Infectivity and Shedding of Mouse Kidney Parvovirus After Oronasal Inoculation of C57BL/6, CD1, and NSG Mice.

Mouse kidney parvovirus (MKPV), the etiology of murine inclusion body nephropathy, has been identified globally in mice used for research, with an estimated prevalence of 10% in academic colonies. In immunodeficient strains, MKPV causes significant morbidity and mortality, and severe renal pathology. In contrast, in immunocompetent mice, the infection is subclinical and causes minimal pathology. We investigated viral infectivity and shedding in inbred C57BL/6NCrl (B6), outbred Crl:CD1(ICR) (CD1), and highly immunocompromised NOD. Cg - Prkdc scid Il2rg tm1Wjl/SzJ (NSG) mice. Four doses, ranging from 1.16 × 10 3 to 1.16 × 10 6 viral copies per microliter, of an MKPV inoculum were administered oronasally to 3 mice per dose per mouse type. All 3 types (B6, CD1, and NSG) had persistent infection with prolonged shedding in urine and feces. Viral copy number in the urine generally increased over time, while shedding in the feces was more variable. Among the 3 populations, CD1 mice developed viral shedding in urine earliest (4 wk after inoculation) and at higher levels (greater than 1 × 10 7 viral copies per microliter). B6 mice become viruric later (7 wk after inoculation), with lesser virus shed (1 × 10 6 viral copies per microliter or less). In CD1 and B6 mice, peak urine shedding occurred at 11 to 14 wk after inoculation, after which levels gradually declined until 35 wk after inoculation (study endpoint). In contrast, NSG mice did not become viruric until 10 wk after inoculation and continued to shed large amounts of virus (greater than 1 × 107 viral copies per microliter) in urine until the study endpoint. Two commercial immunofluorescent serologic assays failed to detect serum antibodies to MKPV nonstructural protein 1 as late as 58 wk after inoculation, whereas immunohistochemistry of infected renal tissue successfully detected anti-MKPV serum antibodies. These results increase our knowledge of the biology of MKPV and have practical application for development of effective screening programs for this pathogen.

Newlavirus, a Novel, Highly Prevalent, and Highly Diverse Protoparvovirus of Foxes (Vulpes spp.).

The genus Protoparvovirus (family Parvoviridae) includes several viruses of carnivores. We describe a novel fox protoparvovirus, which we named Newlavirus as it was discovered in samples from Newfoundland and Labrador, Canada. Analysis of the full non-structural protein (NS1) sequence indicates that this virus is a previously uncharacterized species. Newlavirus showed high prevalence in foxes from both the mainland (Labrador, 54/137, 39.4%) and the island of Newfoundland (22/50, 44%) but was not detected in samples from other carnivores, including coyotes (n = 92), lynx (n = 58), martens (n = 146), mink (n = 47), ermines (n = 17), dogs (n = 48), and ringed (n = 4), harp (n = 6), bearded (n = 6), and harbor (n = 2) seals. Newlavirus was found at similar rates in stool and spleen (24/80, 30% vs. 59/152, 38.8%, p = 0.2) but at lower rates in lymph nodes (2/37, 5.4%, p < 0.01). Sequencing a fragment of approximately 750 nt of the capsid protein gene from 53 samples showed a high frequency of co-infection by more than one strain (33.9%), high genetic diversity with 13 genotypes with low sequence identities (70.5-87.8%), and no geographic segregation of strains. Given the high prevalence, high diversity, and the lack of identification in other species, foxes are likely the natural reservoir of Newlavirus, and further studies should investigate its distribution.

Determination of a novel parvovirus pathogen associated with massive mortality in adult tilapia.

