Swine influenza viruses and pandemic H1N1‐2009 infection in pigs, Myanmar

2020 ◽  
Vol 67 (6) ◽  
pp. 2653-2666
Author(s):  
Pont Pont Mon ◽  
Khin Thurain ◽  
Taveesak Janetanakit ◽  
Chanakarn Nasamran ◽  
Napawan Bunpapong ◽  
...  

2011 ◽  
Vol 17 (10) ◽  
pp. 1897-1899 ◽  
Author(s):  
Ranawaka A.P.M. Perera ◽  
Steven Riley ◽  
Siu K. Ma ◽  
Hua-Chen Zhu ◽  
Yi Guan ◽  
...  


Virus Genes ◽  
2013 ◽  
Vol 47 (1) ◽  
pp. 75-85 ◽  
Author(s):  
Nataya Charoenvisal ◽  
Juthatip Keawcharoen ◽  
Donruethai Sreta ◽  
Supassama Chaiyawong ◽  
Nutthawan Nonthabenjawan ◽  
...  


2010 ◽  
Vol 56 (8) ◽  
pp. 1340-1344 ◽  
Author(s):  
Leo L M Poon ◽  
Polly W Y Mak ◽  
Olive T W Li ◽  
Kwok Hung Chan ◽  
Chung Lam Cheung ◽  
...  

BACKGROUND Influenza viruses can generate novel reassortants in coinfected cells. The global circulation and occasional introductions of pandemic H1N1/2009 virus in humans and in pigs, respectively, may allow this virus to reassort with other influenza viruses. These possible reassortment events might alter virulence and/or transmissibility of the new reassortants. Investigations to detect such possible reassortants should be included as a part of pandemic influenza surveillance plans. METHODS We established a real-time reverse-transcription (RT)-PCR–based strategy for the detection of reassortment of pandemic H1N1/2009 virus. Singleplex SYBR green–based RT-PCR assays specific for each gene segment of pandemic H1N1/2009 were developed. These assays were evaluated with influenza viruses of various genetic backgrounds. RESULTS All human pandemic H1N1 (n = 27) and all seasonal human (n = 58) isolates were positive and negative, respectively, for all 8 segments. Of 48 swine influenza viruses isolated from our ongoing surveillance program of influenza viruses in swine, 10 were positive in all reactions. All 8 viral segments of these 10 samples were confirmed to be of pandemic H1N1 origin, indicating that these were caused by zoonotic transmissions from human to pigs. The 38 swine viruses that were nonpandemic H1N1/2009 had 1–6 gene segments positive in the tests. Further characterization of these nonpandemic H1N1/2009 swine viruses indicated that these PCR-positive genes were the precursor genes of the pandemic H1N1/2009 virus. CONCLUSIONS Our results demonstrated that these assays can detect reintroductions of pandemic H1N1/2009 virus in pigs. These assays might be useful screening tools for identifying viral reassortants derived from pandemic H1N1/2009 or its precursors.



2010 ◽  
Vol 170 (1-2) ◽  
pp. 169-172 ◽  
Author(s):  
Yasuaki Hiromoto ◽  
Yuko Uchida ◽  
Nobuhiro Takemae ◽  
Tsuyoshi Hayashi ◽  
Tomoyuki Tsuda ◽  
...  


Author(s):  
Ranawaka Perera ◽  
Steven Riley ◽  
Siu Ma ◽  
Hua-Chen Zhu ◽  
Yi Guan ◽  
...  


2015 ◽  
Vol 89 (10) ◽  
pp. 5651-5667 ◽  
Author(s):  
Daniel Dlugolenski ◽  
Les Jones ◽  
Elizabeth Howerth ◽  
David Wentworth ◽  
S. Mark Tompkins ◽  
...  

