Pigeon circovirus (PiCV) is considered to be genetically diverse, with a relatively small circular single-stranded DNA genome of 2 kb that encodes for a capsid protein (Cap) and a replication initiator protein (Rep). Australasia is known to be the origin of diverse species of the Order Columbiformes, but limited data on the PiCV genome sequence has hindered phylogeographic studies in this species. To fill this gap, this study was conducted to investigate PiCV in 118 characteristic samples from different birds across Australia using PCR and sequencing. Eighteen partial PiCV Rep sequences and one complete PiCV genome sequence were recovered from reservoir and aberrant hosts. Phylogenetic analyses revealed that PiCV circulating in Australia was scattered across three different subclades. Importantly, one subclade dominated within the PiCV sequenced from Australia and Poland, whereas other PiCV sequenced in this study were more closely related to the PiCV sequenced from China, USA and Japan. In addition, PiCV Rep sequences obtained from clinically affected plumed whistling duck, blue billed duck and Australian magpie demonstrated natural spillover of PiCV unveiled host generalist characteristics of the pigeon circovirus. These findings indicate that PiCV genomes circulating in Australia lack host adapted population structure but demonstrate natural spillover infection.

Columbid alphaherpesvirus 1 (CoHV1) is associated with oral or upper respiratory tract lesions, encephalitis, and occasional fatal systemic disease in naive or immunosuppressed pigeons. Clinical disease is often reported with CoHV1 and coinfecting viruses, including pigeon circovirus (PiCV), which may cause host immunosuppression and augment lesion development. A natural outbreak of CoHV1 and PiCV coinfection occurred in a flock of 60 racing rock pigeons ( Columba livia), in which 4 pigeons succumbed within 7 d of clinical onset. Lesions included suppurative stomatitis, pharyngitis, cloacitis, meningitis, and tympanitis, with eosinophilic intranuclear inclusion bodies consistent with herpesviral infection. In addition, large numbers of botryoid intracytoplasmic inclusion bodies were present in the skin, oral mucosa, and bursa of Fabricius, suggestive of circoviral infection, which was confirmed by immunohistochemistry. The concurrent viral load of CoHV1 and PiCV was high in liver, oropharynx, and bursa of Fabricius. We found PiCV in oro-cloacal swabs from 44 of 46 additional birds of variable clinical status, PiCV alone in 23 birds, and coinfection with CoHV1 in 21 birds. Viral copy numbers were significantly higher ( p < 0.0001) for both viruses in clinically affected pigeons than in subclinical qPCR-positive birds. The CoHV1-induced lesions might have been exacerbated by concomitant PiCV infection.

Background: Birds are known to harbour many pathogens, including circovirus, herpesviruses, adenoviruses and Chlamydia psittaci. Some of these pose zoonotic risks, while others, such as beak and feather disease virus (BFDV), have a significant impact on the conservation of endangered bird species.Objectives: This study was aimed to determine the faecal virome of a group of apparently healthy Monk parakeet using high‐throughput sequencing.Methods: Fresh faecal samples were collected from four Monk parakeets at a pet shop in Melbourne, Australia. Virus enrichment and nucleic acid extraction were performed on the faecal samples, followed by high‐throughput sequencing at the Australian Genome Research Facility (AGRF).Results: Utilising an established pipeline for high‐throughput sequencing data analysis, this study revealed the presence of three viruses of the families Circoviridae, Parvoviridae and Adenoviridae. Subsequent sequence comparison and phylogenetic analyses further confirmed that the detected viruses belong to the genera Chaphamaparvovirus (unassigned species), Circovirus (species Circovirus parrot) and Siadenovirus (species Siadenovirus viridis).Conclusion: Despite non‐pathogenicity, the existence of multiple viruses within a bird species underscores the risk of these viruses spreading into the pet trade. Detection and a better understanding of avian viruses are crucial for the establishment of appropriate management and biosecurity measures in the domestic and international bird trade, which ultimately supports the conservation of vulnerable bird species.

Lumpy skin disease virus (LSDV), a transboundary pathogen threatening cattle health in South and Southeast Asia, presents growing challenges for disease control. This study combined serological, molecular, and genomic approaches to investigate LSDV in Barura Upazila, Bangladesh. Serological screening of 424 cattle using a commercial ELISA revealed a high seroprevalence of 55.5% (95% CI: 50.7–60.3), indicating widespread exposure. Although differences were observed by age and breed, no significant associations were found with seropositivity, suggesting broad regional circulation. Real-time PCR confirmed LSDV DNA in all 20 clinically infected animals, with consistent P32 gene amplification. Two samples with low Cq values underwent whole-genome sequencing. The complete genomes of LSDV-L2/2024 and LSDV-L3/2024 showed >99.6% identity with the reference strain LSDV-29, yet carried unique genomic features, including truncated or variant ORFs and immune-related gene differences. Phylogenetic analysis of the DNA polymerase gene revealed distinct clustering: L2/2024 aligned with South Asian isolates, while L3/2024 grouped with strains from Africa, the Middle East, and Europe. These results highlight co-circulation of genetically diverse strains and possible cross-regional introductions. Overall, our findings underscore the evolutionary plasticity of LSDV and the critical need for ongoing genomic surveillance to guide targeted vaccine development and disease control strategies.

Abalone are highly susceptible to haliotid herpesvirus 1 (HaHV1), the causative agent of abalone viral ganglioneuritis (AVG), a re-emerging disease responsible for significant mortality events in both wild and farmed populations. Currently, there are no effective antiviral treatments or preventive measures available against HaHV1, which is partly due to the limited understanding of the immune responses and viral pathogenesis in this non-model marine invertebrate. This highlights the urgent need for novel intervention strategies, including investigations into the molecular mechanisms underlying HaHV1 infection. In other herpesviruses, the large tegument protein UL36 plays a crucial role in transporting the viral capsid to the host cell’s nuclear pore complex (NPC), mediated by N-terminal nuclear localization signals (NLSs). However, the nuclear import mechanism of UL36 homologue (UL36h) in HaHV1 remains largely uncharacterized. In this study, we identified and functionally characterized the NLS motif within HaHV1 UL36h and elucidated its interactions with the importin alpha (IMPα) nuclear import receptor. Through a combination of high-resolution crystallography and quantitative binding assays, we determined the key residues responsible for binding to IMPα and demonstrated isoform-specific variations in binding affinity. Our biochemical and structural analyses confirmed key interactions within the NLS that are essential for IMPα interactions. These findings advance our molecular understanding of HaHV1 host interactions and pave the way for the development of targeted antiviral strategies against abalone herpesvirus infection.