Tilapia is one of the most important economic and fastest-growing species in aquaculture worldwide. In 2015, an epidemic associated with severe mortality occurred in adult tilapia in Hubei, China. The causative pathogen was identified as Tilapia parvovirus (TiPV) by virus isolation, electron microscopy, experimental challenge, In situ hybridization (ISH), indirect immunofluorescence (IFA), and viral gene sequencing. Electron microscopy revealed large numbers of parvovirus particles in the organs of diseased fish, including kidney, spleen, liver, heart, brain, gill, intestine, etc. The virions were spherical in shape, non-enveloped and approximately 30nm in diameter. The TiPV was isolated and propagated in tilapia brain cells (TiB) and induced a typical cytopathic effect (CPE) after 3 days post-infection (dpi). This virus was used to experimentally infect adult tilapia and clinical disease symptoms similar to those observed naturally were replicated. Additionally, the results of ISH and IFA showed positive signals in kidney and spleen tissues from TiPV-infected fish. To identify TiPV-specific sequences, the near complete genome of TiPV was obtained and determined to be 4269 bp in size. Phylogenetic analysis of the NS1 sequence revealed that TiPV is a novel parvovirus, forms a separate branch in proposed genus Chapparvovirus of Parvoviridae. Results presented here confirm that TiPV is a novel parvovirus pathogen that can cause massive mortality in adult tilapia. This provides a basis for the further studies to define the epidemiology, pathology, diagnosis, prevention and treatment of this emerging viral disease.

A Roadmap for the Success of Oncolytic Parvovirus-Based Anticancer Therapies.

Autonomous rodent protoparvoviruses (PVs) are promising anticancer agents due to their excellent safety profile, natural oncotropism, and oncosuppressive activities. Viral infection can trigger immunogenic cell death, activating the immune system against the tumor. However, the efficacy of this treatment in recent clinical trials is moderate compared with results seen in preclinical work. Various strategies have been employed to improve the anticancer activities of oncolytic PVs, including development of second-generation parvoviruses with enhanced oncolytic and immunostimulatory activities and rational combination of PVs with other therapies. Understanding the cellular factors involved in the PV life cycle is another important area of investigation. Indeed, these studies may lead to the identification of biomarkers that would allow a more personalized use of PV-based therapies. This review focuses on this work and the challenges that still need to be overcome to move PVs forward into clinical practice as an effective therapeutic option for cancer patients.

Tropism, pathology, and transmission of equine parvovirus-hepatitis.

Equine parvovirus-hepatitis (EqPV-H) has recently been associated with cases of Theiler's disease, a form of fulminant hepatic necrosis in horses. To assess whether EqPV-H is the cause of Theiler's disease, we first demonstrated hepatotropism by PCR on tissues from acutely infected horses. We then experimentally inoculated horses with EqPV-H and 8 of 10 horses developed hepatitis. One horse showed clinical signs of liver failure. The onset of hepatitis was temporally associated with seroconversion and a decline in viremia. Liver histology and in situ hybridization showed lymphocytic infiltrates and necrotic EqPV-H-infected hepatocytes. We next investigated potential modes of transmission. Iatrogenic transmission via allogeneic stem cell therapy for orthopedic injuries was previously suggested in a case series of Theiler's disease, and was demonstrated here for the first time. Vertical transmission and mechanical vectoring by horse fly bites could not be demonstrated in this study, potentially due to limited sample size. We found EqPV-H shedding in oral and nasal secretions, and in feces. Importantly, we could demonstrate EqPV-H transmission via oral inoculation with viremic serum. Together, our findings provide additional information that EqPV-H is the likely cause of Theiler's disease and that transmission of EqPV-H occurs via both iatrogenic and natural routes.

Emerging Human Parvoviruses: The Rocky Road to Fame.

Parvoviruses are structurally simple viruses with linear single-stranded DNA genomes and nonenveloped icosahedral capsids. They infect a wide range of animals from insects to humans. Parvovirus B19 is a long-known human pathogen, whereas adeno-associated viruses are nonpathogenic. Since 2005, many parvoviruses have been discovered in human-derived samples: bocaviruses 1-4, parvovirus 4, bufavirus, tusavirus, and cutavirus. Some human parvoviruses have already been shown to cause disease during acute infection, some are associated with chronic diseases, and others still remain to be proven clinically relevant-or harmless commensals, a distinction not as apparent as it might seem. One initially human-labeled parvovirus might not even be a human virus, whereas another was originally overlooked due to inadequate diagnostics. The intention of this review is to follow the rocky road of emerging human parvoviruses from discovery of a DNA sequence to current and future clinical status, highlighting the perils along the way.

