Relationship of mink virus enteritis virus and feline panleukopenia virus: rapid onset of mink virus enteritis virus protection after feline panleukopenia virus infection.
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Animals↗
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A survey of North American migratory waterfowl for duck plague (duck virus enteritis) virus.
A survey of migratory waterfowl for duck plague (DP) virus was conducted in the Mississippi and Central flyways during 1982 and in the Atlantic and Pacific flyways during 1983. Cloacal and pharyngeal swabs were collected from 3,169 migratory waterfowl in these four flyways, principally mallards (Anas platyrhynchos L.), black ducks (Anas rubripes Brewster), and pintails (Anas acuta L.). In addition 1,033 birds were sampled from areas of recurrent DP outbreaks among nonmigratory and captive waterfowl, and 590 from Lake Andes National Wildlife Refuge, the site of the only known major DP outbreak in migratory waterfowl. Duck plague virus was not found in any of the samples. Results support the hypothesis that DP is not established in North American migratory waterfowl as an enzootic disease.
Animals↗
Development of homologous viral internal controls for use in RT-PCR assays of waterborne enteric viruses.
Enteric viruses often contaminate water sources causing frequent outbreaks of gastroenteritis. Reverse transcription-polymerase chain reaction (RT-PCR) assays are commonly used for detection of human enteric viruses in environmental and drinking water samples. RT-PCR provides a means to rapidly detect low levels of these viruses, but it is sensitive to inhibitors that are present in water samples. Inhibitors of RT-PCR are concentrated along with viruses during sample processing. While procedures have been developed to remove inhibitors, none of them completely remove all inhibitors from all types of water matrices. This problem requires that adequate controls be used to distinguish true from potentially false-negative results. To address this problem, we have developed homologous viral internal controls for hepatitis A virus (HAV), poliovirus, Norwalk virus and rotavirus. These internal controls can be used in RT-PCR assays for the detection of the above viruses by competitive amplification, thereby allowing the detection of false negatives in processed water samples. The internal controls developed in this study were successfully tested with virus-seeded environmental water sample concentrates.
Electrophoresis, Polyacrylamide Gel↗
Clinical Impact and Genetic Analysis of Enteric Viruses Associated With Acute Gastroenteritis in Greater Accra, Ghana: A Comprehensive Study of Five Viruses.
Enteric viruses are significantly associated with acute gastroenteritis globally. Despite a decrease in severe rotavirus associated diarrhoea, Ghana still records high diarrhoea burden. Meanwhile aetiological investigations in hospital settings do not routinely include viral testing. Rotavirus vaccination is thought to alter enteric viral populations and impact evolution. To better understand virus-specific effects in acute gastroenteritis in both children and adults, we tested fecal samples from 228 patients at two hospitals in Accra from January to December 2019, using multiplex and singleplex PCR assays. The clinical impact of detected viruses was assessed using a modified Vesikari score system. Partial viral genome sequences were obtained by Sanger Sequencing and their genetic diversity and evolutionary history, traced by phylogenetic analyses. At least one enteric virus was found in 86 (37.7%) patient samples, with 36.9% of the population under five infected. Single infections of rotavirus, norovirus, adenovirus, sapovirus and astrovirus were 33, 14, 8, 6, and 1, respectively, while coinfections were 24. Rotavirus accounted for 33.3% of 24 clinically severe cases (modified Vesikari score > 7). Three out of 10 rotavirus cases with evidence of vaccination experienced severe gastroenteritis. Diverse genotypes, including RVA G2P[4], G1P[8], G12P[8] and G12P[6]; AdV F40 and F41; NoV GII.4 Sydney 2012, GII.6 and GI.3, several of which clustered with contemporary strains from the Americas, Europe and Asia, were detected. This study also provides the first report of SaV GI.1, GI.7 and GII.8 detection in humans in Ghana. RVA G2P[4] and AdV F were associated with higher proportions of hospitalizations. While RVA continues to have a profound clinical impact on gastroenteritis, AdV and SaV produce an equally severe disease. In contrast, NoV and AstV showed a generally mild to moderate impact on clinical disease severity.
Humans↗
Inactivated vaccine for protection against duck virus enteritis.
