scholarly journals Pathogenicity of the Novel A/H7N9 Influenza Virus in Mice

mBio ◽  
2013 ◽  
Vol 4 (4) ◽  
Author(s):  
Chris Ka Pun Mok ◽  
Horace Hok Yeung Lee ◽  
Michael Chi Wai Chan ◽  
Sin Fun Sia ◽  
Maxime Lestra ◽  
...  

ABSTRACT A novel avian-origin influenza A/H7N9 virus infecting humans was first identified in March 2013 and, as of 30 May 2013, has caused 132 human infections leading to 33 deaths. Phylogenetic studies suggest that this virus is a reassortant, with the surface hemagglutinin (HA) and neuraminidase (NA) genes being derived from duck and wild-bird viruses, respectively, while the six “internal gene segments” were derived from poultry H9N2 viruses. Here we determine the pathogenicity of a human A/Shanghai/2/2013 (Sh2/H7N9) virus in healthy adult mice in comparison with that of A/chicken/Hong Kong/HH8/2010 (ck/H9N2) virus, highly pathogenic avian influenza (HPAI) A/Hong Kong/483/1997 (483/H5N1) virus, and a duck influenza A H7N9 virus of different genetic derivation, A/duck/Jiangxi/3286/2009 (dk/H7N9). Intranasal infection of mice with Sh2/H7N9 virus doses of 103, 104, and 105 PFU led to significant weight loss without fatality. This virus was more pathogenic than dk/H7N9 and ck/H9N2 virus, which has six internal gene segments that are genetically similar to Sh2/H7N9. Sh2/H7N9 replicated well in the nasal cavity and lung, but there was no evidence of virus dissemination beyond the respiratory tract. Mice infected with Sh2/H7N9 produced higher levels of proinflammatory cytokines in the lung and serum than did ck/H9N2 and dk/H7N9 but lower levels than 483/H5N1. Cytokine induction was positively correlated with virus load in the lung at early stages of infection. Our results suggest that Sh2/H7N9 virus is able to replicate and cause disease in mice without prior adaptation but is less pathogenic than 483/H5N1 virus. IMPORTANCE An H7N9 virus isolate causing fatal human disease was found to be more pathogenic for mice than other avian H9N2 or H7N9 viruses but less pathogenic than the highly pathogenic avian influenza virus (HPAI) H5N1. Similarly, the ability of Sh2/H7N9 to elicit proinflammatory cytokines in the lung and serum of mice was intermediate to ck/H9N2 and dk/H7N9 on the one hand and HPAI H5N1 on the other. These findings accord with the observed epidemiology in humans, in whom, as with seasonal influenza viruses, H7N9 viruses cause severe disease predominantly in older persons while HPAI H5N1 can cause severe respiratory disease and death in children and young adults.

The Lancet ◽  
1998 ◽  
Vol 351 (9101) ◽  
pp. 472-477 ◽  
Author(s):  
Eric CJ Claas ◽  
Albert DME Osterhaus ◽  
Ruud van Beek ◽  
Jan C De Jong ◽  
Guus F Rimmelzwaan ◽  
...  

The Analyst ◽  
2019 ◽  
Vol 144 (8) ◽  
pp. 2594-2603 ◽  
Author(s):  
Meng Xiao ◽  
Liping Huang ◽  
Xiaohui Dong ◽  
Kaixin Xie ◽  
Haicong Shen ◽  
...  

Outbreaks and potential epidemics of the highly pathogenic avian influenza virus pose serious threats to human health and the global economy.


2017 ◽  
Vol 22 (19) ◽  
Author(s):  
Wenfei Zhu ◽  
Jianfang Zhou ◽  
Zi Li ◽  
Lei Yang ◽  
Xiyan Li ◽  
...  

With no or low virulence in poultry, avian influenza A(H7N9) virus has caused severe infections in humans. In the current fifth epidemic wave, a highly pathogenic avian influenza (HPAI) H7N9 virus emerged. The insertion of four amino acids (KRTA) at the haemagglutinin (HA) cleavage site enabled trypsin-independent infectivity of this virus. Although maintaining dual receptor-binding preference, its HA antigenicity was distinct from low-pathogenic avian influenza A(H7N9). The neuraminidase substitution R292K conferred a multidrug resistance phenotype.


2021 ◽  
Author(s):  
Periyasamy Vijayakumar ◽  
Ashwin Ashok Raut ◽  
Santhalembi Chingtham ◽  
Harshad V Murugkar ◽  
Diwakar D. Kulkarni ◽  
...  

