Limits...
Assessing the fitness of distinct clades of influenza A (H9N2) viruses.

- Emerg Microbes Infect (2013)

Bottom Line: Influenza A (H9N2) viruses are a genetically diverse population that infects wild and domestic avian species and mammals and contributed the internal gene segments to the A/H5N1 and A/H7N9 viruses associated with lethal human infections.However, the A/swine/Hong Kong/9A-1/1998 and A/chicken/Hong Kong/G9/1997 viruses also displayed several features suggesting a fitness profile adapted to human infection and transmission.Therefore, we conclude that comprehensive risk analyses based on surveillance of circulating influenza virus strains are necessary to assess the potential for human infection by emerging influenza A viruses.

View Article: PubMed Central - PubMed

ABSTRACT
Influenza A (H9N2) viruses are a genetically diverse population that infects wild and domestic avian species and mammals and contributed the internal gene segments to the A/H5N1 and A/H7N9 viruses associated with lethal human infections. Here we comprehensively assess the potential risk to mammals of a diverse panel of A/H9N2 viruses, representing the major H9N2 clades, using a combination of in vitro assays (e.g., antiviral susceptibility and virus growth in primary differentiated human airway cells) and in vivo assays (e.g., replication, transmission and/or pathogenicity of viruses in ducks, pigs, mice and ferrets). We observed that viruses isolated from humans, A/Hong Kong/1073/1999 and A/Hong Kong/33982/2009, had the highest risk potential. However, the A/swine/Hong Kong/9A-1/1998 and A/chicken/Hong Kong/G9/1997 viruses also displayed several features suggesting a fitness profile adapted to human infection and transmission. The North American avian H9N2 clade virus had the lowest risk profile, and the other viruses tested displayed various levels of fitness across individual assays. In many cases, the known genotypic polymorphisms alone were not sufficient to accurately predict the virus' phenotype. Therefore, we conclude that comprehensive risk analyses based on surveillance of circulating influenza virus strains are necessary to assess the potential for human infection by emerging influenza A viruses.

No MeSH data available.


Related in: MedlinePlus

Pathogenicity of H9N2 viruses in pigs. Three-week-old pigs were inoculated intranasally with an H9N2 virus or were in DC with inoculated pigs (n=2 pigs/group), and weight was monitored every 2 days for 14 dpi. No significant differences in weight gain were identified across the groups. The data represent the average relative weight change compared to the animals' weights at 0 dpi. Each pig is plotted as a separate line. DC, direct contact.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3924558&req=5

fig3: Pathogenicity of H9N2 viruses in pigs. Three-week-old pigs were inoculated intranasally with an H9N2 virus or were in DC with inoculated pigs (n=2 pigs/group), and weight was monitored every 2 days for 14 dpi. No significant differences in weight gain were identified across the groups. The data represent the average relative weight change compared to the animals' weights at 0 dpi. Each pig is plotted as a separate line. DC, direct contact.

Mentions: None of the pigs showed clinical symptoms (coughing, sneezing or malaise) at any time, and all gained weight with no significant differences between any of the groups (inoculated or direct contact) (Figure 3). Despite the lack of clinical symptoms, one of the HK/33982 virus-inoculated pigs shed virus, reaching titers of 104 TCID50/mL and 102.7 TCID50/mL on 5 and 7 dpi, respectively. The virus also transmitted to one of the direct contact animals, which shed 103.3 TCID50/mL at 9 days post-contact. None of the pigs seroconverted by 14 dpi/post-contact, including the swine/HK virus-infected animals, as determined by HI assay. These results suggest that H9N2 virus replication is limited in pigs, though the HK/33982 (G1 lineage) virus can replicate to moderate titers and transmit by direct contact.


Assessing the fitness of distinct clades of influenza A (H9N2) viruses.

- Emerg Microbes Infect (2013)

Pathogenicity of H9N2 viruses in pigs. Three-week-old pigs were inoculated intranasally with an H9N2 virus or were in DC with inoculated pigs (n=2 pigs/group), and weight was monitored every 2 days for 14 dpi. No significant differences in weight gain were identified across the groups. The data represent the average relative weight change compared to the animals' weights at 0 dpi. Each pig is plotted as a separate line. DC, direct contact.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3924558&req=5

fig3: Pathogenicity of H9N2 viruses in pigs. Three-week-old pigs were inoculated intranasally with an H9N2 virus or were in DC with inoculated pigs (n=2 pigs/group), and weight was monitored every 2 days for 14 dpi. No significant differences in weight gain were identified across the groups. The data represent the average relative weight change compared to the animals' weights at 0 dpi. Each pig is plotted as a separate line. DC, direct contact.
Mentions: None of the pigs showed clinical symptoms (coughing, sneezing or malaise) at any time, and all gained weight with no significant differences between any of the groups (inoculated or direct contact) (Figure 3). Despite the lack of clinical symptoms, one of the HK/33982 virus-inoculated pigs shed virus, reaching titers of 104 TCID50/mL and 102.7 TCID50/mL on 5 and 7 dpi, respectively. The virus also transmitted to one of the direct contact animals, which shed 103.3 TCID50/mL at 9 days post-contact. None of the pigs seroconverted by 14 dpi/post-contact, including the swine/HK virus-infected animals, as determined by HI assay. These results suggest that H9N2 virus replication is limited in pigs, though the HK/33982 (G1 lineage) virus can replicate to moderate titers and transmit by direct contact.

Bottom Line: Influenza A (H9N2) viruses are a genetically diverse population that infects wild and domestic avian species and mammals and contributed the internal gene segments to the A/H5N1 and A/H7N9 viruses associated with lethal human infections.However, the A/swine/Hong Kong/9A-1/1998 and A/chicken/Hong Kong/G9/1997 viruses also displayed several features suggesting a fitness profile adapted to human infection and transmission.Therefore, we conclude that comprehensive risk analyses based on surveillance of circulating influenza virus strains are necessary to assess the potential for human infection by emerging influenza A viruses.

View Article: PubMed Central - PubMed

ABSTRACT
Influenza A (H9N2) viruses are a genetically diverse population that infects wild and domestic avian species and mammals and contributed the internal gene segments to the A/H5N1 and A/H7N9 viruses associated with lethal human infections. Here we comprehensively assess the potential risk to mammals of a diverse panel of A/H9N2 viruses, representing the major H9N2 clades, using a combination of in vitro assays (e.g., antiviral susceptibility and virus growth in primary differentiated human airway cells) and in vivo assays (e.g., replication, transmission and/or pathogenicity of viruses in ducks, pigs, mice and ferrets). We observed that viruses isolated from humans, A/Hong Kong/1073/1999 and A/Hong Kong/33982/2009, had the highest risk potential. However, the A/swine/Hong Kong/9A-1/1998 and A/chicken/Hong Kong/G9/1997 viruses also displayed several features suggesting a fitness profile adapted to human infection and transmission. The North American avian H9N2 clade virus had the lowest risk profile, and the other viruses tested displayed various levels of fitness across individual assays. In many cases, the known genotypic polymorphisms alone were not sufficient to accurately predict the virus' phenotype. Therefore, we conclude that comprehensive risk analyses based on surveillance of circulating influenza virus strains are necessary to assess the potential for human infection by emerging influenza A viruses.

No MeSH data available.


Related in: MedlinePlus