Thermal Inactivation of Avian Influenza and Newcastle Disease Viruses in Chicken Meat

2008 ◽  
Vol 71 (6) ◽  
pp. 1214-1222 ◽  
Author(s):  
COLLEEN THOMAS ◽  
DANIEL J. KING ◽  
DAVID E. SWAYNE
Keyword(s):  
Avian Influenza ◽  
Newcastle Disease ◽  
Thermal Inactivation ◽  
Systemic Disease ◽  
Virus Titer ◽  
Chicken Meat ◽  
Influenza Viruses ◽  
Linear Regression Models ◽  
Log Reduction ◽  
High Pathogenicity

Avian influenza viruses (AIV) and Newcastle disease viruses (NDV) of high pathogenicity cause severe systemic disease with high mortality in chickens and can be isolated from the meat of infected chickens. Although AIV and NDV strains of low pathogenicity are typically not present in chicken meat, virus particles in respiratory secretions or feces are possible sources of carcass contamination. Because spread of AIV and NDV is associated with movement of infected birds or their products, the presence of these viruses in chicken meat is cause for concern. This study presents thermal inactivation data for two viruses of high pathogenicity in chickens (AIV strain A/chicken/Pennsylvania/1370/1983 and NDV strain APMV-1/chicken/California/S0212676/2002) and two viruses of low pathogenicity in chickens (AIV strain A/chicken/Texas/298313/2004 and NDV strain APMV-1/chicken/Northern Ireland/Ulster/1967). Under the conditions of the assay, high-pathogenicity AIV was inactivated more slowly in meat from naturally infected chickens than in artificially infected chicken meat with a similar virus titer. In contrast, high-pathogenicity NDV was inactivated similarly in naturally and artificially infected meat. Linear regression models predicted that the current U.S. Department of Agriculture–Food Safety and Inspection Service time-temperature guidelines for cooking chicken meat to achieve a 7-log reduction of Salmonella also would effectively inactivate the AIV and NDV strains tested. Experimentally, the AIV and NDV strains used in this study (and the previously studied H5N1 high-pathogenicity AIV strain A/chicken/Korea/ES/2003) were effectively inactivated in chicken meat held at 70 or 73.9°C for less than 1 s.

Thermal Inactivation of H5N2 High-Pathogenicity Avian Influenza Virus in Dried Egg White with 7.5% Moisture

2009 ◽  
Vol 72 (9) ◽  
pp. 1997-2000 ◽  
Author(s):  
COLLEEN THOMAS ◽  
DAVID E. SWAYNE
Keyword(s):  
Linear Regression ◽  
Avian Influenza ◽  
Thermal Inactivation ◽  
Systemic Disease ◽  
Egg White ◽  
Influenza Viruses ◽  
Log Reduction ◽  
Poultry Products ◽  
High Pathogenicity ◽  
D Values

High-pathogenicity avian influenza viruses (HPAIV) cause severe systemic disease with high mortality in chickens. Isolation of HPAIV from the internal contents of chicken eggs has been reported, and this is cause for concern because HPAIV can be spread by movement of poultry products during marketing and trade activity. This study presents thermal inactivation data for the HPAIV strain A/chicken/PA/1370/83 (H5N2) (PA/83) in dried egg white with a moisture content (7.5%) similar to that found in commercially available spray-dried egg white products. The 95% upper confidence limits for D-values calculated from linear regression of the survival curves at 54.4, 60.0, 65.5, and 71.1°C were 475.4, 192.2, 141.0, and 50.1 min, respectively. The line equation y = [0.05494 × °C] + 5.5693 (root mean square error = 0.0711) was obtained by linear regression of experimental D-values versus temperature. Conservative predictions based on the thermal inactivation data suggest that standard industry pasteurization protocols would be very effective for HPAIV inactivation in dried egg white. For example, these calculations predict that a 7-log reduction would take only 2.6 days at 54.4°C.