ABSTRACTSwine are susceptible to infection by both avian and human influenza viruses, and this feature is thought to contribute to novel reassortant influenza viruses. In this study, the influenza virus reassortment rate in swine and human cells was determined. Coinfection of swine cells with 2009 pandemic H1N1 virus (huH1N1) and an endemic swine H1N2 (A/swine/Illinois/02860/09) virus (swH1N2) resulted in a 23% reassortment rate that was independent of α2,3- or α2,6-sialic acid distribution on the cells. The reassortants had altered pathogenic phenotypes linked to introduction of the swine virus PA and neuraminidase (NA) into huH1N1. In mice, the huH1N1 PA and NA mediated increased MIP-2 expression early postinfection, resulting in substantial pulmonary neutrophilia with enhanced lung pathology and disease. The findings support the notion that swine are a mixing vessel for influenza virus reassortants independent of sialic acid distribution. These results show the potential for continued reassortment of the 2009 pandemic H1N1 virus with endemic swine viruses and for reassortants to have increased pathogenicity linked to the swine virus NA and PA genes which are associated with increased pulmonary neutrophil trafficking that is related to MIP-2 expression.IMPORTANCEInfluenza A viruses can change rapidly via reassortment to create a novel virus, and reassortment can result in possible pandemics. Reassortments among subtypes from avian and human viruses led to the 1957 (H2N2 subtype) and 1968 (H3N2 subtype) human influenza pandemics. Recent analyses of circulating isolates have shown that multiple genes can be recombined from human, avian, and swine influenza viruses, leading to triple reassortants. Understanding the factors that can affect influenza A virus reassortment is needed for the establishment of disease intervention strategies that may reduce or preclude pandemics. The findings from this study show that swine cells provide a mixing vessel for influenza virus reassortment independent of differential sialic acid distribution. The findings also establish that circulating neuraminidase (NA) and PA genes could alter the pathogenic phenotype of the pandemic H1N1 virus, resulting in enhanced disease. The identification of such factors provides a framework for pandemic modeling and surveillance.



2019 ◽  
Vol 79 ◽  
pp. 9
Author(s):  
O. Smutko ◽  
A. Fesenko ◽  
L. Radchenko ◽  
O. Onishchenko ◽  
L. Leibenko ◽  
...  


2012 ◽  
Vol 93 (6) ◽  
pp. 1261-1268 ◽  
Author(s):  
Wenjun Ma ◽  
Qinfang Liu ◽  
Bhupinder Bawa ◽  
Chuanling Qiao ◽  
Wenbao Qi ◽  
...  

The 2009 pandemic H1N1 virus (pH1N1) contains neuraminidase (NA) and matrix (M) genes from Eurasian avian-like swine influenza viruses (SIVs), with the remaining six genes from North American triple-reassortant SIVs. To characterize the role of the pH1N1 NA and M genes in pathogenesis and transmission, their impact was evaluated in the background of an H1N1 triple-reassortant (tr1930) SIV in which the HA (H3) and NA (N2) of influenza A/swine/Texas/4199-2/98 virus were replaced with those from the classical H1N1 A/swine/Iowa/15/30 (1930) virus. The laboratory-adapted 1930 virus did not shed nor transmit in pigs, but tr1930 was able to shed in infected pigs. The NA, M or both genes of the tr1930 virus were then substituted by those of pH1N1. The resulting virus with both NA and M from pH1N1 grew to significantly higher titre in cell cultures than the viruses with single NA or M from pH1N1. In a pig model, only the virus containing both NA and M from pH1N1 was transmitted to and infected sentinels, whereas the viruses with single NA or M from pH1N1 did not. These results demonstrate that the right combination of NA and M genes is critical for the replication and transmissibility of influenza viruses in pigs.



2011 ◽  
Vol 85 (9) ◽  
pp. 4596-4601 ◽  
Author(s):  
M. Ozawa ◽  
S. Basnet ◽  
L. M. Burley ◽  
G. Neumann ◽  
M. Hatta ◽  
...  


2011 ◽  
Vol 149 (3-4) ◽  
pp. 472-477 ◽  
Author(s):  
Ana Moreno ◽  
Livia Di Trani ◽  
Silvia Faccini ◽  
Gabriele Vaccari ◽  
Daniele Nigrelli ◽  
...  


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