Pathogenesis of influenza virus infections: The good, the bad and the ugly
Current Opinion in Virology , Volume 2 - Issue 3 p. 276- 286
The clinical outcome of different influenza virus infections ranges from subclinical upper respiratory tract disease to fatal lower respiratory tract disease. An important determinant in the pathogenesis of these diseases is the tissue tropism of the influenza virus. Furthermore, virulence is often correlated with virus replication and is regulated by multiple virus genes. Host defense against virus infection consists of both innate and adaptive immune responses. However, excessive or dysbalanced immune response may result in lung tissue damage, reduced respiratory capacity, and severe disease or even death. By interdisciplinary efforts to better understand the intricate interaction between virus, tissue, and immune response, we may be able to find new ways to improve the outcome of influenza virus infections.
|virus pathogenesis, Influenza virus, adaptive immunity, host resistance, human, immune dysregulation, immunity, influenza, innate immunity, lung injury, nonhuman, pneumonia, priority journal, review, upper respiratory tract infection, viral tropism, virus gene, virus replication|
|Current Opinion in Virology|
|This work was funded by the European Commission 7th Framework Programme; grant id fp7/223498 - European management platform for emerging and re-emerging infectious disease entities (EMPERIE), This work was funded by the European Commission 7th Framework Programme; grant id fp7/278976 - ANTIcipating the Global Onset of Novel Epidemics (ANTIGONE), This work was funded by the European Commission 7th Framework Programme; grant id fp7/258084 - Pathogenesis and transmission of influenza virus in pigs (FLUPIG)|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Kuiken, T, Riteau, B, Fouchier, R.A.M, & Rimmelzwaan, G.F. (2012). Pathogenesis of influenza virus infections: The good, the bad and the ugly. Current Opinion in Virology (Vol. 2, pp. 276–286). doi:10.1016/j.coviro.2012.02.013