Thermal Inactivation of H5N1 High Pathogenicity Avian Influenza Virus in Naturally Infected Chicken Meat

2007 ◽  
Vol 70 (3) ◽  
pp. 674-680 ◽  
Author(s):  
COLLEEN THOMAS ◽  
DAVID E. SWAYNE
Keyword(s):  
Linear Regression ◽  
Avian Influenza ◽  
Thermal Inactivation ◽  
Chicken Meat ◽  
Meat Sample ◽  
Breast Meat ◽  
Infectious Dose ◽  
High Pathogenicity ◽  
Z Value ◽  
D Values

Thermal inactivation of the H5N1 high pathogenicity avian influenza (HPAI) virus strain A/chicken/Korea/ES/2003 (Korea/03) was quantitatively measured in thigh and breast meat harvested from infected chickens. The Korea/03 titers were recorded as the mean embryo infectious dose (EID50) and were 108.0 EID50/g in uncooked thigh samples and 107.5 EID50/g in uncooked breast samples. Survival curves were constructed for Korea/03 in chicken thigh and breast meat at 1°C intervals for temperatures of 57 to 61°C. Although some curves had a slightly biphasic shape, a linear model provided a fair-to-good fit at all temperatures, with R2 values of 0.85 to 0.93. Stepwise linear regression revealed that meat type did not contribute significantly to the regression model and generated a single linear regression equation for z-value calculations and D-value predictions for Korea/03 in both meat types. The z-value and the upper limit of the 95% confidence interval for the z-value were 4.64 and 5.32°C, respectively. From the lowest temperature to the highest, the predicted D-values and the upper limits of their 95% prediction intervals (conservative D-values) for 57 to 61°C were 241.2 and 321.1 s, 146.8 and 195.4 s, 89.3 and 118.9 s, 54.4 and 72.4 s, and 33.1 and 44.0 s. D-values and conservative D-values predicted for higher temperatures were 0.28 and 0.50 s for 70°C and 0.041 and 0.073 s for 73.9°C. Calculations with the conservative D-values predicted that cooking chicken meat according to current U.S. Department of Agriculture Food Safety and Inspection Service time-temperature guidelines will inactivate Korea/03 in a heavily contaminated meat sample, such as those tested in this study, with a large margin of safety.

Evaluation of the U.S. Department of Agriculture's Egg Pasteurization Processes on the Inactivation of High-Pathogenicity Avian Influenza Virus and Velogenic Newcastle Disease Virus in Processed Egg Products

2013 ◽  
Vol 76 (4) ◽  
pp. 640-645 ◽  
Author(s):  
REVIS A. CHMIELEWSKI ◽  
JOAN R. BECK ◽  
DAVID E. SWAYNE
Keyword(s):  
Avian Influenza ◽  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Thermal Inactivation ◽  
Egg Yolk ◽  
Log Reduction ◽  
Egg Products ◽  
Velogenic Newcastle Disease Virus ◽  
Lower Temperature

Globally, 230,662 metric tons of liquid egg products are marketed each year. The presence of highly pathogenic avian influenza (HPAI) or Newcastle disease in an exporting country can legitimately inhibit trade in eggs and processed egg products; development and validation of pasteurization parameters are essential for safe trade to continue. The HPAI virus (HPAIV) A/chicken/Pennsylvania/1370/1983 (H5N2) and velogenic Newcastle disease virus (vNDV) AMPV-1/chicken/California/S01212676/2002 were inoculated into five egg products and heat treated at various times and temperatures to determine thermal inactivation rates to effect a 5-log viral reduction. For HPAIV and vNDV, the pasteurization processes for fortified, sugared, plain, and salted egg yolk, and homogenized whole egg (HPAIV only) products resulted in >5-log reductions in virus at the lower temperature–longer times of U.S. Department of Agriculture (USDA)–approved Salmonella pasteurization processes. In addition, a >5-log reduction of HPAIV was also demonstrated for the five products at the higher temperatures–shorter times of USDA-approved pasteurization processes, whereas the vNDV virus was adequately inactivated in only fortified and plain egg yolk products. For the salted and sugared egg yolk products, an additional 0.65 and 1.6 min of treatment, respectively, at 63.3°C was necessary to inactivate 5 log of vNDV. Egg substitute with fat does not have standard USDA pasteurization criteria, but the D59-value was 0.75 min, adequate to inactivate 5 log of vNDV in <4 min.

scholarly journals Amino Acid Residue 217 in the Hemagglutinin Glycoprotein Is a Key Mediator of Avian Influenza H7N9 Virus Antigenicity

2018 ◽  
Vol 93 (1) ◽  
Author(s):  
Pengxiang Chang ◽  
Joshua E. Sealy ◽  
Jean-Remy Sadeyen ◽  
Munir Iqbal
Keyword(s):  
Amino Acid ◽  
Avian Influenza ◽  
Immune Escape ◽  
Influenza Viruses ◽  
Single Mutation ◽  
H7n9 Virus ◽  
Avian Influenza Viruses ◽  
Antigenic Analysis ◽  
Neutralizing Capacity ◽  
High Pathogenicity

