scholarly journals The Pathobiology of H7N3 Low and High Pathogenicity Avian Influenza Viruses from the United States Outbreak in 2020 Differs between Turkeys and Chickens

Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1851
Author(s):  
Miriã F. Criado ◽  
Christina M. Leyson ◽  
Sungsu Youk ◽  
Suzanne DeBlois ◽  
Tim Olivier ◽  
...  
Keyword(s):  
United States ◽  
Influenza Virus ◽  
South Carolina ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
The United States ◽  
Influenza Viruses ◽  
Infectious Dose ◽  
High Pathogenicity ◽  
Commercial Turkey

An outbreak caused by H7N3 low pathogenicity avian influenza virus (LPAIV) occurred in commercial turkey farms in the states of North Carolina (NC) and South Carolina (SC), United States in March of 2020. Subsequently, H7N3 high pathogenicity avian influenza virus (HPAIV) was detected on a turkey farm in SC. The infectivity, transmissibility, and pathogenicity of the H7N3 HPAIV and two LPAIV isolates, including one with a deletion in the neuraminidase (NA) protein stalk, were studied in turkeys and chickens. High infectivity [<2 log10 50% bird infectious dose (BID50)] and transmission to birds exposed by direct contact were observed with the HPAIV in turkeys. In contrast, the HPAIV dose to infect chickens was higher than for turkeys (3.7 log10 BID50), and no transmission was observed. Similarly, higher infectivity (<2–2.5 log10 BID50) and transmissibility were observed with the H7N3 LPAIVs in turkeys compared to chickens, which required higher virus doses to become infected (5.4–5.7 log10 BID50). The LPAIV with the NA stalk deletion was more infectious in turkeys but did not have enhanced infectivity in chickens. These results show clear differences in the pathobiology of AIVs in turkeys and chickens and corroborate the high susceptibility of turkeys to both LPAIV and HPAIV infections.

Surveillance for High Pathogenicity Avian Influenza Virus in Wild Birds in the Pacific Flyway of the United States, 2006–2007

2009 ◽  
Vol 4 (2) ◽  
pp. e9-e10
Author(s):  
Robert J. Dusek ◽  
J. Bradley Bortner ◽  
Thomas J. Deliberto ◽  
Jenny Hoskins ◽  
J. Christian Franson ◽  
...  
Keyword(s):  
United States ◽  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
The United States ◽  
Wild Birds ◽  
The Pacific ◽  
Pacific Flyway ◽  
High Pathogenicity

Surveillance for High Pathogenicity Avian Influenza Virus in Wild Birds in the Pacific Flyway of the United States, 2006–2007

2009 ◽  
Vol 53 (2) ◽  
pp. 222-230 ◽  
Author(s):  
Robert J. Dusek ◽  
J. Bradley Bortner ◽  
Thomas J. DeLiberto ◽  
Jenny Hoskins ◽  
J. Christian Franson ◽  
...  
Keyword(s):  
United States ◽  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
The United States ◽  
Wild Birds ◽  
The Pacific ◽  
Pacific Flyway ◽  
High Pathogenicity

scholarly journals Simulated Flock-Level Shedding Characteristics of Turkeys in Ten Thousand Bird Houses Infected with H7 Low Pathogenicity Avian Influenza Virus Strains

Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2509
Author(s):  
Peter J. Bonney ◽  
Sasidhar Malladi ◽  
Amos Ssematimba ◽  
Kaitlyn M. St. Charles ◽  
Emily Walz ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
The United States ◽  
Infection Process ◽  
Infectious Dose ◽  
Viral Shedding ◽  
Polymerase Chain ◽  
Commercial Turkey ◽  
Over Time

Understanding the amount of virus shed at the flock level by birds infected with low pathogenicity avian influenza virus (LPAIV) over time can help inform the type and timing of activities performed in response to a confirmed LPAIV-positive premises. To this end, we developed a mathematical model which allows us to estimate viral shedding by 10,000 turkey toms raised in commercial turkey production in the United States, and infected by H7 LPAIV strains. We simulated the amount of virus shed orally and from the cloaca over time, as well as the amount of virus in manure. In addition, we simulated the threshold cycle value (Ct) of pooled oropharyngeal swabs from birds in the infected flock tested by real-time reverse transcription polymerase chain reaction. The simulation model predicted that little to no shedding would occur once the highest threshold of seroconversion was reached. Substantial amounts of virus in manure (median 1.5×108 and 5.8×109; 50% egg infectious dose) were predicted at the peak. Lastly, the model results suggested that higher Ct values, indicating less viral shedding, are more likely to be observed later in the infection process as the flock approaches recovery.

Avian Influenza Virus Prevalence in Migratory Waterfowl in the United States, 2007–2009

2014 ◽  
Vol 58 (4) ◽  
pp. 531-540 ◽  
Author(s):  
Scott R. Groepper ◽  
Thomas J. DeLiberto ◽  
Mark P. Vrtiska ◽  
Kerri Pedersen ◽  
Seth R. Swafford ◽  
...  
Keyword(s):  
United States ◽  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
The United States ◽  
Migratory Waterfowl ◽  
Virus Prevalence

scholarly journals H5N2 Avian Influenza Outbreak in Texas in 2004: the First Highly Pathogenic Strain in the United States in 20 Years?

2005 ◽  
Vol 79 (17) ◽  
pp. 11412-11421 ◽  
Author(s):  
Chang-Won Lee ◽  
David E. Swayne ◽  
Jose A. Linares ◽  
Dennis A. Senne ◽  
David L. Suarez
Keyword(s):  
United States ◽  
Amino Acid ◽  
Avian Influenza ◽  
Cleavage Site ◽  
Basic Amino Acid ◽  
The United States ◽  
Influenza Viruses ◽  
Single Point Mutation ◽  
Highly Pathogenic

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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