INFLUENZA virus
The recent H1N1 influenza pandemic, and the looming threat of a new pandemic evolving out of the highly pathogenic H5N1 avian strains now circulating in Asia, has prompted the use of macaque infection models to better understand influenza pathogenesis and to improve rapid diagnostic, therapeutic, and vaccine strategies. Macaque genomic and proteomic resources are central to maximizing the gains to be realized from this animal model.
Recent studies used cynomolgus macaques to determine the host response to two genetically similar but clinically distinct swine-origin H1N1 isolates from the 2009 pandemic (Safronetz et al.). The pandemic isolates caused greater clinical disease in macaques than did a seasonal strain and also showed heterogeneity in virus replication and transcriptional and cytokine responses that correlated with disease progression.
The cynomolgus macaque model was also used to characterize the host response to the influenza virus that caused the devastating 1918 "Spanish flu" pandemic, which resulted in an estimated 50 million deaths worldwide (Kobasa et al.). This study revealed that the reconstructed 1918 virus replicated to high levels and spread rapidly throughout the respiratory tract of infected animals, causing severe damage and massive infiltration of immune cells. Genomic analyses revealed that the 1918 virus triggered unusually high and sustained expression of numerous genes involved in the innate immune response, including those encoding proinflammatory cytokines and chemokines.