Sequence analysis of the equine H7 influenza virus haemagglutinin gene

Gibson, C.A.; Daniels, Rod S.; Oxford, John; McCauley, John W.

doi:10.1016/0168-1702(92)90037-a

Cited by 26 publications

(21 citation statements)

References 34 publications

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“…However, the origin of the recombinant insert remains a mystery. Previous analysis of either sense of the nucleotide sequence in the nucleotide databases failed to identify significant homology (Gibson et al, 1992), and re-analysis by our laboratory has confirmed a lack of homology with currently available database sequences. Therefore, it is possible that emergence of a HPAI, at least in part, can occur by novel insertions in the cleavage site and should be considered in surveillance studies.…”

Section: Discussionsupporting

confidence: 51%

“…However, only four basic residues are found in the equine H7N7 HA cleavage site. This is intriguing, since intracellular cleavage was observed for the equine H7 HA (Gibson et al, 1992), (Takeuchi et al, 1994), but in contrast, was not observed by mutational analysis of other HA subtypes when the cleavage site contained only four basic residues (Gohrbandt et al, 2011, Walker and Kawaoka, 1993). A unique feature of the equine H7 HA cleavage site is the presence of an eleven amino acid insertion (consensus sequence=NSTHKQLTHHM) directly N-terminal to the tetrabasic cleavage site (RKKR) (Fig.…”

Section: Introductionmentioning

confidence: 98%

“…1). This insertion appears to have occurred coincident with the transmission of an avian H7N7 to horses (Gibson et al, 1992). It remains unclear whether there is a functional role of this unique eleven amino acid insertion, but it may play a role in HA stability or cleavage due to the presence of three ionizable histidine residues and the addition of a predicted glycosylation site within the insertion.…”

Section: Introductionmentioning

confidence: 99%

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Acquisition of a novel eleven amino acid insertion directly N-terminal to a tetrabasic cleavage site confers intracellular cleavage of an H7N7 influenza virus hemagglutinin

et al. 2012

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A critical feature of highly pathogenic avian influenza viruses (H5N1 and H7N7) is the efficient intracellular cleavage of the hemagglutinin (HA) protein. H7N7 viruses also exist in equine species, and a unique feature of the equine H7N7 HA is the presence of an eleven amino acid insertion directly N-terminal to a tetrabasic cleavage site. Here, we show that three histidine residues within the unique insertion of the equine H7N7 HA are essential for intracellular cleavage. An asparagine residue within the insertion-derived glycosylation site was also found to be essential for intracellular cleavage. The presence of the histidine residues also appear to be involved in triggering fusion, since mutation of the histidine residues resulted in a destabilizing effect. Importantly, the addition of a tetrabasic site and the eleven amino acid insertion conferred efficient intracellular cleavage to the HA of an H7N3 low pathogenicity avian influenza virus. Our studies show that acquisition of the eleven amino acid insertion offers an alternative mechanism for intracellular cleavage of influenza HA.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Acquisition of a novel eleven amino acid insertion directly N-terminal to a tetrabasic cleavage site confers intracellular cleavage of an H7N7 influenza virus hemagglutinin

et al. 2012

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“…Other influenza viruses have been observed with 10 additional amino acids at the HA cleavage site including the equine type 1 (H7N7) viruses, with A/Equine/Prague/56 as the prototype virus. These viruses have four basic amino acids at the cleavage site and can grow in cell culture without trypsin ( 28 ), a characteristic for avian viruses of the highly pathogenic phenotype. However, the H7N7 viruses are not considered to cause a systemic disease in horses, but they have been described as causing systemic infection in mice without prior adaptation ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Recombination Resulting in Virulence Shift in Avian Influenza Outbreak, Chile

Suarez

Senne

Banks

et al. 2004

Emerg. Infect. Dis.

