Dose Response of Influenza A/Washington/897/80 (H3N2) Avian-Human Reassortant Virus in Adult Volunteers

1985 ◽  
Vol 152 (1) ◽  
pp. 225-229 ◽  
Author(s):  
B. R. Murphy ◽  
M. L. Clements ◽  
E. L. Tierney ◽  
R. E. Black ◽  
J. Stienberg ◽  
...  
1984 ◽  
Vol 149 (5) ◽  
pp. 814-815 ◽  
Author(s):  
M. L. Clements ◽  
R. F. Betts ◽  
H. F. Maassab ◽  
B. R. Murphy

1984 ◽  
Vol 149 (5) ◽  
pp. 816-816 ◽  
Author(s):  
B. R. Murphy ◽  
M. L. Clements ◽  
H. P. Madore ◽  
J. Steinberg ◽  
S. O'Donnell ◽  
...  

2015 ◽  
Vol 89 (17) ◽  
pp. 8806-8815 ◽  
Author(s):  
Yang Yu ◽  
Xingbo Wang ◽  
Tao Jin ◽  
Hailong Wang ◽  
Weiying Si ◽  
...  

ABSTRACTThe novel H7N9 avian influenza virus (AIV) was demonstrated to cause severe human respiratory infections in China. Here, we examined poultry specimens from live bird markets linked to human H7N9 infection in Hangzhou, China. Metagenomic sequencing revealed mixed subtypes (H5, H7, H9, N1, N2, and N9). Subsequently, AIV subtypes H5N9, H7N9, and H9N2 were isolated. Evolutionary analysis showed that the hemagglutinin gene of the novel H5N9 virus originated from A/Muscovy duck/Vietnam/LBM227/2012 (H5N1), which belongs to clade 2.3.2.1. The neuraminidase gene of the novel H5N9 virus originated from human-infective A/Hangzhou/1/2013 (H7N9). The six internal genes were similar to those of other H5N1, H7N9, and H9N2 virus strains. The virus harbored the PQRERRRKR/GL motif characteristic of highly pathogenic AIVs at the HA cleavage site. Receptor-binding experiments demonstrated that the virus binds α-2,3 sialic acid but not α-2,6 sialic acid. Identically, pathogenicity experiments also showed that the virus caused low mortality rates in mice. This newly isolated H5N9 virus is a highly pathogenic reassortant virus originating from H5N1, H7N9, and H9N2 subtypes. Live bird markets represent a potential transmission risk to public health and the poultry industry.IMPORTANCEThis investigation confirms that the novel H5N9 subtype avian influenza A virus is a reassortant strain originating from H5N1, H7N9, and H9N2 subtypes and is totally different from the H5N9 viruses reported before. The novel H5N9 virus acquired a highly pathogenic H5 gene and an N9 gene from human-infecting subtype H7N9 but caused low mortality rates in mice. Whether this novel H5N9 virus will cause human infections from its avian host and become a pandemic subtype is not known yet. It is therefore imperative to assess the risk of emergence of this novel reassortant virus with potential transmissibility to public health.


1984 ◽  
Vol 92 (2) ◽  
pp. 231-242 ◽  
Author(s):  
N. Yamane ◽  
Y. Nakamura ◽  
M. Yuki ◽  
T. Odagiri ◽  
N. Ishida

SUMMARYA cold-adapted influenza A virus, CR-37 (H1N1), derived from genetic reassortment between A/Ann Arbor/6/60 (H2N2) cold-adapted variant virus and A/California/10/78 (H1N1) wild-type virus, was tested in Japanese adult volunteers. The CR-37 live virus preparation induced only low-grade clinical reactionsin volunteers for the first 3–4 days after inoculation. Two vaccinees who did not show any antibody changes became febrile (over 38–0 °C). Skin tests using the vaccine preparation and uninfected allantoic fluid were performed, and indicated that one of these two vaccinees was positive for the CR-37 vaccine preparation. A high proportion of the vaccinees whose sera had a haemagglutination-inhibition (HI) antibody titre against thevaccine strain of ≤ 64 before inoculation, seroconverted in both HI and neuraminidase-inhibition (NA1) antibody titrations, and only a few seroconverted in the titration of antibody against type-specific internal antigens. The serological examinations against heterotypic H1N1 variants indicated that the cold-adapted live influenza virus vaccine could induce a broad spectrum of HI antibody reactivity and immunity of long duration.


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