scholarly journals Genetic analysis and antigenic characterization of swine origin influenza viruses isolated from humans in the United States, 1990–2010

Virology ◽  
2012 ◽  
Vol 422 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Bo Shu ◽  
Rebecca Garten ◽  
Shannon Emery ◽  
Amanda Balish ◽  
Lynn Cooper ◽  
...  
Virology ◽  
2019 ◽  
Vol 535 ◽  
pp. 279-282 ◽  
Author(s):  
John D. Neill ◽  
Beate M. Crossley ◽  
Ana C. Mosena ◽  
Julia F. Ridpath ◽  
Darrell O. Bayles ◽  
...  

2010 ◽  
Vol 92 (4) ◽  
pp. 919-930 ◽  
Author(s):  
A. Lorusso ◽  
A. L. Vincent ◽  
M. L. Harland ◽  
D. Alt ◽  
D. O. Bayles ◽  
...  

Virology ◽  
1999 ◽  
Vol 256 (1) ◽  
pp. 45-53 ◽  
Author(s):  
Carl D. Kirkwood ◽  
Jon R. Gentsch ◽  
Yasutaka Hoshino ◽  
H.Fred Clark ◽  
Roger I. Glass

2002 ◽  
Vol 13 (6) ◽  
pp. 391-396 ◽  
Author(s):  
Raymond SW Tsang ◽  
Susan G Squires ◽  
Wendell D Zollinger ◽  
Fraser E Ashton

The relative frequency of serogroups ofNeisseria meningitidisassociated with meningococcal disease in Canada during the period January 1, 1999 to June 30, 2001 was examined. Of the 552 strains ofN meningitidiscollected from clinical specimens of normally sterile sites, 191 (34.6%), 276 (50.0%), 61 (11.1%) and 23 (4.2%) were identified by serological and molecular methods as serogroups B, C, Y and W135, respectively. About half (50.8%) of the serogroup Y isolates were isolated in the province of Ontario. The two most common serotypes found were 2c and 14. Most of the serogroup Y strains isolated from patients in Ontario were serotype 2c, while serotype 14 was the most common serotype associated with disease in the province of Quebec. The two most common serosubtypes found among the serogroup Y meningococci were P1.5 and P1.2,5. Laboratory findings, based on antigenic analysis, did not suggest that these serogroup Y strains arise by capsule switching from serogroups B and C strains. This study documented a higher incidence of finding serogroup Y meningococci in clinical specimens from patients in Ontario compared to the rest of Canada, and parallels the increase in serogroup Y meningococcal disease reported in some parts of the United States.


Author(s):  
Mark W Tenforde ◽  
H Keipp Talbot ◽  
Christopher H Trabue ◽  
Manjusha Gaglani ◽  
Tresa M McNeal ◽  
...  

Abstract Background Influenza causes significant morbidity and mortality and stresses hospital resources during periods of increased circulation. We evaluated the effectiveness of the 2019-2020 influenza vaccine against influenza-associated hospitalizations in the United States. Methods We included adults hospitalized with acute respiratory illness at 14 hospitals and tested for influenza viruses by reserve transcription polymerase chain reaction. Vaccine effectiveness (VE) was estimated by comparing the odds of current-season influenza vaccination in test-positive influenza cases versus test-negative controls, adjusting for confounders. VE was stratified by age and major circulating influenza types along with A(H1N1)pdm09 genetic subgroups. Results 3116 participants were included, including 18% (553) influenza-positive cases. Median age was 63 years. Sixty-seven percent (2079) received vaccination. Overall adjusted VE against influenza viruses was 41% (95% confidence interval [CI]: 27-52). VE against A(H1N1)pdm09 viruses was 40% (95% CI: 24-53) and 33% against B viruses (95% CI: 0-56). Of the two major A(H1N1)pdm09 subgroups (representing 90% of sequenced H1N1 viruses), VE against one group (5A+187A,189E) was 59% (95% CI: 34-75) whereas no significant VE was observed against the other group (5A+156K) [-1%, 95% CI: -61-37]. Conclusions In a primarily older population, influenza vaccination was associated with a 41% reduction in risk of hospitalized influenza illness.


2005 ◽  
Vol 79 (17) ◽  
pp. 11412-11421 ◽  
Author(s):  
Chang-Won Lee ◽  
David E. Swayne ◽  
Jose A. Linares ◽  
Dennis A. Senne ◽  
David L. Suarez

ABSTRACT In early 2004, an H5N2 avian influenza virus (AIV) that met the molecular criteria for classification as a highly pathogenic AIV was isolated from chickens in the state of Texas in the United States. However, clinical manifestations in the affected flock were consistent with avian influenza caused by a low-pathogenicity AIV and the representative virus (A/chicken/Texas/298313/04 [TX/04]) was not virulent for experimentally inoculated chickens. The hemagglutinin (HA) gene of the TX/04 isolate was similar in sequence to A/chicken/Texas/167280-4/02 (TX/02), a low-pathogenicity AIV isolate recovered from chickens in Texas in 2002. However, the TX/04 isolate had one additional basic amino acid at the HA cleavage site, which could be attributed to a single point mutation. The TX/04 isolate was similar in sequence to TX/02 isolate in several internal genes (NP, M, and NS), but some genes (PA, PB1, and PB2) had sequence of a clearly different origin. The TX/04 isolate also had a stalk deletion in the NA gene, characteristic of a chicken-adapted AIV. By analyzing viruses constructed by in vitro mutagenesis followed by reverse genetics, we found that the pathogenicity of the TX/04 virus could be increased in vitro and in vivo by the insertion of an additional basic amino acid at the HA cleavage site and not by the loss of a glycosylation site near the cleavage site. Our study provides the genetic and biologic characteristics of the TX/04 isolate, which highlight the complexity of the polygenic nature of the virulence of influenza viruses.


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