Genetic characterization of H5N1 influenza A viruses isolated from zoo tigers in Thailand

Amonsin, Alongkorn; Payungporn, Sunchai; Theamboonlers, Apiradee; Thanawongnuwech, Roongroje; Suradhat, Sanipa; Pariyothorn, Nuananong; Tantilertcharoen, Rachod; Damrongwantanapokin, Sudarat; Buranathai, Chantanee; Chaisingh, Arunee; Songserm, Thaweesak; Poovorawan, Yong

doi:10.1016/j.virol.2005.08.032

Cited by 91 publications

(58 citation statements)

References 33 publications

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“…Their study used a human H5N1 virus isolate of clade 1 (A/Vietnam/1203/2004) which bears 627K. Within the clade 1 virus group, some viruses isolated from human and feline cases contained the 627K mutation, but the majority of natural avian isolates retained 627E (Table 1) (34,51). Interestingly, Schat and coworkers (42) also performed in vivo studies with viruses engineered to be LPAIVs by removal of the multibasic cleavage site in the HA protein.…”

Section: Discussionmentioning

confidence: 99%

The Effect of the PB2 Mutation 627K on Highly Pathogenic H5N1 Avian Influenza Virus Is Dependent on the Virus Lineage

Long

Howard

Núñez

et al. 2013

J Virol

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The 50-92 PB2 627K was genetically unstable during virus propagation, resulting in reversion to PB2 627E or the accumulation of the additional mutation PB2 628R and/or a synonymous mutation from an A to a G nucleotide at nucleotide position 1869 (PB2 A1869G). Intriguingly, PB2 628R and/or A1869G appeared to improve the genetic stability of 50-92 PB2 627K. However, the replication of 50-92 PB2 627K in conjunction with these stabilizing mutations was significantly restricted in experimentally infected chickens, where reversion to PB2 627E occurred. In contrast, no significant effects on viral fitness were observed for Ty/05 PB2 627E or 627K in in vitro or in vivo experiments. Our observations suggest that PB2 627K is supported in Eurasianlineage viruses; in contrast, PB2 627K carries a significant fitness cost in the historical pre-Asian 50-92 virus.

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Section: Discussionmentioning

confidence: 99%

The Effect of the PB2 Mutation 627K on Highly Pathogenic H5N1 Avian Influenza Virus Is Dependent on the Virus Lineage

Long

Howard

Núñez

et al. 2013

J Virol

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“…It was reported that the H5N1 virus can infect and cause death in mammals such as mice (5,9,12,14,29), cats (21), tigers (2), ferrets (11,26), monkeys (40), and humans (7,49,55). High-level inductions of proinflammatory cytokines in mammals infected with the H5N1 viruses, referred to as "cytokine storms," have been hypothesized to contribute to the severity of pathological changes and ultimate death (4,7,13,45,55).…”

mentioning

confidence: 99%

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

Okada

Itoh

et al. 2009

J Virol

141

123

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The Asian H5N1 highly pathogenic avian influenza (HPAI) viruses have been increasing in 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 times (MDTs) of chickens infected with the Asian H5N1 A/chicken/Yamaguchi/7/04 (CkYM7) strain with those infected with the H5N1 Duck/Yokohama/aq10/03 (DkYK10) strain, using a wireless thermosensor. Asian H5N1 CkYM7 caused peracute 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 antiviral and proinflammatory cytokine mRNA expressions at 24 h postinfection (hpi) that suddenly decreased 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 the low-pathogenicity H5N2 A/chicken/Ibaraki/1/2004 strain. 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 twofold 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 replication of the virus in macrophages and vascular endothelial cells, which resulted in disruption of the thermoregulation system and innate immune responses.

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“…At necropsy, affected organs, intestinal content and pleural fluid are sampled. After nucleic acid extraction, a RT-PCR is performed using primers designed to identify the haemagglutinin and neuraminidase genes (Keawcharoen et al, 2004) as well as the nucleocapsid gene (Amonsin et al, 2006). H5N1 virus antigens are identified by immunohistochemistry on sections of affected organs, using a monoclonal antibody specific for the nucleocapsid of influenza A virus (Keawcharoen et al, 2004;Rimmelzwaan et al, 2006); a polyclonal goat antiserum against H5N1 virus has also been used (Songserm et al, 2006a).…”

Section: Diagnosismentioning

confidence: 99%

Highly pathogenic avian influenza H5N1 virus in cats and other carnivores

Thiry¹,

Zicola²,

Addie³

et al. 2007

Veterinary Microbiology

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The Asian lineage highly pathogenic avian influenza (HPAI) H5N1 virus is a known pathogen of birds. Only recently, the virus has been reported to cause sporadic fatal disease in carnivores, and its zoonotic potential has been dominating the popular media. Attention to felids was drawn by two outbreaks with high mortality in tigers, leopards and other exotic felids in Thailand. Subsequently, domestic cats were found naturally infected and experimentally susceptible to H5N1 virus. A high susceptibility of the dog to H3N8 equine influenza A virus had been reported earlier, and recently also HPAI H5N1 virus has been identified as a canine pathogen. The ferret, hamster and mouse are suitable as experimental animals; importantly, these species are also kept as pets. Experimental intratracheal and oral infection of cats with an HPAI H5N1 virus isolate from a human case resulted in lethal disease; furthermore, cats have been infected by the feeding of infected chickens. Spread of the infection from experimentally infected to in-contact cats has been reported. The epidemiological role of the cat and other pet animal species in transmitting HPAI H5N1 virus to humans needs continuous consideration and attention. #

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Genetic characterization of H5N1 influenza A viruses isolated from zoo tigers in Thailand

Cited by 91 publications

References 33 publications

The Effect of the PB2 Mutation 627K on Highly Pathogenic H5N1 Avian Influenza Virus Is Dependent on the Virus Lineage

The Effect of the PB2 Mutation 627K on Highly Pathogenic H5N1 Avian Influenza Virus Is Dependent on the Virus Lineage

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

Highly pathogenic avian influenza H5N1 virus in cats and other carnivores

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