Giuseppe
Emeritus
J Virol. 2009 Mar 18. [Epub ahead of print]
Early Control of H5N1 Influenza Virus Replication by the Type I Interferon Response in Mice.
Szretter KJ, Gangappa S, Belser JA, Zeng H, Chen H, Matsuoka Y, Sambhara S, Swayne DE, Tumpey TM, Katz JM. - Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333; Emory University, Atlanta, Georgia 30322; and Southeast Poultry Research Laboratory, Agricultural Research Service, U.S. Department of Agriculture, Athens, Georgia 30606.
Widespread distribution of highly pathogenic avian H5N1 influenza viruses in domesticated and wild birds continues to pose a threat to public health as interspecies transmission of virus has resulted in increasing numbers of human disease.
Although the pathogenic mechanism(s) of H5N1 influenza viruses have not been fully elucidated, it has been suggested that the ability to evade host innate responses, such as the type I interferon response may contribute to the virulence of these viruses in mammals.
We investigated the role of type I interferons (IFNalphabeta) might play in H5N1 pathogenicity in vivo, by comparing the kinetics and outcome of H5N1 virus infection in IFNalphabetaR-deficient and SvEv129 wildtype mice using two avian influenza A viruses isolated from humans, A/Hong Kong/483/97 (HK/483) and A/Hong Kong/486/97 (HK/486) that exhibit high and low lethality in mice, respectively.
IFNalphabetaR-deficient mice experienced significantly more weight-loss and more rapid time-to-death compared to wildtype mice. HK/486 virus caused a systemic infection similar to HK/483 virus in IFNalphabetaR-deficient mice, suggesting a role for IFNalphabeta in controlling the systemic spread of this H5N1 virus.
HK/483 virus replicated more efficiently than HK/486 virus both in vivo and in vitro. However, replication of both viruses was significantly reduced following pretreatment with IFNalphabeta.
These results suggest a role for IFNalphabeta response in the control of H5N1 virus replication both in vivo and in vitro and as such may provide some degree of protection to the host in the early stages of infection.
PMID: 19297490 [PubMed - as supplied by publisher]
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Early Control of H5N1 Influenza Virus Replication by the Type I Interferon Response in Mice.
Szretter KJ, Gangappa S, Belser JA, Zeng H, Chen H, Matsuoka Y, Sambhara S, Swayne DE, Tumpey TM, Katz JM. - Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333; Emory University, Atlanta, Georgia 30322; and Southeast Poultry Research Laboratory, Agricultural Research Service, U.S. Department of Agriculture, Athens, Georgia 30606.
Widespread distribution of highly pathogenic avian H5N1 influenza viruses in domesticated and wild birds continues to pose a threat to public health as interspecies transmission of virus has resulted in increasing numbers of human disease.
Although the pathogenic mechanism(s) of H5N1 influenza viruses have not been fully elucidated, it has been suggested that the ability to evade host innate responses, such as the type I interferon response may contribute to the virulence of these viruses in mammals.
We investigated the role of type I interferons (IFNalphabeta) might play in H5N1 pathogenicity in vivo, by comparing the kinetics and outcome of H5N1 virus infection in IFNalphabetaR-deficient and SvEv129 wildtype mice using two avian influenza A viruses isolated from humans, A/Hong Kong/483/97 (HK/483) and A/Hong Kong/486/97 (HK/486) that exhibit high and low lethality in mice, respectively.
IFNalphabetaR-deficient mice experienced significantly more weight-loss and more rapid time-to-death compared to wildtype mice. HK/486 virus caused a systemic infection similar to HK/483 virus in IFNalphabetaR-deficient mice, suggesting a role for IFNalphabeta in controlling the systemic spread of this H5N1 virus.
HK/483 virus replicated more efficiently than HK/486 virus both in vivo and in vitro. However, replication of both viruses was significantly reduced following pretreatment with IFNalphabeta.
These results suggest a role for IFNalphabeta response in the control of H5N1 virus replication both in vivo and in vitro and as such may provide some degree of protection to the host in the early stages of infection.
PMID: 19297490 [PubMed - as supplied by publisher]
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