Retrospective investigation and molecular characteristics of the recombinant Muscovy duck parvovirus circulating in Muscovy duck flocks in China.

The recombinant Muscovy duck parvovirus (rMDPV) has been recently characterized and identified in China. However, whether other additional rMDPV field isolates exist, and whether these strains possess common molecular characteristics, remain to be explored. In this retrospective study, two new rMDPV isolates, namely, JH06 and JH10, were identified through genome sequencing and recombination analysis. JH06, JH10, and four previously characterized rMDPV strains (SAAS-SHNH, ZW, FJM3, and PT97) underwent the same recombination events in a 1.1-kb region in their VP3 genes and displayed highly consistent beginning and ending breakpoints. JH06, JH10, SAAS-SHNH, ZW, and FJM3, but not PT97, underwent recombination in their P9 promoter regions. In both recombination events, the classical MDPV strain YY acted as the major parent, whereas the virulent strain DY16 and the vaccine strain SYG61v of goose parvovirus (GPV) served as the minor parents. The sequence alignments of inverted terminal repeats (ITRs) revealed that rMDPV strains shared higher identities (96.0%-97.2%) with classical MDPV strains than with GPV and contained typical one-nucleotide-pair deletions in the palindromic stems of their ITRs. This work elucidated the common molecular characteristics and differences of six rMDPV strains. The results of this work will facilitate the preparation of an efficacious vaccine for the protection of Muscovy ducks against rMDPV infection.

Pulpitis de las piscinas asociada a exantema por parvovirus / Pool palms associated with a parvovirus rash

La entidad denominada pulpitis de las piscinas es un proceso benigno, relativamente frecuente, debido al incremento de las actividades deportivas en las piscinas. Presentamos el caso de un niño de nueve años con lesiones bilaterales en los pulpejos de ambas manos de cinco días de evolución

The entity known as pool palms is a benign process that is relatively frequent due to the increase in sports activities in swimming pools. We report a 9-year-old boy with intense redness on the fingertips of both hands of 5 days of evolution

Avian parvovirus: classification, phylogeny, pathogenesis and diagnosis.

Poultry parvoviruses identified during the early 1980s are found worldwide in intestines from young birds with enteric disease syndromes as well as healthy birds. The chicken parvovirus (ChPV) and turkey parvovirus (TuPV) belong to the Aveparvovirus genus within the subfamily Parvovirinae. Poultry parvoviruses are small, non-enveloped, single-stranded DNA viruses consisting of three open reading frames, the first two encoding the non-structural protein (NS) and nuclear phosphoprotein (NP) and the third encoding the viral capsid proteins 1 (VP1 and VP2). In contrast to other parvoviruses, the VP1-unique region does not contain the phospholipase A2 sequence motif. Recent experimental studies suggested the parvoviruses to be the candidate pathogens in cases of enteric disease syndrome. Current diagnostic methods for poultry parvovirus detection include PCR, real-time PCR, enzyme linked immunosorbent assay using recombinant VP2 or VP1 capsid proteins. Moreover, sequence-independent amplification techniques combined with next-generation sequencing platforms have allowed rapid and simultaneous detection of the parvovirus from affected and healthy birds. There is no commercial vaccine; hence, the development of an effective vaccine to control the spread of infection should be of primary importance. This review presents the current knowledge on poultry parvoviruses with emphasis on taxonomy, phylogenetic relationship, genomic analysis, epidemiology, pathogenesis and diagnostic methods.

An Atypical Parvovirus Drives Chronic Tubulointerstitial Nephropathy and Kidney Fibrosis.

