scholarly journals Role of domestic ducks in the emergence of a new genotype of highly pathogenic H5N1 avian influenza A viruses in Bangladesh

2017 ◽  
Vol 6 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Subrata Barman ◽  
Atanaska Marinova-Petkova ◽  
M Kamrul Hasan ◽  
Sharmin Akhtar ◽  
Rabeh El-Shesheny ◽  
...  
Virology ◽  
2017 ◽  
Vol 503 ◽  
pp. 83-93 ◽  
Author(s):  
Ben Peeters ◽  
Sylvia Reemers ◽  
Jos Dortmans ◽  
Erik de Vries ◽  
Mart de Jong ◽  
...  

2007 ◽  
Vol 4 (1) ◽  
pp. 43 ◽  
Author(s):  
Karoline Bragstad ◽  
Poul H Jørgensen ◽  
Kurt Handberg ◽  
Anne S Hammer ◽  
Susanne Kabell ◽  
...  

2010 ◽  
Vol 84 (6) ◽  
pp. 3068-3078 ◽  
Author(s):  
Mayo Ueda ◽  
Tomo Daidoji ◽  
Anariwa Du ◽  
Cheng-Song Yang ◽  
Madiha S. Ibrahim ◽  
...  

ABSTRACT In this study, we show that the highly pathogenic H5N1 avian influenza virus (AIV) (A/crow/Kyoto/53/04 and A/chicken/Egypt/CL6/07) induced apoptosis in duck embryonic fibroblasts (DEF). In contrast, apoptosis was reduced among cells infected with low-pathogenic AIVs (A/duck/HK/342/78 [H5N2], A/duck/HK/820/80 [H5N3], A/wigeon/Osaka/1/01 [H7N7], and A/turkey/Wisconsin/1/66 [H9N2]). Thus, we investigated the molecular mechanisms of apoptosis induced by H5N1-AIV infection. Caspase-dependent and -independent pathways contributed to the cytopathic effects. We further showed that, in the induction of apoptosis, the hemagglutinin of H5N1-AIV played a major role and its cleavage sequence was not critical. We also observed outer membrane permeabilization and loss of the transmembrane potential of the mitochondria of infected DEF, indicating that mitochondrial dysfunction was caused by the H5N1-AIV infection. We then analyzed Ca2+ dynamics in the infected cells and demonstrated an increase in the concentration of Ca2+ in the cytosol ([Ca2+]i) and mitochondria ([Ca2+]m) after H5N1-AIV infection. Regardless, gene expression important for regulating Ca2+ efflux from the endoplasmic reticulum did not significantly change after H5N1-AIV infection. These results suggest that extracellular Ca2+ may enter H5N1-AIV-infected cells. Indeed, EGTA, which chelates extracellular free Ca2+, significantly reduced the [Ca2+]i, [Ca2+]m, and apoptosis induced by H5N1-AIV infection. In conclusion, we identified a novel mechanism for influenza A virus-mediated cell death, which involved the acceleration of extracellular Ca2+ influx, leading to mitochondrial dysfunction and apoptosis. These findings may be useful for understanding the pathogenesis of H5N1-AIV in avian species as well as the impact of Ca2+ homeostasis on influenza A virus infection.


2007 ◽  
Vol 275 (1630) ◽  
pp. 19-28 ◽  
Author(s):  
Kieran J Sharkey ◽  
Roger G Bowers ◽  
Kenton L Morgan ◽  
Susan E Robinson ◽  
Robert M Christley

Highly pathogenic avian influenza and in particular the H5N1 strain has resulted in the culling of millions of birds and continues to pose a threat to poultry industries worldwide. The recent outbreak of H5N1 in the UK highlights the need for detailed assessment of the consequences of an incursion and of the efficacy of control strategies. Here, we present results from a model of H5N1 propagation within the British poultry industry. We find that although the majority of randomly seeded incursions do not spread beyond the initial infected premises, there is significant potential for widespread infection. The efficacy of the European Union strategy for disease control is evaluated and our simulations emphasize the pivotal role of duck farms in spreading H5N1.


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