Sequence analysis of reassortants within H3N2 subtype influenza A virus circulated in Hong Kong, 2014–2017

2020 ◽  
Vol 33 ◽  
pp. 101510
Author(s):  
Liang Chen ◽  
Jiasheng Xiong ◽  
Li Peng ◽  
Pengfei Yang ◽  
Hao Yu ◽  
...  
2005 ◽  
Vol 79 (15) ◽  
pp. 9926-9932 ◽  
Author(s):  
Kyoko Shinya ◽  
Masato Hatta ◽  
Shinya Yamada ◽  
Ayato Takada ◽  
Shinji Watanabe ◽  
...  

ABSTRACT In 2003, H5N1 avian influenza virus infections were diagnosed in two Hong Kong residents who had visited the Fujian province in mainland China, affording us the opportunity to characterize one of the viral isolates, A/Hong Kong/213/03 (HK213; H5N1). In contrast to H5N1 viruses isolated from humans during the 1997 outbreak in Hong Kong, HK213 retained several features of aquatic bird viruses, including the lack of a deletion in the neuraminidase stalk and the absence of additional oligosaccharide chains at the globular head of the hemagglutinin molecule. It demonstrated weak pathogenicity in mice and ferrets but caused lethal infection in chickens. The original isolate failed to produce disease in ducks but became more pathogenic after five passages. Taken together, these findings portray the HK213 isolate as an aquatic avian influenza A virus without the molecular changes associated with the replication of H5N1 avian viruses in land-based poultry such as chickens. This case challenges the view that adaptation to land-based poultry is a prerequisite for the replication of aquatic avian influenza A viruses in humans.


PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e92914 ◽  
Author(s):  
Susan S. Chiu ◽  
Janice Y. C. Lo ◽  
Kwok-Hung Chan ◽  
Eunice L. Y. Chan ◽  
Lok-Yee So ◽  
...  

2009 ◽  
Vol 52 (5) ◽  
pp. 439-449 ◽  
Author(s):  
Andy Ka-Leung Ng ◽  
Jia-Huai Wang ◽  
Pang-Chui Shaw

1999 ◽  
Vol 179 (5) ◽  
pp. 1132-1138 ◽  
Author(s):  
Shengqiang Li ◽  
Chongguang Liu ◽  
Alexander Klimov ◽  
Kanta Subbarao ◽  
Michael L. Perdue ◽  
...  

1993 ◽  
Vol 90 (3) ◽  
pp. 397-402 ◽  
Author(s):  
N. Masurel ◽  
R. A. Heijtin

SUMMARYSera from people born between 1883 and 1930 and collected in 1977 were tested for the presence of HI antibodies to A/FM/1/47 (H1N1) virus and three recently (1977 and 1978) isolated influenza A-H1N1 viruses. The highest frequency of high-titred antibody to the four H1N1 viruses was detected in sera from people born in 1903–4, i.e. 42,54,38, and 22% had antibody against A/FM/1/47, A/Hong Kong/117/77, A/Brazil/11/78, and A/Fukushima/103/78 respectively. The birthdate groups 1896–1907 showed a higher percentage of HI antibody titres ≥18, ≥50, ≥100 or ≥1600 against the four H1N1 viruses than the birthdate groups 1907–30. This indicates the existence of an era, 1908–18, in which, apart from the H3N2 virus (1900–18), the H1N1 virus was epidemic among the human population.


1980 ◽  
Vol 28 (3) ◽  
pp. 792-798
Author(s):  
Brian R. Murphy ◽  
Nanette T. Hosier ◽  
Robert M. Chanock

The influenza A/Udorn/72- ts -1A2 virus possesses temperature-sensitive mutations in the genes coding for the P1 and P3 polymerase proteins. It is being evaluated as a donor of its attenuating temperature-sensitive genes to produce recombinant live vaccine strains of epidemic variants of influenza A virus. Transfer of the P1 and P3 genes to two viruses within the H3N2 subtype of influenza A virus (i.e., the A/Victoria/3/75 and A/Alaska/6/77 viruses) conferred on each variant the following properties: (i) 37°C shutoff temperature for plaque formation, (ii) almost complete restriction of viral replication in the lungs, (iii) a 100-fold restriction of viral replication in the nasal turbinates, and (iv) genetic stability after replication in hamsters. This study was undertaken to determine whether the transfer of the two ts -1A2 temperature-sensitive genes into a virus belonging to the H1N1 subtype (i.e., the A/Hong Kong/123/77 virus) would result in a restriction of replication in vitro and in vivo comparable to that observed with the previously studied H3N2 recombinant viruses in hamsters. This was found to be the case. In addition, infection of hamsters with the A/Hong Kong/77- ts -1A2 virus induced significant resistance to infection with wild-type A/Hong Kong/77 virus. Thus, the two ts -1A2 temperature-sensitive genes attenuated influenza A viruses belonging to two distinct subtypes to a specific and predictable level. An unexpected genetic interaction was observed between several A/Hong Kong/77- ts -1A2 segregants bearing the group 5 (P1) temperature-sensitive lesion. One interpretation of these results is that intracistronic complementation occurred between these segregants.


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