Abstract Elucidation of molecular pathogenesis underlying virus-host interaction is important for the development of new diagnostic and therapeutic strategies against highly pathogenic avian influenza (HPAI) infection in chicken. However, chicken HPAI viral pathogenesis is not completely understood. To elucidate the intracellular signaling pathways and critical host proteins associated with influenza pathogenesis, we characterized the lung proteome of chicken infected with HPAI H5N1 virus (A/duck/India/02CA10/2011/Agartala). The chicken mass spectra data sets comprised1, 47, 451 MS scans and 19, 917 MS/MS scans. At local FDR 5% level, we identified total 3313 chicken proteins with presence of at least one unique peptide. At 12 hrs, 247 proteins are downregulated while 1754 proteins are downregulated at 48 hrs indicating that the host has succumbed to infection. There is expression of proteins of the predominant signaling pathways, such as TLR, RLR, NLR and JAK-STAT signaling. Activation of these pathways is associated with cytokine storm effect and thus may be the cause of severity of HPAI H5N1 infection in chicken. Further we identified proteins like MyD88, IKBKB, IRAK4, RELA, and MAVS involved in the critical signaling pathways and some other novel proteins (HNF4A, ELAVL1, FN1, COPS5, CUL1, BRCA1 and FYN) as main hub proteins that might play important roles in influenza pathogenesis in chicken. Taken together, we characterized the signaling pathways and the proteomic determinants responsible for disease pathogenesis in chicken infected with HPAI H5N1 virus.


2020 ◽  
Vol 26 (2) ◽  
pp. 379-380 ◽  
Author(s):  
Wenming Jiang ◽  
Guangyu Hou ◽  
Jinping Li ◽  
Cheng Peng ◽  
Suchun Wang ◽  
...  

2020 ◽  
Vol 33 (1) ◽  
pp. 124-128
Author(s):  
Tanjin T. Mumu ◽  
Mohammed Nooruzzaman ◽  
Azmary Hasnat ◽  
Rokshana Parvin ◽  
Emdadul H. Chowdhury ◽  
...  

A mixed-aged flock of 130 turkeys in Bangladesh reported the sudden death of 1 bird in September 2017. Highly pathogenic avian influenza A(H5N1) virus was detected in 3 turkeys, and phylogenetic analysis placed the viruses in the reassortant clade 2.3.2.1a. The birds had clinical signs of depression, diarrhea, weakness, closed eyes, and finally death. The mortality rate of the flock was 13% over the 6 d prior to the flock being euthanized. At autopsy, we observed congestion in lungs and brain, hemorrhages in the trachea, pancreas, breast muscle, coronary fat, intestine, bursa of Fabricius, and kidneys. Histopathology revealed hemorrhagic pneumonia, hemorrhages in the liver and kidneys, and hemorrhages and necrosis in the spleen and pancreas. Significant changes in the brain included gliosis, focal encephalomalacia and encephalitis, and neuronophagia.


PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e73200 ◽  
Author(s):  
Sharifa Nasreen ◽  
Salah Uddin Khan ◽  
Eduardo Azziz-Baumgartner ◽  
Kathy Hancock ◽  
Vic Veguilla ◽  
...  

2009 ◽  
Vol 46 (5) ◽  
pp. 971-976 ◽  
Author(s):  
D. Van Riel ◽  
J. M. A. Van Den Brand ◽  
V. J. Munster ◽  
T. M. Besteboer ◽  
R. A. M. Fouchier ◽  
...  

The largest recorded outbreak of highly pathogenic avian influenza virus of the subtype H7N7 occurred in the Netherlands in 2003. We describe the immunohistochemical and histopathologic findings of 3 chickens naturally infected during this outbreak. Influenza virus antigen occurred in endothelial cells and mononuclear cells of all tissues examined and occurred in parenchymal cells of heart, lung, kidney, pancreas, and trachea, often associated with multifocal inflammation and necrosis. These findings are consistent with the acute stage of highly pathogenic avian influenza from other subtypes. In the severely edematous wattle skin, most endothelial cells contained virus antigen, while in all other tissues virus antigen was only detected in a few endothelial cells. Virus histochemistry showed that this H7N7 virus attached to more endothelial cells in wattle skin than in other vascular beds. This might explain, at least partly, the tropism of the virus and the associated severity of lesions in this tissue.


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