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Like their cellular host counterparts, many invading viral pathogens must contend with, modulate, and utilize the host cell’s chromatin machinery to promote efficient lytic infection or control persistent–latent states. While not intended to be comprehensive, this review represents a compilation of conceptual snapshots of the dynamic interplay of viruses with the chromatin environment. Contributions...
Nonspecific anti-inflammatory drugs have been purported to reduce the burden of severe influenza disease. We demonstrate that, unlike oseltamivir administration, simvastatin administration did not reduce morbidity, mortality, or viral load of mice infected with H1N1 or H5N1 viruses. No added benefit to the efficacy of oseltamivir therapy was observed when mice were treated in combination with simvastatin...
PB1F2 is the 11th protein of the influenza A virus. The protein has variable sizes with truncations either at the C- or N-terminal ends. The most recent example being the 2009 pandemic H1N1 virus which codes for only 11 amino-acids of the C-terminus. A review of the reports since the discovery of PB1F2 in 2001 suggests a multifunctional role for this protein that includes a proapoptotic function in...
The in vivo role of alveolar macrophages in the infections with 2009 pandemic H1N1 influenza virus is not as yet known. Ferret study shows that alveolar macrophages are critical for lowering the risk of severe outcomes in 2009 pandemic H1N1 influenza virus infections. Up to 40% of the infected ferrets depleted of alveolar macrophages died, with elevated body temperature and major loss of body weight...
Human influenza viruses predominantly bind α2,6 linked sialic acid (SA) while avian viruses bind α2,3 SA-containing complex glycans. Virulence and tissue tropism of influenza viruses have been ascribed to this binding preference. We generated 2009 pandemic H1N1 (pH1N1) viruses with either predominant α2,3 or α2,6 SA binding and evaluated these viruses in mice and ferrets. The α2,3 pH1N1 virus had...
Understanding the host response to influenza A virus infection is essential for developing intervention approaches. We show that infection of human alveolar epithelial cells and human bronchial epithelial cells with influenza A for 3h resulted in down-regulation of host hsa-miRNA-548an (miRNA-548an) which triggered the overexpression of influenza non-structural-1A binding protein (IVNS1ABP, herein...
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