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Transmission of equine influenza virus to English foxhounds.

Daly JM, Blunden AS, Macrae S, Miller J, Bowman SJ, Kolodziejek J, Nowotny N, Smith KC - Emerging Infect. Dis. (2008)

Bottom Line: We retrospectively demonstrated that an outbreak of severe respiratory disease in a pack of English foxhounds in the United Kingdom in September 2002 was caused by an equine influenza A virus (H3N8).We also demonstrated that canine respiratory tissue possesses the relevant receptors for infection with equine influenza virus.

View Article: PubMed Central - PubMed

Affiliation: Animal Health Trust, Kentford, Newmarket, Suffolk, UK. jshaw@liverpool.ac.uk

ABSTRACT
We retrospectively demonstrated that an outbreak of severe respiratory disease in a pack of English foxhounds in the United Kingdom in September 2002 was caused by an equine influenza A virus (H3N8). We also demonstrated that canine respiratory tissue possesses the relevant receptors for infection with equine influenza virus.

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Related in: MedlinePlus

Lectin staining for α2,3 sialic acid linkages on A) equine trachea and B) canine trachea; magnification x200; cell nuclei counterstained with Hoechst 33342 solution.
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Figure 2: Lectin staining for α2,3 sialic acid linkages on A) equine trachea and B) canine trachea; magnification x200; cell nuclei counterstained with Hoechst 33342 solution.

Mentions: An important factor in interspecies transmission is the ability of the hemagglutinin protein of the virus to bind to certain receptors on the host cells before the virus is internalized. Although all influenza A viruses recognize cell surface oligosaccharides with a terminal sialic acid, their receptor specificity varies; it is thought that species-specific differences in the distribution of linkages on respiratory epithelial cells influences the ability of influenza A viruses to transmit between species. Respiratory tract tissue samples were obtained within 2–4 hours of death from a horse and a greyhound, each euthanized for reasons other than this study, and rinsed extensively to remove surface mucous. The tissues were stained by immunofluorescence by using the lectins Sambucus nigra (SNA, specific for SAα2,6 galactose(Gal)/N-acetylgalactosaminide) and Maackia amurensis (MAA, specific for SAα2,3) as previously described (7). The MAA lectin bound strongly to the equine tracheal epithelium (Figure 2, panel A), which confirms the finding that the NeuAc2,3Gal linkage preferentially bound by equine influenza viruses is found on sialyloligosaccharides in the equine trachea (7). The MAA lectin also bound strongly to the canine respiratory epithelium (Figure 2, panel B) at all levels of the respiratory tract examined (distal, medial and proximal trachea; primary and secondary bronchi), which suggests that receptors with the required linkage for recognition by equine influenza virus are available on canine respiratory epithelial cells, although further subtle differences in receptor specificity may exist. The SNA lectin, specific for SAα2,6Gal, which did not bind to the equine tracheal epithelium, showed some binding to the canine epithelium (data not shown).


Transmission of equine influenza virus to English foxhounds.

Daly JM, Blunden AS, Macrae S, Miller J, Bowman SJ, Kolodziejek J, Nowotny N, Smith KC - Emerging Infect. Dis. (2008)

Lectin staining for α2,3 sialic acid linkages on A) equine trachea and B) canine trachea; magnification x200; cell nuclei counterstained with Hoechst 33342 solution.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2570814&req=5

Figure 2: Lectin staining for α2,3 sialic acid linkages on A) equine trachea and B) canine trachea; magnification x200; cell nuclei counterstained with Hoechst 33342 solution.
Mentions: An important factor in interspecies transmission is the ability of the hemagglutinin protein of the virus to bind to certain receptors on the host cells before the virus is internalized. Although all influenza A viruses recognize cell surface oligosaccharides with a terminal sialic acid, their receptor specificity varies; it is thought that species-specific differences in the distribution of linkages on respiratory epithelial cells influences the ability of influenza A viruses to transmit between species. Respiratory tract tissue samples were obtained within 2–4 hours of death from a horse and a greyhound, each euthanized for reasons other than this study, and rinsed extensively to remove surface mucous. The tissues were stained by immunofluorescence by using the lectins Sambucus nigra (SNA, specific for SAα2,6 galactose(Gal)/N-acetylgalactosaminide) and Maackia amurensis (MAA, specific for SAα2,3) as previously described (7). The MAA lectin bound strongly to the equine tracheal epithelium (Figure 2, panel A), which confirms the finding that the NeuAc2,3Gal linkage preferentially bound by equine influenza viruses is found on sialyloligosaccharides in the equine trachea (7). The MAA lectin also bound strongly to the canine respiratory epithelium (Figure 2, panel B) at all levels of the respiratory tract examined (distal, medial and proximal trachea; primary and secondary bronchi), which suggests that receptors with the required linkage for recognition by equine influenza virus are available on canine respiratory epithelial cells, although further subtle differences in receptor specificity may exist. The SNA lectin, specific for SAα2,6Gal, which did not bind to the equine tracheal epithelium, showed some binding to the canine epithelium (data not shown).

Bottom Line: We retrospectively demonstrated that an outbreak of severe respiratory disease in a pack of English foxhounds in the United Kingdom in September 2002 was caused by an equine influenza A virus (H3N8).We also demonstrated that canine respiratory tissue possesses the relevant receptors for infection with equine influenza virus.

View Article: PubMed Central - PubMed

Affiliation: Animal Health Trust, Kentford, Newmarket, Suffolk, UK. jshaw@liverpool.ac.uk

ABSTRACT
We retrospectively demonstrated that an outbreak of severe respiratory disease in a pack of English foxhounds in the United Kingdom in September 2002 was caused by an equine influenza A virus (H3N8). We also demonstrated that canine respiratory tissue possesses the relevant receptors for infection with equine influenza virus.

Show MeSH
Related in: MedlinePlus