multifaceted, broad-spectrum protection is key to successful antiviral responses.