ABSTRACTAvian influenza viruses continue to evolve and acquire mutations that facilitate antigenic drift and virulence change. In 2017, low-pathogenicity H7N9 avian influenza viruses evolved to a high-pathogenicity phenotype in China. Comparative antigenic analysis of the low- and high-pathogenicity virus strains showed marked variability. In order to identify residues that may be linked to the antigenic change among the H7N9 viruses, we serially passaged the viruses in the presence of homologous ferret antiserum. Progeny viruses able to overcome the neutralizing capacity of the antiserum were sequenced. The analysis showed that the emergent immune escape viruses contained mutations A125T, A151T, and L217Q in the hemagglutinin (HA) glycoprotein as early as passage 5 and that these mutations persisted until passage 10. The results revealed that a single mutation, L217Q, in the HA of H7N9 virus led to 23- and 8-fold reductions in hemagglutination inhibition (HI) titer with ferret and chicken antisera, respectively. Further analysis showed that this change also contributed to antigenic differences between the low- and high-pathogenicity H7N9 viruses, thus playing a major role in their antigenic diversification. Therefore, evolutionary changes at amino acid position 217 in the H7N9 viruses can serve as a genetic marker for virus antigenic diversity during vaccine seed matching and selection. Thein vitroimmune escape mutant selection method used in this study could also aid in the prediction of emerging antigenic variants in naturally infected or immunized animals.IMPORTANCEAvian influenza H7N9 viruses circulating in poultry and wild birds continue to evolve and acquire important phenotypic changes. Mutations to the virus hemagglutinin (HA) glycoprotein can modulate virus antigenicity and facilitate virus escape from natural or vaccine-induced immunity. The focus of this study was to identify evolutionary markers in the HA of H7N9 that drive escape from antibody-based immunity. To achieve this, we propagated low-pathogenicity H7N9 virus in the presence of polyclonal antiserum derived from ferrets infected with the same strain of virus (homologous antiserum). This selection process was repeated 10 times. The HA gene sequences of viruses recovered after the fifth passage showed that the viruses readily acquired mutations at three different amino acid positions (A125T, A151T, and L217Q). Further functional analysis of these mutations confirmed that the mutation at residue 217 in the HA was responsible for mediating changes to the immunological properties of the H7N9 virus.

scholarly journals Insights into the Acquisition of Virulence of Avian Influenza Viruses during a Single Passage in Ferrets

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 915
Author(s):  
Butler ◽  
Middleton ◽  
Haining ◽  
Layton ◽  
Rockman ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Respiratory Tract ◽  
Severe Disease ◽  
Influenza Viruses ◽  
Mammalian Host ◽  
Upper Respiratory Tract ◽  
Avian Influenza Viruses ◽  
Single Passage ◽  
H5n1 Isolate ◽  
High Pathogenicity

Circulating avian influenza viruses pose a significant threat, with human infections occurring infrequently but with potentially severe consequences. To examine the dynamics and locale of the adaptation process of avian influenza viruses when introduced to a mammalian host, we infected ferrets with H5N1 viruses. As expected, all ferrets infected with the human H5N1 isolate A/Vietnam/1203/2004 showed severe disease and virus replication outside the respiratory tract in multiple organs including the brain. In contrast infection of ferrets with the avian H5N1 virus A/Chicken/Laos/Xaythiani26/2006 showed a different collective pattern of infection; many ferrets developed and cleared a mild respiratory infection but a subset (25–50%), showed extended replication in the upper respiratory tract and developed infection in distal sites. Virus from these severely infected ferrets was commonly found in tissues that included liver and small intestine. In most instances the virus had acquired the common virulence substitution PB2 E627K but, in one case, a previously unidentified combination of two amino acid substitutions at PB2 S489P and NP V408I, which enhanced polymerase activity, was found. We noted that virus with high pathogenicity adaptations could be dominant in an extra-respiratory site without being equally represented in the nasal wash. Further ferret passage of these mutated viruses resulted in high pathogenicity in all ferrets. These findings illustrate the remarkable ability of avian influenza viruses that avoid clearance in the respiratory tract, to mutate towards a high pathogenicity phenotype during just a single passage in ferrets and also indicate a window of less than 5 days in which treatment may curtail systemic infection.

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