Background: Both male and female pigeons have the ability to produce a nutrient solution in their crop for the nourishment of their young. The production of the nutrient solution has been likened to lactation in mammals, and hence the product has been called pigeon 'milk'. It has been shown that pigeon 'milk' is essential for growth and development of the pigeon squab, and without it they fail to thrive. Studies have investigated the nutritional value of pigeon 'milk' but very little else is known about what it is or how it is produced. This study aimed to gain insight into the process by studying gene expression in the 'lactating' crop. Results: Macroscopic comparison of 'lactating' and non-'lactating' crop reveals that the 'lactating' crop is enlarged and thickened with two very obvious lateral lobes that contain discrete rice-shaped pellets of pigeon 'milk'. This was characterised histologically by an increase in the number and depth of rete pegs extending from the basal layer of the epithelium to the lamina propria, and extensive proliferation and folding of the germinal layer into the superficial epithelium. A global gene expression profile comparison between 'lactating' crop and non-'lactating' crop showed that 542 genes are up-regulated in the 'lactating' crop, and 639 genes are down-regulated. Pathway analysis revealed that genes up-regulated in 'lactating' crop were involved in the proliferation of melanocytes, extracellular matrix-receptor interaction, the adherens junction and the wingless (wnt) signalling pathway. Gene ontology analysis showed that antioxidant response and microtubule transport were enriched in 'lactating' crop. Conclusions: There is a hyperplastic response in the pigeon crop epithelium during 'lactation' that leads to localised cellular stress and expression of antioxidant protein-encoding genes. The differentiated, cornified cells that form the pigeon 'milk' are of keratinocyte lineage and contain triglycerides that are likely endocytosed as very low density lipoprotein (VLDL) and repackaged as triglyceride in vesicles that are transported intracellularly by microtubules. This mechanism is an interesting example of the evolution of a system with analogies to mammalian lactation, as pigeon 'milk' fulfils a similar function to mammalian milk, but is produced by a different mechanism.

Cyprinid herpesvirus 3 (CyHV-3) infects koi and common carp and causes widespread mortalities. While the virus is a significant concern for aquaculture operations in many countries, in Australia the virus may be a useful biocontrol agent for pest carp. However, carp immune responses to CyHV-3, and the molecular mechanisms underpinning resistance, are not well understood. Here we used RNA-Seq on carp during different phases of CyHV-3 infection to detect the gene expression dynamics of both host and virus simultaneously. During acute CyHV-3 infection, the carp host modified the expression of genes involved in various immune systems and detoxification pathways. Moreover, the activated pathways were skewed toward humoral immune responses, which may have been influenced by the virus itself. Many immune-related genes were duplicated in the carp genome, and often these were expressed differently across the infection phases. Of particular interest were two interleukin-10 homologues that were not expressed synchronously, suggesting neo- or sub-functionalization. The carp immunoglobulin repertoire significantly diversified during active CyHV-3 infection, which was followed by the selection of high-affinity B-cells. This is indicative of a developing adaptive immune response, and is the first attempt to use RNA-Seq to understand this process in fish during a viral infection.

The rabbit caliciviruses Lagovirus europaeus GI.1 and GI.2 both cause acute necrotizing hepatitis in European rabbits (Oryctolagus cuniculus). Whilst GI.2 is highly virulent in both young and adult rabbits, rabbits younger than eight weeks of age are highly resistant to disease caused by GI.1, although they are still permissive to infection and viral replication. To investigate the underlying mechanism(s) of this age related resistance to GI.1, we compared liver transcriptomes of young rabbits infected with GI.1 to those of adult rabbits infected with GI.1 and young rabbits infected with GI.2. Our data suggest that kittens have constitutively heightened innate immune responses compared to adult rabbits, particularly associated with increased expression of major histocompatibility class II molecules and activity of natural killer cells, macrophages, and cholangiocytes. This enables them to respond more rapidly to GI.1 infection than adult rabbits and thus limit virus-induced pathology. In contrast, these responses were not fully developed during GI.2 infection. We speculate that the observed downregulation of multiple genes associated with innate immunity in kittens during GI.2 infection may be due to virally-mediated immunomodulation, permitting fatal disease to develop. Our study provides insight into the fundamental host–pathogen interactions responsible for the differences in age-related susceptibility, which likely plays a critical role in defining the success of GI.2 in outcompeting GI.1 in the field.

Biological invasions are a major threat to global biodiversity. Australia has experienced many invasive species, with the common carp (Cyprinus carpio L.) a prominent example. Cyprinid herpesvirus 3 (CyHV-3) has been proposed as a biological control (biocontrol) agent for invasive carp in Australia. Safety and efficacy are critical factors in assessing the suitability of biocontrol agents, and extensive host-specificity testing suggests that CyHV-3 is safe. Efficacy depends on the relationship between virus transmissibility and virulence. Based on observations from natural outbreaks, as well as the biology of virus-host interactions, we hypothesize that (i) close contact between carp provides the most efficient transmission of virus, (ii) transmission occurs at regular aggregations of carp that favour recrudescence of latent virus, and (iii) the initially high virulence of CyHV-3 will decline following its release in Australia. We also suggest that the evolution of carp resistance to CyHV-3 will likely necessitate the future release of progressively more virulent strains of CyHV-3, and/or an additional broad-scale measure(s) to complement the effect of the virus. If the release of CyHV-3 does go ahead, longitudinal studies are required to track the evolution of a virus-host relationship from its inception, and particularly the complex interplay between transmission, virulence and host resistance.