Birds have a smaller repertoire of immune genes than mammals. In our efforts to study antiviral responses to influenza in avian hosts, we have noted key genes that appear to be missing. As a result, we speculate that birds have impaired detection of viruses and intracellular pathogens. Birds are missing TLR8, a detector for single-stranded RNA. Chickens also lack RIG-I, the intracellular detector for single-stranded viral RNA. Riplet, an activator for RIG-I, is also missing in chickens. IRF3, the nuclear activator of interferon-beta in the RIG-I pathway is missing in birds. Downstream of interferon (IFN) signaling, some of the antiviral effectors are missing, including ISG15, and ISG54 and ISG56 (IFITs). Birds have only three antibody isotypes and IgD is missing. Ducks, but not chickens, make an unusual truncated IgY antibody that is missing the Fc fragment. Chickens have an expanded family of LILR leukocyte receptor genes, called CHIR genes, with hundreds of members, including several that encode IgY Fc receptors. Intriguingly, LILR homologues appear to be missing in ducks, including these IgY Fc receptors. The truncated IgY in ducks, and the duplicated IgY receptor genes in chickens may both have resulted from selective pressure by a pathogen on IgY FcR interactions. Birds have a minimal MHC, and the TAP transport and presentation of peptides on MHC class I is constrained, limiting function. Perhaps removing some constraint, ducks appear to lack tapasin, a chaperone involved in loading peptides on MHC class I. Finally, the absence of lymphotoxin-alpha and beta may account for the observed lack of lymph nodes in birds. As illustrated by these examples, the picture that emerges is some impairment of immune response to viruses in birds, either a cause or consequence of the host-pathogen arms race and long evolutionary relationship of birds and RNA viruses.

Wild waterfowl, including mallard ducks, are the natural reservoir of avian influenza A virus and they are resistant to strains that would cause fatal infection in chickens. Here we investigate potential involvement of TRIM proteins in the differential response of ducks and chickens to influenza. We examine a cluster of TRIM genes located on a single scaffold in the duck genome, which is a conserved synteny group with a TRIM cluster located in the extended MHC region in chickens and turkeys. We note a TRIM27-like gene is present in ducks, and absent in chickens and turkeys. Orthologous genes are predicted in many birds and reptiles, suggesting the gene has been lost in chickens and turkeys. Using quantitative real-time PCR (qPCR) we show that TRIM27-L, and the related TRIM27.1, are upregulated 5- and 9-fold at 1 day post-infection with highly pathogenic A/Vietnam/1203/2004. To assess whether TRIM27.1 or TRIM27-L are involved in modulation of antiviral gene expression, we overexpressed them in DF1 chicken cells, and neither show any direct effect on innate immune gene expression. However, when co-transfected with duck RIG-I-N (d2CARD) to constitutively activate the MAVS pathway, TRIM27.1 weakly decreases, while TRIM27-L strongly activates innate immune signalling leading to increased transcription of antiviral genes MX1 and IFN-β. Furthermore, when both are co-expressed, the activation of the MAVS signalling pathway by TRIM27-L over-rides the inhibition by TRIM27.1. Thus ducks have an activating TRIM27-L to augment MAVS signalling following RIG-I detection, while chickens lack both TRIM27-L and RIG-I itself.

Aims: This study aimed to determine whether host-adapted lactobacilli exhibit superior survival during intestinal transit relative to nomadic and free-living organisms, and to characterize the impact of probiotic lactobacilli on autochthonous lactobacilli. Methods and Results: Mixed cultures of Lactobacillus casei K9-1 and Lactobacillus fermentum K9-2, or reutericyclin producing Lactobacillus reuteri and its isogenic mutant were fed to piglets as freeze-dried culture, or as part of fermented feed. Lactobacilli in digesta and faecal samples were quantified by strain-specific quantitative PCR (qPCR), high-resolution-melting curve qPCR, and high-throughput sequencing of 16S rRNA gene sequence tags. The abundance of the host adapted L. reuteri in digesta and faeces was higher (P < 0Á05) when compared to L. casei or L. fermentum. Feed fermentation or chemical acidification of feed reduced (P < 0Á05) cell counts of Lactobacillus salivarius in colonic digesta. The reutericyclin producing L. reuteri TMW1.656 transiently reduced (P < 0Á05) the faecal abundance of lactobacilli. However, the overall impact of probiotic intervention on autochthonous lactobacilli was minor. Conclusions: The vertebrate host-adapted L. reuteri survives better during intestinal transit of piglets compared to L. casei and L. fermentum. Significance and Impact of the Study: Ecology and lifestyle of Lactobacillus strains may be suitable criteria for selection of probiotic strains for use in swine production.

Enterococcus canintestini 49, isolated from dog feces, is active against Clostridium perfringens, vancomycin-resistant enterococci, and Listeria monocytogenes. Its draft genome sequence reported herein contains a gene cluster encoding multiple bacteriocins and indicates the absence of genes for virulence factors. These characteristics signify the strain’s potential for use as a probiotic.

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