The occurrence of a spontaneous nephropathy with intranuclear inclusions in laboratory mice has puzzled pathologists for over 4 decades, because its etiology remains elusive. The condition is more severe in immunodeficient animals, suggesting an infectious cause. Using metagenomics, we identify the causative agent as an atypical virus, termed "mouse kidney parvovirus" (MKPV), belonging to a divergent genus of Parvoviridae. MKPV was identified in animal facilities in Australia and North America, is transmitted via a fecal-oral or urinary-oral route, and is controlled by the adaptive immune system. Detailed analysis of the clinical course and histopathological features demonstrated a stepwise progression of pathology ranging from sporadic tubular inclusions to tubular degeneration and interstitial fibrosis and culminating in renal failure. In summary, we identify a widely distributed pathogen in laboratory mice and establish MKPV-induced nephropathy as a new tool for elucidating mechanisms of tubulointerstitial fibrosis that shares molecular features with chronic kidney disease in humans.

Antibodies against canine distemper virus, parvovirus and Ehrlichia spp. in wild captive carnivores in midwestern Brazil / Anticorpos contra o vírus da cinomose canina, parvovírus e Ehrlichia spp. em carnívoros selvagens cativos no centro-oeste do Brasil

The occurrence of antibodies against canine distemper virus (CDV), parvovirus and Ehrlichia spp. in wild captive carnivores was evaluated in a zoological park in midwestern Brazil. Serum samples were collected between 2007 and 2014 from 45 carnivores. Antibodies were evaluated by virus neutralization assay for CDV, hemagglutination inhibition test for parvovirus, indirect immunofluorescent and Enzyme-linked immunosorbent assay for Ehrlichia spp. Antibodies against CDV and parvovirus were detected in 75% of Canidae and Felidae. Procyonidae were negative for CDV, although one Mustelidae was positive. TwoCanidae presented antibodies reactive to E. canis antigens. The high antibodies rates to CDV and parvovirus suggest the contact with both pathogens, however since no clinical history of disease are registered in the Zoo-UFMT, we can presume that carnivores have responded satisfactorily against the antigens. The low serological rates observed against Ehrlichia spp. may be resulted to the low occurrence of ticks among carnivores.(AU)

A ocorrência de anticorpos contra o vírus da cinomose canina (CDV), parvovírus e Ehrlichia spp. em carnívoros selvagens em cativeiro foi avaliada em um parque zoológico do centro oeste do Brasil. As amostras de soro foram coletadas entre 2007 e 2014 de 45 carnívoros. Os anticorpos foram avaliados por ensaio de neutralização de vírus para CDV, teste de inibição de hemaglutinação para parvovírus, imunofluorescência indireta e ensaio imunoenzimático ligado à enzima para Ehrlichia spp. Anticorpos contra CDV e parvovírus foram detectados em 75% de canídeos e felídeos. Procionídeos foram negativos para CDV, embora um mustelídeo fora positivo. Dois canídeos apresentaram anticorpos reativos aos antígenos de E. canis. As altas taxas de anticorpos para CDV e parvovírus sugerem o contato com ambos os patógenos, entretanto desde que nenhuma história clínica de doença está registrada no Zoo-UFMT, podemos presumir que os carnívoros têm respondido satisfatoriamente contra os antígenos. As baixas taxas serológicas observadas contra Ehrlichia spp. pode ser resultado da baixa ocorrência de carrapatos entre os carnívoros.(AU)

Complex and Dynamic Interactions between Parvovirus Capsids, Transferrin Receptors, and Antibodies Control Cell Infection and Host Range.

