Abstract
Highly pathogenic avian influenza virus (HPAIV) of the H5N1 subtype has been reported to infect pigeons asymptomatically or induce mild symptoms. However, host immune responses of pigeons inoculated with HPAIVs have not been well documented. To assess host responses of pigeons against HPAIV infection, we compared lethality, viral distribution and mRNA expression of immune related genes of pigeons infected with two HPAIVs (A/Pigeon/Thailand/VSMU-7-NPT/2004; Pigeon04 and A/Tree sparrow/Ratchaburi/VSMU-16-RBR/2005; T.sparrow05) isolated from wild birds in Thailand. The survival experiment showed that 25% of pigeons died within 2 weeks after the inoculation of two HPAIVs or medium only, suggesting that these viruses did not cause lethal infection in pigeons. Pigeon04 replicated in the lungs more efficiently than T.sparrow05 and spread to multiple extrapulmonary organs such as the brain, spleen, liver, kidney and rectum on days 2, 5 and 9 post infection. No severe lesion was observed in the lungs infected with Pigeon04 as well as T.sparrow05 throughout the collection periods. Encephalitis was occasionally observed in Pigeon04- or T.sparrow05-infected brain, the severity, however was mostly mild. To analyze the expression of immune-related genes in the infected pigeons, we established a quantitative real-time PCR analysis for 14 genes of pigeons. On day 2 post infection, Pigeon04 induced mRNA expression of Mx1, PKR and OAS to a greater extent than T.sparrow05 in the lungs, however their expressions were not up-regulated concomitantly on day 5 post infection when the peak viral replication was observed. Expressions of TLR3, IFNα, IL6, IL8 and CCL5 in the lungs following infection with the two HPAIVs were low. In sum, Pigeon04 exhibited efficient replication in the lungs compared to T.sparrow05, but did not induce excessive host cytokine expressions. Our study has provided the first insight into host immune responses of pigeons against HPAIV infection.
Highlights
The highly pathogenic avian influenza virus (HPAIV) of subtype H5N1, that is currently spread worldwide was first isolated from domestic goose in Guangdong Province, China in 1996 [1]
The following year, sporadic outbreaks of H5N1 HPAIVs occurred in poultries across Hong Kong and were accompanied by human infections that resulted in the deaths of 6 of 18 Hong Kong residents infected with the virus [2]
H5N1 HPAIV and 1918 H1N1 viruses have been reported to have increased virulence in mice and macaques accompanied by increased viral replication and aberrant hostcytokine responses, compared to the seasonal influenza A virus
Summary
The highly pathogenic avian influenza virus (HPAIV) of subtype H5N1, that is currently spread worldwide was first isolated from domestic goose in Guangdong Province, China in 1996 [1]. In late 2002, H5N1 HPAIV outbreaks in Hong Kong occurred in waterfowls and wild birds, resulting in the deaths of many resident avian species including ducks, geese, swans, pigeons and tree sparrows [3]. These H5N1 HPAIVs, were reported to differ antigenetically from those isolated between 1997 and 2001, and were lethal to ducks in a laboratory experiment [4]. In Thailand, HPAIVs were isolated from mammalian species including tigers, leopards, dogs and cats and wild birds including open-bill storks, pigeons and tree sparrows during the HPAI outbreaks in poultries in 2004–2005 [6,7,8,9,10,11]. These reports suggest that current HPAIVs appear to be more lethal to mammals and wild birds compared to those isolated before 2001
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