Apoptosis Triggered by ORF3 Proteins of the Circoviridae Family

Apoptosis, a form of the programmed cell death, is an indispensable defense mechanism regulating cellular homeostasis and is triggered by multiple stimuli. Because of the regulation of apoptosis in cellular homeostasis, viral proteins with apoptotic activity are particular foci of on antitumor therapy. One representative viral protein is the open reading frame 3 (ORF3) protein, also named as apoptin in the Circoviridae chicken anemia virus (CAV), and has the ability to induce tumor-specific apoptosis. Proteins encoded by ORF3 in other circovirus species, such as porcine circovirus (PCV) and duck circovirus (DuCV), have also been reported to induce apoptosis, with subtle differences in apoptotic activity based on cell types. This article is aimed at reviewing the latest research advancements in understanding ORF3 protein-mediated apoptosis mechanisms of Circoviridae from three perspectives: subcellular localization, interactions with host proteins, and participation in multiple apoptotic signaling pathways, providing a scientific basis for circovirus pathogenesis and a reference on its potential anticancer function.

Short Beak and Dwarfism Syndrome in Ducks in Poland Caused by Novel Goose Parvovirus

Short beak and dwarfism syndrome (SBDS), which was previously identified only in mule ducks, is now an emerging disease of Pekin ducks in China and Egypt. The disease is caused by the infection of ducks with a genetic variant of goose parvovirus—novel goose parvovirus (nGPV). In 2019, SBDS was observed for the first time in Poland in eight farms of Pekin ducks. Birds in the affected flock were found to show growth retardation and beak atrophy with tongue protrusions. Morbidity ranged between 15% and 40% (in one flock), while the mortality rate was 4–6%. Co-infection with duck circovirus, a known immunosuppressive agent, was observed in 85.7% of ducks. The complete coding regions of four isolates were sequenced and submitted to GenBank. The phylogenetic analysis revealed a close relationship of Polish viral sequences with the Chinese nGPV. Genomic sequence alignments showed 98.57–99.28% identity with the nGPV sequences obtained in China, and 96.42% identity with the classical GPV (cGPV; Derzsy’s disease). The rate of amino acid mutations in comparison to cGPV and Chinese nGPV was higher in the Rep protein than in the Vp1 protein. To our knowledge, this is the first report of nGPV infection in Pekin ducks in Poland and Europe. It should be emphasized that monitoring and sequencing of waterfowl parvoviruses is important for tracking the viral genetic changes that enable adaptation to new species of waterbirds.

Effect of goose parvovirus and duck circovirus coinfection in ducks

IntroductionCoinfection of goose parvovirus (GPV) and duck circovirus (DuCV) occurs commonly in field cases of short beak and dwarfism syndrome (SBDS). However, whether there is synergism between the two viruses in replication and pathogenicity remains undetermined.Material and MethodsWe established a coinfection model of GPV and DuCV in Cherry Valley ducks. Tissue samples were examined histopathologically. The viral loads in tissues were detected by qPCR, and the distribution of the virus in tissues was detected by immunohistochemistry (IHC).ResultsCoinfection of GPV and DuCV significantly inhibited growth and development of ducks, and caused atrophy and pallor of the immune organs and necrosis of the liver. GPV and DuCV synergistically amplified pathogenicity in coinfected ducks. In the early stage of infection, viral loads of both pathogens in coinfected ducks were significantly lower than those in monoinfected ducks (P < 0.05). With the development of the infection process, GPV and DuCV loads in coinfected ducks were significantly higher than those in monoinfected ducks (P < 0.05). Extended viral distribution in the liver, kidney, duodenum, spleen, and bursa of Fabricius was consistent with the viral load increases in GPV and DuCV coinfected ducks.ConclusionThese results indicate that GPV and DuCV synergistically potentiate their replication and pathogenicity in coinfected ducks.