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The pathogenicity of swan derived H5N1 virus in birds and mammals and its gene analysis.

Tabynov K, Sansyzbay A, Sandybayev N, Mambetaliyev M - Virol. J. (2014)

Bottom Line: SW/3/06 does not possess the prime virulence determinant of HPAIV - a polybasic HA cleavage site - and is highly pathogenic in chickens.The HI assay demonstrated all not diseased animals infected with the SW/3/06 virus had undergone seroconversion by 14, 21 and 28 dpi.Eleven mutations in the seven genes were present in SW/3/06.

View Article: PubMed Central - PubMed

Affiliation: The Research Institute for Biological Safety Problems, Zhambylskaya oblast, Kordayskiy rayon, Gvardeiskiy, 080409, Republic of Kazakhstan. tabynov777@mail.ru.

ABSTRACT

Background: Highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in poultry and can infect and cause mortality in birds and mammals; the genetic determinants of their increased virulence are largely unknown. The main purpose of this work was to determine the correlation between known molecular determinants of virulence in different avian influenza virus (AIV) genes and the results of experimental infection of birds and mammals with AIV strain A/swan/Mangistau/3/06 (H5N1; SW/3/06).

Methods and results: We examined the virulence of SW/3/06 in four species of birds (chickens, ducks, turkeys, geese) and five species of mammals (mice, guinea pigs, cats, dogs, pigs), and identified the molecular determinants of virulence in 11 genes (HA, NA, PB1, PB1-F2, PB2, PA, NS1, NS2, M1, M2 and NP). SW/3/06 does not possess the prime virulence determinant of HPAIV - a polybasic HA cleavage site - and is highly pathogenic in chickens. SW/3/06 replicated efficiently in chickens, ducks, turkeys, mice and dogs, causing 100% mortality within 1.6-5.2 days. In addition, no mortalities were observed in geese, guinea pigs, cats and pigs. The HI assay demonstrated all not diseased animals infected with the SW/3/06 virus had undergone seroconversion by 14, 21 and 28 dpi. Eleven mutations in the seven genes were present in SW/3/06. These mutations may play a role in the pathogenicity of this strain in chickens, ducks, turkeys, mice and dogs. Together or separately, mutations 228S-103S-318I in HA may play a role in the efficient replication of SW/3/06 in mammals (mice, dogs, pigs).

Conclusions: This study provides new information on the pathogenicity of the newly-isolated swan derived H5N1 virus in birds and mammals, and explored the role of molecular determinants of virulence in different genes; such studies may help to identify key virulence or adaptation markers that can be used for global surveillance of viruses threatening to emerge into the human population.

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Viral titers of nasal swabs collected from pigs inoculated with the SW/3/06 virus. Each data point and rhombus represents the mean ± SEM viral titer (log10 EID50/ml of sample media) for pigs positive for the influenza virus in Rapid Test Kit Н5 AIV Ag. Numbers of pigs shedding virus are shown in each point and rhombus. The lower virus detection limit was 100.75 EID50/mL (**P <0.01, ***P <0.001; two-way ANOVA followed by Tukey's multiple comparisons test).
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Fig7: Viral titers of nasal swabs collected from pigs inoculated with the SW/3/06 virus. Each data point and rhombus represents the mean ± SEM viral titer (log10 EID50/ml of sample media) for pigs positive for the influenza virus in Rapid Test Kit Н5 AIV Ag. Numbers of pigs shedding virus are shown in each point and rhombus. The lower virus detection limit was 100.75 EID50/mL (**P <0.01, ***P <0.001; two-way ANOVA followed by Tukey's multiple comparisons test).

Mentions: To detect the virus and determine infective titers, nasal and rectal swabs were collected from the infected pigs. The virus was not detected in any rectal swabs. However, the virus was detected in nasal swabs taken on 1, 3, 5 and 7 dpi in all inoculated pigs (Figure 7). The viral titers of the swabs taken from the animals in the i.n. inoculated group were significantly higher than that of the i.m. inoculated group (from P <0.01 to P <0.001; Figure 7). In general, the H5N1 viral titers were similar in nasal samples collected from the i.n. and i.m. inoculated groups on days 1, 3 and 5, and were higher than the titer of samples collected on day 7 (P <0.01, Figure 7).Figure 7


The pathogenicity of swan derived H5N1 virus in birds and mammals and its gene analysis.

