Immune response in the duck intestine following infection with low-pathogenic avian influenza viruses or stimulation with a Toll-like receptor 7 agonist administered orally

Abstract

This study analysed the immune response in the intestinal tract of ducks infected with low-pathogenic avian influenza viruses compared with ducks treated orally with R848, a synthetic Toll-like receptor 7 (TLR7) agonist. Influenza virus infection induced a type I interferon (IFN)-dependent immune response characterized by the expression of Mx transcripts in the ileum at levels that were proportional to viral load. Mx transcripts were detected in differentiated enterocytes from influenza virus-infected ducks. By contrast, in R848-treated ducks, Mx transcripts were detected solely in intraepithelial round cells of haematopoietic origin. An increase was detected in the number of intraepithelial TLR7-positive cells and intraepithelial IFN-aproducing cells in influenza virus-infected ducks, albeit to a lower level than in R848-treated ducks. IFN-c expression was also upregulated in the intestine of influenza virus-infected and R848-treated ducks. Finally, interleukin (IL)-1b and IL-8 transcripts were expressed at high levels in R848-treated ducks but were not increased in influenza virus-infected ducks. These findings suggest that a type I IFN-mediated immune response in enterocytes and the activation of IFN-c-secreting cells contribute to the control of influenza virus replication in the duck intestine. INTRODUCTIONDucks are frequently infected with avian influenza viruses and have been shown to shed viruses belonging to multiple subtypes (Olsen et al., 2006). They represent an important reservoir species of avian influenza viruses. These viruses can occasionally be transmitted from ducks to other bird species, such as gallinaceous poultry, or to mammals, including humans (Taubenberger & Kash, 2010). Ducks thus have a central role in the epidemiology of influenza virus infection.The vast majority of viruses isolated from ducks are lowpathogenic avian influenza (LPAI) viruses (Munster et al., 2007). LPAI viruses replicate asymptomatically in epithelial cells from the duck intestine and are excreted in the faeces (Kida et al., 1980;Webster et al., 1978). Highly pathogenic avian influenza (HPAI) viruses have also been isolated from ducks (De Marco et al., 2005;Sturm-Ramirez et al., 2005). Interestingly, whilst abrupt death is the usual outcome of HPAI virus infection in gallinaceous poultry, HPAI virus-infected ducks usually present only mild clinical signs and recover from infection (Perkins & Swayne, 2003;Wood et al., 1995). Asian HPAI H5N1 viruses from the clade 2.2 genotype represent an exception, as they have been described as being lethal to ducks (Kim et al., 2008). However, lethality is mainly observed and reproduced experimentally in young ducks (Löndt et al., 2010;Pantin-Jackwood et al., 2007). By contrast, older ducks are able to survive infection with the Asian HPAI H5N1 viruses from the clade 2.2 genotype, suggesting that ducks have the ability to control the replication of the most virulent HPAI viruses. Importantly, HPAI viruses have a similar tropism in poultry and ducks, and comparative analyses have ...

Protection Patterns in Duck and Chicken after Homo- or Hetero-Subtypic Reinfections with H5 and H7 Low Pathogenicity Avian Influenza Viruses: A Comparative Study

“…This was accompanied by a moderate antibody response. These data are in agreement with previous studies performed in mallard ducks [3], [4] or when cross-immunity between H3N8 and H4N6 was compared in mallards, quails and pheasants [14]. The mechanisms sustaining this protection and the duration of this protective immunity still need to be elucidated.…”

“…Among aquatic birds, mallards ( Anas platyrhynchos ) and their domestic counterparts Pekin ducks ( Anas platyrhynchos domesticus ), are of particular epidemiological importance [2]. In ducks, LPAIV infections are mainly asymptomatic and restricted to the epithelial cells lining the distal digestive tract [3]. The subsequent release of virus in feces is therefore a main source of contamination for the environment [4].…”

Tissue tropism and pathology of natural influenza virus infection in black-headed gulls (Chroicocephalus ridibundus)

“…The findings of Daoust et al (2011) correspond with those for experimental LPAIV infection in domestic ducks by Slemons & Easterday (1978) and Kida et al (1980), who found virus replication primarily in the epithelium of cloacal bursa and the large intestine. However, they do not correspond with the results of the study of Volmer et al (2010), who found virus replication more frequently in the small intestine than in the large intestine of domestic ducks experimentally infected with a genetically engineered virus possessing both human-type and avian-type amino acid motifs in the NS1 protein.…”

Differences in highly pathogenic avian influenza viral pathogenesis and associated early inflammatory response in chickens and ducks

“…was detected in the lung (Rebel et al, 2011), although high levels of the IFN-inducible genes Mx and PKR were found in the lung of H5N1-infected chickens (Daviet et al, 2009). The production of cytokines after a virus infection is mediated by pathogen recognition receptors (PRRs), including Toll-like receptors (TLRs) and RIG-I-like receptors (Kawai & Akira, 2008;Diebold, 2009) Induction of these receptors has been studied in lowpathogenic avian influenza infections in both chickens and ducks (Volmer et al, 2011;Karpala et al, 2011b;Cornelissen et al, 2012;Liniger et al, 2012). Barber et al (2010) reported the absence of RIG-I in chickens and suggested that the severity of HPAI infection in chickens may be explained by the absence of RIG-I activity.…”