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J Virol. 2009 May 20. [Epub ahead of print]
Association of Increased Pathogenicity of Asian H5N1 Highly Pathogenic Avian Influenza Viruses in Chickens with Highly Efficient Viral Replication Accompanied by Early Destruction of Innate Immune Responses.
Suzuki K, Okada H, Itoh T, Tada T, Mase M, Nakamura K, Kubo M, Tsukamoto K. Research Team for Zoonotic Diseases, Research Team for Viral Disease, and Research Team for Epidemiology, National Institute of Animal Health (NIAH), National Agriculture and Food Research Organization (NARO), 3-1-5 Kannondai, Tsukuba, Ibaraki 305-0856, Japan; National Institute of Advanced Industrial Science and Technology (AIST), 1-2-1 Namiki, Tsukuba, Ibaraki305-8564 Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation.
The Asian H5N1 highly pathogenic (HP) avian influenza (AI) viruses have been increasing pathogenicity in diverse avian species since 1996, and are now widespread in Asian, European, and African countries.
To better understand the basis of the increased pathogenicity of recent Asian H5N1 HPAI viruses in chickens, we compared the fevers and mean death time (MDT) of chickens infected with the Asian H5N1 A/chicken/Yamaguchi/7/04 (CkYM7) with those infected with H5N1 Duck/Yokohama/aq10/03 (DkYK10) using a wireless thermo-sensor.
Asian H5N1 CkYM7 caused per-acute death in chickens before fever could be induced, whereas DkYK10 virus induced high fevers and had a long MDT. Real-time PCR analyses of cytokine mRNA expressions showed that CkYM7 quickly induced anti-viral and proinflammatory cytokine mRNA expressions at 24 hpi that suddenly depressed at 32 hpi.
In contrast, these cytokine mRNA expressions increased at 24 hpi in the DkYK10 group, but decreased from 48 hpi onward to levels similar to those resulting from infection with low pathogenic H5N2 A/chicken/Ibaraki/1/2004 (CkIB1).
Sequential titrations of viruses in lungs, spleens, and kidneys demonstrated that CkYM7 replicated rapidly and efficiently in infected chickens, and that the viral titers were more than two fold higher than those of DkYK10.
CkYM7 preferentially and efficiently replicated in macrophages and vascular endothelial cells while DkYK10 grew moderately in macrophages.
These results indicate that the increased pathogenicity in chickens of the recent Asian H5N1 HPAI viruses may be associated with extremely rapid and high viral replication of the virus in macrophages and vascular endothelial cells, which resulted in disruption of thermoregulation and innate immune responses.
PMID: 19457987 [PubMed - as supplied by publisher]
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Association of Increased Pathogenicity of Asian H5N1 Highly Pathogenic Avian Influenza Viruses in Chickens with Highly Efficient Viral Replication Accompanied by Early Destruction of Innate Immune Responses.
Suzuki K, Okada H, Itoh T, Tada T, Mase M, Nakamura K, Kubo M, Tsukamoto K. Research Team for Zoonotic Diseases, Research Team for Viral Disease, and Research Team for Epidemiology, National Institute of Animal Health (NIAH), National Agriculture and Food Research Organization (NARO), 3-1-5 Kannondai, Tsukuba, Ibaraki 305-0856, Japan; National Institute of Advanced Industrial Science and Technology (AIST), 1-2-1 Namiki, Tsukuba, Ibaraki305-8564 Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation.
The Asian H5N1 highly pathogenic (HP) avian influenza (AI) viruses have been increasing pathogenicity in diverse avian species since 1996, and are now widespread in Asian, European, and African countries.
To better understand the basis of the increased pathogenicity of recent Asian H5N1 HPAI viruses in chickens, we compared the fevers and mean death time (MDT) of chickens infected with the Asian H5N1 A/chicken/Yamaguchi/7/04 (CkYM7) with those infected with H5N1 Duck/Yokohama/aq10/03 (DkYK10) using a wireless thermo-sensor.
Asian H5N1 CkYM7 caused per-acute death in chickens before fever could be induced, whereas DkYK10 virus induced high fevers and had a long MDT. Real-time PCR analyses of cytokine mRNA expressions showed that CkYM7 quickly induced anti-viral and proinflammatory cytokine mRNA expressions at 24 hpi that suddenly depressed at 32 hpi.
In contrast, these cytokine mRNA expressions increased at 24 hpi in the DkYK10 group, but decreased from 48 hpi onward to levels similar to those resulting from infection with low pathogenic H5N2 A/chicken/Ibaraki/1/2004 (CkIB1).
Sequential titrations of viruses in lungs, spleens, and kidneys demonstrated that CkYM7 replicated rapidly and efficiently in infected chickens, and that the viral titers were more than two fold higher than those of DkYK10.
CkYM7 preferentially and efficiently replicated in macrophages and vascular endothelial cells while DkYK10 grew moderately in macrophages.
These results indicate that the increased pathogenicity in chickens of the recent Asian H5N1 HPAI viruses may be associated with extremely rapid and high viral replication of the virus in macrophages and vascular endothelial cells, which resulted in disruption of thermoregulation and innate immune responses.
PMID: 19457987 [PubMed - as supplied by publisher]
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