scholarly journals Genetic diversity of avian influenza virus strains A/H3N8

2020 ◽  
Vol 85 (4) ◽  
Author(s):  
K. K. Jekebekov ◽  
K. K. Akylbaeva ◽  
A. M. Melisbek ◽  
A. T. Zhunushov ◽  
E. D. Burashev ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Virus Strains

scholarly journals Controlling Avian Influenza Virus in Bangladesh: Challenges and Recommendations

Viruses ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 751
Author(s):  
Rokshana Parvin ◽  
Mohammed Nooruzzaman ◽  
Congriev Kumar Kabiraj ◽  
Jahan Ara Begum ◽  
Emdadul Haque Chowdhury ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Control Strategies ◽  
Poultry Production ◽  
New Host ◽  
Multiple Virus ◽  
Virus Spreading ◽  
Virus Strains ◽  
New Host Species

Avian influenza virus (AIV) remains a huge challenge for poultry production with negative repercussions for micro- and macro-economy and public health in Bangladesh. High (HP) H5N1 and low pathogenicity (LP) H9N2 AIV are currently endemic in poultry, and both have been reported to infect humans sporadically. Multiple virus introductions of different clades of HPAIV H5N1, reassorted genotypes, and on-going diversification of LPAIV H9N2 create a highly volatile virological environment which potentially implicates increased virulence, adaptation to new host species, and subsequent zoonotic transmission. Allotropy of poultry rearing systems and supply chains further increase the risk of virus spreading, which leads to human exposure and fosters the emergence of new potentially pre-pandemic virus strains. Here, we review the epidemiology, focusing on (i) risk factors for virus spreading, (ii) viral genetic evolution, and (iii) options for AIV control in Bangladesh. It is concluded that improved control strategies would profit from the integration of various intervention tools, including effective vaccination, enhanced biosecurity practice, and improved awareness of producers and traders, although widespread household poultry rearing significantly interferes with any such strategies. Nevertheless, continuous surveillance associated with rapid diagnosis and thorough virus characterization is the basis of such strategies.

scholarly journals Killing of Avian and Swine Influenza Virus by Natural Killer Cells

2010 ◽  
Vol 84 (8) ◽  
pp. 3993-4001 ◽  
Author(s):  
Hagit Achdout ◽  
Tal Meningher ◽  
Shira Hirsh ◽  
Ariella Glasner ◽  
Yotam Bar-On ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Natural Killer ◽  
H5n1 Virus ◽  
Swine Influenza Virus ◽  
Mortality Rates ◽  
Influenza Viruses ◽  
Direct Killing ◽  
Virus Strains

ABSTRACT Today, global attention is focused on two influenza virus strains: the current pandemic strain, swine origin influenza virus (H1N1-2009), and the highly pathogenic avian influenza virus, H5N1. At present, the infection caused by the H1N1-2009 is moderate, with mortality rates of less <1%. In contrast, infection with the H5N1 virus resulted in high mortality rates, and ca. 60% of the infected patients succumb to the infection. Thus, one of the world greatest concerns is that the H5N1 virus will evolve to allow an efficient human infection and human-to-human transmission. Natural killer (NK) cells are one of the innate immune components playing an important role in fighting against influenza viruses. One of the major NK activating receptors involved in NK cell cytotoxicity is NKp46. We previously demonstrated that NKp46 recognizes the hemagglutinin proteins of B and A influenza virus strains. Whether NKp46 could also interact with H1N1-2009 virus or with the avian influenza virus is still unknown. We analyzed the immunological properties of both the avian and the H1N1-2009 influenza viruses. We show that NKp46 recognizes the hemagglutinins of H1N1-2009 and H5 and that this recognition leads to virus killing both in vitro and in vivo. However, importantly, while the swine H1-NKp46 interactions lead to the direct killing of the infected cells, the H5-NKp46 interactions were unable to elicit direct killing, probably because the NKp46 binding sites for these two viruses are different.

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