Abstract
BackgroundThe plateau pika (Ochotona curzoniae) is a small rabbit-like mammal that lives at high altitudes in the Qinghai-Tibet plateau and is in close contact with birds. Following the outbreak of highly pathogenic avian influenza (HPAI) H5N1 during 2005 in the migratory birds of Qinghai Lake, two clades of H5N1 have been found in pikas. However, the influenza virus receptor distribution in different tissues of this animal and its susceptibility to influenza A viruses have remained unclear.MethodsThe sialic acid receptor distribution tropism in pika was investigated using fluorescent Sambucus nigra and biotinylated Maackia amurensis I and II. Furthermore, the replication of three influenza A viruses H1N1, H3N2, and H5N1 in this animal was examined by immunohistochemistry and RT-PCR. Morphological and histopathological changes caused by infection were also analyzed with hematoxylin and eosin (H & E) staining.ResultsHuman influenza virus-recognizing SAα2,6Gal receptors are widely expressed in the lung, kidney, liver, spleen, duodenum, ileum, rectum, and heart, whereas avian influenza virus-recognizing SAα2,3Gal receptors are strongly expressed in the trachea and lung of pika. M1 could be detected in the lungs of pikas infected with H1N1, H3N2, and H5N1 by either immunostaining or RT-PCR, and in the brain of H5N1-infected pikas. Additionally, three subtypes of influenza A viruses were able to infect pika and caused varying degrees of pneumonia with epithelial desquamation and alveolar inflammatory cell infiltration. Slight pathological changes were observed in H1N1-infected lungs. A few small bronchi and terminal bronchioles were infiltrated by lymphocytic cells in H3N2-infected lungs. In contrast, serious lung damage, such as alveolar capillary hyperemia, edema, alveolar collapse, and lymphocytic infiltrations was observed in H5N1-infected group. Furthermore, neural system changes were present in the brains of H5N1-infected pikas.ConclusionsSAα2,6Gal receptors are extensively present in many of the tissues and organs in wild plateau pika, whereas SA2,3Gal-linked receptors are dominant on the tracheal epithelial cells. H1N1, H3N2, and H5N1 were able to infect pika and caused different degrees of pathogenic changes in the lungs. Altogether, these results suggest that wild pika has the potential to be a host for different subtypes of influenza A viruses.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-015-0290-8) contains supplementary material, which is available to authorized users.
Highlights
The plateau pika (Ochotona curzoniae) is a small rabbit-like mammal that lives at high altitudes in the Qinghai-Tibet plateau and is in close contact with birds
Distribution of SAα2,3Gal and SAα2,6Gal receptors in the different organs of pika To evaluate the potential role of receptor distribution in the susceptibility of pika to influenza virus infection, we investigated the distributions of SAα2,3Gal and SAα2,6Gal receptors in various organs, such as the trachea, lung, duodenum, ileum, rectum, heart, liver, kidney, brain, and spleen, by using biotinylated Maackia amurensis (MAA) lectin I (MAAI) and II (MAAII) for SAα2,3Gal binding and FITC-labeled Sambucus nigra (SNA) lectin for SAα2,6Gal binding
We found that the tracheal lamina propria and mucous glands express both SAα2,3Gal and SAα2,6Gal linked receptors when MAAI, MAAII, and SNA were used for staining (Figure 1A-a and B-a)
Summary
The plateau pika (Ochotona curzoniae) is a small rabbit-like mammal that lives at high altitudes in the Qinghai-Tibet plateau and is in close contact with birds. Two novel bat-derived subtypes of influenza A viruses, H17N10 and H18N11, were recently discovered respectively in little yellow-shouldered bats (Sturnira lilium, family Phyllostomidae) and flat-faced fruit bats (Artibeus planirostris) by sequencing analyses [2,3,4]. As yet, those two novel influenza viruses lack classical functions for the viral envelope proteins, the HA cannot bind to any traditional influenza virus receptors, and NA loses the neuraminidase activity to remove sialic acid [3,4,5,6,7,8]. The novel H7N9 virus that emerged in March 2013 has caused 419 infections and 127 deaths until July, 2014 [20]
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