Tabynov K, Sansyzbay A, Sandybayev N, Mambetaliyev M - Virol. J. (2014)

Viral titers of nasal swabs collected from pigs inoculated with the SW/3/06 virus. Each data point and rhombus represents the mean ± SEM viral titer (log10 EID50/ml of sample media) for pigs positive for the influenza virus in Rapid Test Kit Н5 AIV Ag. Numbers of pigs shedding virus are shown in each point and rhombus. The lower virus detection limit was 100.75 EID50/mL (**P <0.01, ***P <0.001; two-way ANOVA followed by Tukey's multiple comparisons test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4264262&req=5

Fig7: Viral titers of nasal swabs collected from pigs inoculated with the SW/3/06 virus. Each data point and rhombus represents the mean ± SEM viral titer (log10 EID50/ml of sample media) for pigs positive for the influenza virus in Rapid Test Kit Н5 AIV Ag. Numbers of pigs shedding virus are shown in each point and rhombus. The lower virus detection limit was 100.75 EID50/mL (**P <0.01, ***P <0.001; two-way ANOVA followed by Tukey's multiple comparisons test).
Mentions: To detect the virus and determine infective titers, nasal and rectal swabs were collected from the infected pigs. The virus was not detected in any rectal swabs. However, the virus was detected in nasal swabs taken on 1, 3, 5 and 7 dpi in all inoculated pigs (Figure 7). The viral titers of the swabs taken from the animals in the i.n. inoculated group were significantly higher than that of the i.m. inoculated group (from P <0.01 to P <0.001; Figure 7). In general, the H5N1 viral titers were similar in nasal samples collected from the i.n. and i.m. inoculated groups on days 1, 3 and 5, and were higher than the titer of samples collected on day 7 (P <0.01, Figure 7).Figure 7

Bottom Line: SW/3/06 does not possess the prime virulence determinant of HPAIV - a polybasic HA cleavage site - and is highly pathogenic in chickens.The HI assay demonstrated all not diseased animals infected with the SW/3/06 virus had undergone seroconversion by 14, 21 and 28 dpi.Eleven mutations in the seven genes were present in SW/3/06.

View Article: PubMed Central - PubMed

Affiliation: The Research Institute for Biological Safety Problems, Zhambylskaya oblast, Kordayskiy rayon, Gvardeiskiy, 080409, Republic of Kazakhstan. tabynov777@mail.ru.

ABSTRACT

Background: Highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in poultry and can infect and cause mortality in birds and mammals; the genetic determinants of their increased virulence are largely unknown. The main purpose of this work was to determine the correlation between known molecular determinants of virulence in different avian influenza virus (AIV) genes and the results of experimental infection of birds and mammals with AIV strain A/swan/Mangistau/3/06 (H5N1; SW/3/06).

Methods and results: We examined the virulence of SW/3/06 in four species of birds (chickens, ducks, turkeys, geese) and five species of mammals (mice, guinea pigs, cats, dogs, pigs), and identified the molecular determinants of virulence in 11 genes (HA, NA, PB1, PB1-F2, PB2, PA, NS1, NS2, M1, M2 and NP). SW/3/06 does not possess the prime virulence determinant of HPAIV - a polybasic HA cleavage site - and is highly pathogenic in chickens. SW/3/06 replicated efficiently in chickens, ducks, turkeys, mice and dogs, causing 100% mortality within 1.6-5.2 days. In addition, no mortalities were observed in geese, guinea pigs, cats and pigs. The HI assay demonstrated all not diseased animals infected with the SW/3/06 virus had undergone seroconversion by 14, 21 and 28 dpi. Eleven mutations in the seven genes were present in SW/3/06. These mutations may play a role in the pathogenicity of this strain in chickens, ducks, turkeys, mice and dogs. Together or separately, mutations 228S-103S-318I in HA may play a role in the efficient replication of SW/3/06 in mammals (mice, dogs, pigs).

Conclusions: This study provides new information on the pathogenicity of the newly-isolated swan derived H5N1 virus in birds and mammals, and explored the role of molecular determinants of virulence in different genes; such studies may help to identify key virulence or adaptation markers that can be used for global surveillance of viruses threatening to emerge into the human population.

Show MeSH
Related in: MedlinePlus