Antibody and receptor binding are key virus-host interactions that control host range and determine the success of infection. Canine and feline parvovirus capsids bind the transferrin receptor type 1 (TfR) to enter host cells, and specific structural interactions appear necessary to prepare the stable capsids for infection. Here, we define the details of binding, competition, and occupancy of wild-type and mutant parvovirus capsids with purified receptors and antibodies. TfR-capsid binding interactions depended on the TfR species and varied widely, with no direct relationship between binding affinity and infection. Capsids bound feline, raccoon, and black-backed jackal TfRs at high affinity but barely bound canine TfRs, which mediated infection efficiently. TfRs from different species also occupied capsids to different levels, with an estimated 1 to 2 feline TfRs but 12 black-backed jackal TfRs binding each capsid. Multiple alanine substitutions within loop 1 on the capsid surface reduced TfR binding but substitutions within loop 3 did not, suggesting that loop 1 directly engaged the TfR and loop 3 sterically affected that interaction. Binding and competition between different TfRs and/or antibodies showed complex relationships. Both antibodies 14 and E competed capsids off TfRs, but antibody E could also compete capsids off itself and antibody 14, likely by inducing capsid structural changes. In some cases, the initial TfR or antibody binding event affected subsequent TfR binding, suggesting that capsid structure changes occur after TfR or antibody binding and may impact infection. This shows that precise, host-specific TfR-capsid interactions, beyond simple attachment, are important for successful infection.IMPORTANCE Host receptor binding is a key step during viral infection and may control both infection and host range. In addition to binding, some viruses require specific interactions with host receptors in order to infect, and anti-capsid antibodies can potentially disrupt these interactions, leading to neutralization. Here, we examine the interactions between parvovirus capsids, the receptors from different hosts, and anti-capsid antibodies. We show that interactions between parvovirus capsids and host-specific TfRs vary in both affinity and in the numbers of receptors bound, with complex effects on infection. In addition, antibodies binding to two sites on the capsids had different effects on TfR-capsid binding. These experiments confirm that receptor and antibody binding to parvovirus capsids are complex processes, and the infection outcome is not determined simply by the affinity of attachment.

Comparative genetic analysis and pathological characteristics of goose parvovirus isolated in Heilongjiang, China.

BACKGROUND: Goose parvovirus (GPV) causes acute enteritis, hepatitis, myocarditis and high morbidity and mortality in geese and ducks. GPV H strain was isolated from a Heilongjiang goose farm where the geese were showing signs of hemorrhage in the brain, liver, and intestinal tract. In this study, we explored the genetic diversity among waterfowl parvovirus isolates and the pathological characteristics of GPV H in Shaoxing ducklings. METHODS: The complete capsid protein (VP) and non-structural (NS) sequences of the isolated H strain were sequenced, and phylogenetic trees of VP and NS were constructed in MEGA version 5.05 using the neighbor-joining method. Three-day-old Shaoxing ducklings were inoculated with GPV and were euthanized at 1, 2, 4, 6, and 8 days post-inoculation (PI), and their organs were removed and collected. The organs of 6-day PI ducklings were fixed in formalin, embedded in paraffin, sectioned for histology, stained with HE and analyzed for pathological lesions. The distribution of the GPV H strain in the tissues of the inoculated ducklings was detected using the polymerase chain reaction (PCR) method. RESULTS: Genetic analysis of the NS and VP genes indicated that the H strain was closely related to strains circulating in China during 1999-2014, and the nucleic acid identity of those strains was 98%-99%. Classical symptoms were observed in the inoculated ducklings. GPV remained in many tissues and replicated in a majority of the tissues, leading to histopathological lesions in four tissues. CONCLUSIONS: We first reported the distribution and histopathological lesions of a Chinese strain of GPV in infected shaoxing ducklings. This H strain was moderate pathogenic for Shaoxing ducklings.

Optimizing the Targeting of Mouse Parvovirus 1 to Murine Melanoma Selects for Recombinant Genomes and Novel Mutations in the Viral Capsid Gene.

