Different progress of MDCK cell death after infection by two different influenza virus isolates

Abstract

The effect of influenza strains A (H3N2) and B, isolated during the seasons of 1994 and 1995 in the Czech Republic, on MDCK cells was studied. Various concentrations of virus and conditions of nutrition were used during the cell culture. The virus replication and consequently fragmentation of genomic DNA together with cytotoxicity were investigated in the absence and presence of 10 per cent calf serum. Virus replication, regardless of type A or B, caused earlier DNA fragmentation in comparison to non-infected cells in tissue culture. The results showed that the influenza B strain had a greater cytotoxic effect on MDCK cells than influenza A. A higher infection dose of influenza A virus accelerated the onset of apoptosis; conversely, a higher infection dose of influenza B virus delayed the onset of apoptosis. The absence of serum enhanced the progress of influenza-induced apoptosis in conditions in vitro.

A single NS2 mutation of K86R promotes PR8 vaccine donor virus growth in Vero cells

“…Many strategies have been applied for the development of efficient, robust, scalable cellbased influenza vaccine production systems, including experimentation with the culture conditions, cellular metabolism and the bioreactor model (Hornickova, 1997;Kaverin and Webster, 1995;Mohler et al, 2005). Efforts have also been made to modify the vaccine strain genetically to improve viral growth and vaccine production.…”

The 2009 Pandemic H1N1 and Triple-Reassortant Swine H1N1 Influenza Viruses Replicate Efficiently but Elicit an Attenuated Inflammatory Response in Polarized Human Bronchial Epithelial Cells

“…These cytokines and chemokines are of particular interest because they are produced by a variety of pulmonary cells and can instigate a cascade of physiological changes, including recruitment, proliferation, and activation of immune cells. In particular, a key regulator of virus-induced interferon production, RNA helicase RIG-I, and the interferon-stimulated gene 15 (ISG-15) (13,30). Apoptosis is known to be induced by several influenza virus subtypes through both extracellular and intracellular apoptotic pathways and can contribute to the pathogenesis of influenza.…”

“…Influenza virus infection of epithelial cells of the airway results in cellular apoptosis or necrosis (13,30). Apoptosis is known to be induced by several influenza virus subtypes through both extracellular and intracellular apoptotic pathways and can contribute to the pathogenesis of influenza.…”

A review of mathematical models of influenza A infections within a host or cell culture: lessons learned and challenges ahead

“…Lifespan of interferon 3.5h [74], 60h [75] Direct experimental measures Average lifespan of an infected cell 12-48h [80][81][82][83][84][85][86] Average infectious lifespan of a virion 0.5-3h [87][88][89][90] Length of the latent (eclipse) phase 3-12h [42,80,[82][83][84]87,88,[91][92][93] Lifespan is defined as the inverse of the rate parameters (the sometimes alternatively used half-life contains an extra factor of log( 2)). Note that some of the studies are in vitro and some in vivo.…”