BackgroundInfluenza A viruses have an envelope made of a lipid bilayer and two surface glycoproteins, the hemagglutinin and the neuraminidase. The structure of the virus is directly dependent on the genetic makeup of the viral genome except the glycosylation moieties and the composition of the lipid bilayer. They both depend on the host cell and are in direct contact with the environment, such as air or water. Virus survival is important for virus transmission from contaminated waters in the case of wild aquatic birds or from contaminated surface or air for humans.ObjectiveThe objective of this study was to check whether the origin species of the host cell has an influence on influenza A virus survival.MethodThe persistence in water at 35°C of viruses grown on either mammalian cells or avian cells and belonging to two different subtypes H1N1 and H5N1 was compared.ResultsBoth H5N1 and H1N1 viruses remained infectious for periods of time as long as 19–25 days, respectively. However, within the same subtype, viruses grown on mammalian cells were more stable in water at 35°C than their counterparts grown on avian cells, even for viruses sharing the same genetic background.ConclusionsThis difference in virus stability outside the host is probably connected to the nature of the lipid bilayer taken from the cell or to the carbohydrate side chains of the virus surface glycoproteins. Moreover, the long-lasting survival time might have a critical role in the ecology of influenza viruses, especially for avian viruses.
Several cell stresses induce nuclear factor-kappaB (NF-kB) activation, which include irradiation, oxidation, and UV. Interestingly, serum-starving stress-induced NF-kB activation in COS cells, but not in COS-A717 cells. COS-A717 is a mutant cell line of COS cells that is defective of the NF-kB signaling pathway. We isolated genes with compensating activity for the NF-kB pathway and one gene encoded the G protein b2 (Gb2). Gb2 is one of the G protein-coupled receptor signaling effectors. In COS-A717 cells, Gb2 expression is significantly reduced. In Gb2 cDNA-transfected COS-A717 cells, the NF-kB activity was increased along with the recovery of Gb2 expression. Furthermore, serum-starving stress induced the NF-kB activity in Gb2-transfected COS-A717 cells. Consistently, the serum-starved COS cells with siRNA-reduced Gb2 protein expression showed decreased NF-kB activity.These results indicate that Gb2 is required for starvation-induced NF-kB activation and constitutive NF-kB activity. We propose that serum contains some molecule(s) that strongly inhibits NF-kB activation mediated through Gb2 signaling.
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