Combining virus-enhanced immunogenicity with direct delivery of immunomodulatory molecules would represent a novel treatment modality for melanoma, and would require development of new viral vectors capable of targeting melanoma cells preferentially. Here we explore the use of rodent protoparvoviruses targeting cells of the murine melanoma model B16F10. An uncloned stock of mouse parvovirus 1 (MPV1) showed some efficacy, which was substantially enhanced following serial passage in the target cell. Molecular cloning of the genes of both starter and selected virus pools revealed considerable sequence diversity. Chimera analysis mapped the majority of the improved infectivity to the product of the major coat protein gene, VP2, in which linked blocks of amino acid changes and one or other of two apparently spontaneous mutations were selected. Intragenic chimeras showed that these represented separable components, both contributing to enhanced infection. Comparison of biochemical parameters of infection by clonal viruses indicated that the enhancement due to changes in VP2 operates after the virus has bound to the cell surface and penetrated into the cell. Construction of an in silico homology model for MPV1 allowed placement of these changes within the capsid shell, and revealed aspects of the capsid involved in infection initiation that had not been previously recognized.

Pathogenicity of Pekin duck- and goose-origin parvoviruses in Pekin ducklings.

Goose parvovirus (GPV) usually affects goslings and Muscovy ducks but not Pekin ducks. Earlier works showed that a variant GPV can cause short beak and dwarfism syndrome (SBDS) in Pekin ducks. Here, we investigated the pathogenicity of a variant GPV of Pekin duck-origin (JS1) and a classical GPV of goose-origin (H) in Pekin ducklings. Following intramuscular infection at two days of age, both JS1 and H strains influenced weight gain and development of beaks and bones of wings and legs, and caused microscopic lesions of internal organs of ducks. However, the clinical signs typical of SBDS could only be replicated with the JS1 isolate. The findings suggest that both variant and classical GPVs are pathogenic for Pekin ducklings, while the former is more virulent than the latter. Using a quantitative real-time PCR assay, high levels of viral load were detected from bloods, internal organs, leg muscles, and ileac contents in JS1- and H-infected ducks from 6h to 35days postinfection (DPI). Using a GPV VP3-based ELISA, antibodies in sera of JS1- and H-infected ducks were detectable at 1 DPI and then persistently rose during the subsequent five weeks. These results suggest that both variant and classical GPVs can infect Pekin ducklings. The present work contributes to the understanding of pathogenicity of GPV to Pekin ducks and may provide clues to pathogenesis of GPV-related SBDS.

Implication of the intestinal microbiome as a potential surrogate marker of immune responsiveness to experimental therapies in autoimmune diabetes.

Type 1 diabetes (T1D) is an autoimmune proinflammatory disease with no effective intervention. A major obstacle in developing new immunotherapies for T1D is the lack of means for monitoring immune responsiveness to experimental therapies. The LEW1.WR1 rat develops autoimmunity following infection with the parvovirus Kilham rat virus (KRV) via mechanisms linked with activation of proinflammatory pathways and alterations in the gut bacterial composition. We used this animal to test the hypothesis that intervention with agents that block innate immunity and diabetes is associated with a shift in the gut microbiota. We observed that infection with KRV results in the induction of proinflammatory gene activation in both the spleen and pancreatic lymph nodes. Furthermore, administering animals the histone deacetylase inhibitor ITF-2357 and IL-1 receptor antagonist (Anakinra) induced differential STAT-1 and the p40 unit of IL-12/IL-23 gene expression. Sequencing of bacterial 16S rRNA genes demonstrated that both ITF-2357 and Anakinra alter microbial diversity. ITF-2357 and Anakinra modulated the abundance of 23 and 8 bacterial taxa in KRV-infected animals, respectively, of which 5 overlapped between the two agents. Lastly, principal component analysis implied that ITF-2357 and Anakinra induce distinct gut microbiomes compared with those from untreated animals or rats provided KRV only. Together, the data suggest that ITF-2357 and Anakinra differentially influence the innate immune system and the intestinal microbiota and highlight the potential use of the gut microbiome as a surrogate means of assessing anti-inflammatory immune effects in type 1 diabetes.

Immune-Related Gene Expression Patterns in GPV- or H9N2-Infected Goose Spleens.

