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Forskningsartikel2003Vetenskapligt granskad

Experimental infection of ponies with equine influenza A2 (H3N8) virus strains of different pathogenicity elicits varying interferon and interleukin-6 responses

Wattrang E, Jessett DM, Yates P, Fuxler L, Hannant D

Sammanfattning

The production of interferon (IFN), interleukin-6 (IL-6), and tumor necrosis factor (TNF) was monitored in horses during the course of influenza A2 virus infections. The effects of two virus strains, Newmarket/2/93 and Sussex/89, were compared, of which the latter is considered the more pathogenic in terms of clinical signs. Ten naive ponies were infected with influenza A/equine/Sussex/89 and 10 with influenza A/equine/Newmarket/2/93, respectively. As expected ponies infected with Sussex/89 showed the most pronounced clinical signs but there was no notable difference in viral excretion compared with Newmarket/2/93. IFN was detected in nasal secretions of all ponies infected with Sussex/89 but only in 2 ponies infected with Newmarktet/2/93. IFN was not detected in serum of any animal. IL-6 activity was detected in nasal secretions of all experimental animals from day 2 and onwards, but showed markedly higher IL-6 responses were observed in ponies infected with Sussex/89. No TNF activity was detected in any of the samples collected. In summary, equine influenza A 2 infections elicited local, and in some cases systemic, IFN and IL-6 responses in the ponies. Interestingly, there was some evidence that the duration and levels of cytokine responses may be related to the pathogenicity of the influenza strains

Publicerad i

Viral Immunology
2003, Volym: 16, nummer: 1, sidor: 57-67
Utgivare: MARY ANN LIEBERT INC PUBL

      SLU författare

    • Wattrang, Eva

      • Institutionen för molekylär biovetenskap, Sveriges lantbruksuniversitet
      • Fuxler, Lisbeth

        • Institutionen för molekylär biovetenskap, Sveriges lantbruksuniversitet

      Publikationens identifierare

      DOI: https://doi.org/10.1089/088282403763635456

      Permanent länk till denna sida (URI)

      https://res.slu.se/id/publ/1041