312

242

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Influenza A viruses occur worldwide in wild birds and are occasionally associated with outbreaks in commercial chickens and turkeys. However, avian influenza viruses have not been isolated from wild birds or poultry in South America. A recent outbreak in chickens of H7N3 low pathogenic avian influenza (LPAI) occurred in Chile. One month later, after a sudden increase in deaths, H7N3 highly pathogenic avian influenza (HPAI) virus was isolated. Sequence analysis of all eight genes of the LPAI virus and the HPAI viruses showed minor differences between the viruses except at the hemagglutinin (HA) cleavage site. The LPAI virus had a cleavage site similar to other low pathogenic H7 viruses, but the HPAI isolates had a 30 nucleotide insert. The insertion likely occurred by recombination between the HA and nucleoprotein genes of the LPAI virus, resulting in a virulence shift. Sequence comparison of all eight gene segments showed the Chilean viruses were also distinct from all other avian influenza viruses and represent a distinct South American clade.

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“…ow-pathogenic (LP) avian influenza A viruses (AIVs) of the H5 and H7 subtypes in wild avian species are unique compared to the other 14 AIV subtypes, as they can become highly pathogenic and infect both poultry and mammalian species, including humans, seals, swine, and horses (1)(2)(3)(4)(5). The first studied AIV was an H7 virus originally described by Perroncito in northern Italy in 1878 as "fowl plague" (6).…”

mentioning

confidence: 99%

Potential for Low-Pathogenic Avian H7 Influenza A Viruses To Replicate and Cause Disease in a Mammalian Model

Zanin

Koçer

Poulson

et al. 2017

J Virol

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H7 subtype influenza A viruses are widely distributed and have been responsible for human infections and numerous outbreaks in poultry with significant impact. Despite this, the disease-causing potential of the precursor low-pathogenic (LP) H7 viruses from the wild bird reservoir has not been investigated. Our objective was to assess the disease-causing potential of 30 LP H7 viruses isolated from wild avian species in the United States and Canada using the DBA/2J mouse model. Without prior mammalian adaptation, the majority of viruses, 27 (90%), caused mortality in mice. Of these, 17 (56.7%) caused 100% mortality and 24 were of pathogenicity similar to that of A/Anhui/1/2013 (H7N9), which is highly pathogenic in mice. Viruses of duck origin were more pathogenic than those of shorebird origin, as 13 of 18 (72.2%) duck origin viruses caused 100% mortality while 4 of 12 (33.3%) shorebird origin viruses caused 100% mortality, despite there being no difference in mean lung viral titers between the groups. Replication beyond the respiratory tract was also evident, particularly in the heart and brain. Of the 16 viruses studied for fecal shedding, 11 were detected in fecal samples. These viruses exhibited a strong preference for avian-type ␣2,3-linked sialic acids; however, binding to mammalian-type ␣2,6-linked sialic acids was also detected. These findings indicate that LP avian H7 influenza A viruses are able to infect and cause disease in mammals without prior adaptation and therefore pose a potential public health risk.IMPORTANCE Low-pathogenic (LP) avian H7 influenza A viruses are widely distributed in the avian reservoir and are the precursors of numerous outbreaks of highly pathogenic avian influenza viruses in commercial poultry farms. However, unlike highly pathogenic H7 viruses, the disease-causing potential of LP H7 viruses from the wild bird reservoir has not been investigated. To address this, we studied 30 LP avian H7 viruses isolated from wild avian species in the United States and Canada using the DBA/2J mouse model. Surprisingly, the majority of these viruses, 90%, caused mortality in mice without prior mammalian adaptation, and 56.7% caused 100% mortality. There was also evidence of spread beyond the respiratory tract and fecal shedding. Therefore, the disease-causing potential of LP avian H7 influenza A viruses in mammals may be underestimated, and these viruses therefore pose a potential public health risk.KEYWORDS H7, influenza, avian viruses, viral pathogenesis

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Sequence analysis of the equine H7 influenza virus haemagglutinin gene

Cited by 26 publications

References 34 publications

Acquisition of a novel eleven amino acid insertion directly N-terminal to a tetrabasic cleavage site confers intracellular cleavage of an H7N7 influenza virus hemagglutinin

Acquisition of a novel eleven amino acid insertion directly N-terminal to a tetrabasic cleavage site confers intracellular cleavage of an H7N7 influenza virus hemagglutinin

Recombination Resulting in Virulence Shift in Avian Influenza Outbreak, Chile

Potential for Low-Pathogenic Avian H7 Influenza A Viruses To Replicate and Cause Disease in a Mammalian Model

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