Goose parvovirus (GPV) and avian influenza virus subtype H9N2 are single-stranded DNA (ssDNA) and single-stranded RNA (ssRNA) viruses, respectively, both of which can spread in goslings and cause a significant economic loss. To explore the comprehensive transcriptome of GPV- or H9N2-infected goose spleens and to understand the immune responses induced by a DNA virus (GPV) or a RNA virus (H9N2), RNA-seq was performed on the spleens of goslings at the fifth day post infection. In the present study, 2604 and 2409 differentially expressed unigenes were identified in the GPV- and H9N2-infected groups, respectively. Through KEGG pathway enrichment analyses, the up-regulated transcripts in the two virus-infected groups were mainly involved in immune-related pathways. In addition, the two virus-infected groups displayed similar expression patterns in the immune response pathways, including pattern-recognition receptor signaling pathways, the antigen processing and presentation pathway, the NF-κB signaling pathway and the JAK-STAT signaling pathway, as well as cytokines. Furthermore, most of the immune-related genes, particularly TLR7, TRAF3, Mx, TRIM25, CD4, and CD8α, increased in response to GPV and H9N2 infection. However, the depression of NF-κB signaling may be a mechanism by which the viruses evade the host immune system or a strategy to achieve immune homeostasis.

Chicken parvovirus viral loads in cloacal swabs from malabsorption syndrome-affected and healthy broilers.

Chicken parvovirus (ChPV) has been associated with malabsorption syndrome (MAS) in broilers. However, the participation of this virus in such syndrome is unclear, since it may be detected in diseased and healthy chickens. In the course of these studies, it was argued whether ChPV genome loads might be correlated to the occurrence of MAS. To check such a hypothesis, a SYBR green-based quantitative polymerase chain reaction was developed to detect and quantify ChPV genomes. Cloacal swabs from 68 broilers with MAS and 59 from healthy animals were collected from different poultry farms. Genomes of ChPV were detected in all samples, regardless of their health status. However, viral genome loads in MAS-affected broilers were significantly higher (1 × 105 genome copies per 100 ng DNA) than in healthy animals (1.3 × 103 GC/100 ng DNA). These findings indicate that there is an association between high ChPV genome loads and the occurrence of MAS in broilers.

Novel duck parvovirus identified in Cherry Valley ducks (Anas platyrhynchos domesticus), China.

An unknown infectious disease in Cherry Valley ducks (Anas platyrhynchos domesticus) characterized by short beak and strong growth retardation occurred in China during 2015. The causative agent of this disease, tentatively named duck short beak and dwarfism syndrome (DSBDS), as well as the evolutionary relationships between this causative agent and all currently known avian-origin parvoviruses were clarified by virus isolation, transmission electron microscope (TEM) observation, analysis of nuclear acid type, (RT-)PCR identification, whole genome sequencing, and NS1 protein sequences-based phylogenetic analyses. The results indicated that the causative agent of DSBDS is closely related with the goose parvovirus-like virus, which is divergent from all currently known avian-origin parvoviruses and should be a novel duck parvovirus (NDPV).

Isolation and characterization of a distinct duck-origin goose parvovirus causing an outbreak of duckling short beak and dwarfism syndrome in China.

Many mule duck and Cherry Valley duck flocks in different duck-producing regions of China have shown signs of an apparently new disease designated "short beak and dwarfism syndrome" (SBDS) since 2015. The disease is characterized by dyspraxia, weight loss, a protruding tongue, and high morbidity and low mortality rates. In order to characterize the etiological agent, a virus designated SBDSV M15 was isolated from allantoic fluid of dead embryos following serial passage in duck embryos. This virus causes a cytopathic effect in duck embryo fibroblast (DEF) cells. Using monoclonal antibody diagnostic assays, the SBDSV M15 isolate was positive for the antigen of goose parvovirus but not Muscovy duck parvovirus. A 348-bp (2604-2951) VP1gene fragment was amplified, and its sequence indicated that the virus was most closely related to a Hungarian GPV strain that was also isolated from mule ducks with SBDS disease. A similar disease was reproduced by inoculating birds with SBDSV M15. Together, these data indicate that SBDSV M15 is a GPV-related parvovirus causing SBDS disease and that it is divergent from classical GPV isolates.