Immunogenicity of inactivated tissue-culture-derived duck enteritis virus (DEV) vaccines was evaluated in white Pekin and mallard ducks. DEV from a Lake Andes outbreak was propagated in chicken embryo fibroblast cells, inactivated with beta-propiolactone, and emulsified with Freund's adjuvant (FA), multiple-oil emulsion (MOE), or Squalane-pluronic L121 (L121). White Pekin and mallard ducklings were vaccinated at 2 or 3 wk of age, respectively. Challenge at 2 wk postvaccination with a virulent DEV isolated from a Long Island outbreak indicated that inactivated Lake Andes (ILA) vaccine mixed with any of the above adjuvants conferred protection, even with a single-dose inoculation. Antibody responses to vaccination, as determined by indirect enzyme-linked immunosorbent assay, showed that ILA virus with FA induced an early production of antibodies similar to that induced by commercially available modified live virus (MLV) vaccine. However, the mean anti-duck virus enteritis (DVE) IgG titers determined by multiple samplings during the first 35 days postvaccination showed titers from ILA virus with FA to be at least 10 times higher than those induced by MLV vaccine. The highest antibody titers were induced by ILA mixed with FA followed by ILA mixed with the MOE and L121. The results of this study indicated that inactivated vaccine is as efficacious as modified live vaccine in enhancing protection against virulent DEV in waterfowl.
Animals↗
[Relation of the amount of the virus administered, enteral virus multiplication and antibody formation following oral administration of Teschen virus. Contribution to the understanding of the action mechanism of oral vaccinations].
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Animals↗
Antigenic structure and variation of canine parvovirus type-2, feline panleukopenia virus, and mink enteritis virus.
The antigenic structure and variation of canine parvovirus type-2 (CPV), feline panleukopenia virus (FPV), mink enteritis virus (MEV), and a closely related virus of raccoons (RPV) was investigated using a panel of 13 monoclonal antibodies (mAb) formed against CPV and 8 mAb formed against FPV. Each mAb both neutralized and inhibited the hemagglutination of the homologous virus. All mAb tested immunoprecipitated the two capsid proteins. Five mAb were specific for the CPV isolates and one reacted with the FPV, MEV, and RV isolates, but not the CPV. Another mAb reacted only with certain FPV and MEV isolates. The remaining 14 mAb reacted with most parvoviral isolates from the four animal species. Antigenic variation was observed both within and between the parvovirus isolates from each species. The 12 MEV isolates could be grouped into three antigenic types based on their reactivity with the panel of mAb. Antigenic variants of either CPV or FPV were readily selected with several mAb. Analysis of these variant viruses by direct serological tests and competition radioimmune assays between different mAb revealed that the capsid surface contained at least two determinants, each being comprised of many different but overlapping epitopes.
Animals↗
Latency sites and reactivation of duck enteritis virus.
Duck virus enteritis (DVE) is a contagious disease caused by herpesvirus in waterfowl populations. Recovered birds become carriers and shed the virus periodically. Reactivation of latent duck enteritis virus (DEV) has been implicated in outbreaks of DVE in domestic and migrating waterfowl populations. In this study, the sites for virus latency were determined in white Pekin ducks infected with the DEV-97 strain. At 3 wk postinfection, infectious virus was not detectable in tissues or cloacal swabs (CSs). At 7 and 9 weeks postinfection, the viral DNA was detected by polymerase chain reaction in the trigeminal ganglia (TG), suggesting that the virus is latent. Viral DNA was detected in the peripheral blood lymphocytes (PBL), spleen, thymus, bursa, and CSs only after in vitro cocultivation. In vivo virus reactivation was demonstrated when dexamethasone or a combination of dexamethasone and cyclophosphamide was inoculated in latently infected ducks. The reactivation of DEV occurred without any clinical evidence of the disease, but the virus was detected in PBL and CSs. We conclude from this study that DEV establishes latency in TG and lymphoid tissues including PBL.
Animals↗
Antigenic relationships between canine parvovirus type 2, feline panleukopenia virus and mink enteritis virus using conventional antisera and monoclonal antibodies.
The antigenic relationships between three similar parvoviruses, canine parvovirus type 2 (CPV), feline panleukopenia virus (FPV) and mink enteritis virus (MEV) were investigated. Antisera against all 3 viruses and monoclonal antibodies (mAb) to CPV were prepared and the viruses compared using several serological methods. When conventional sera were used in the hemagglutination-inhibition and agar gel precipitin (AGP) tests there were no differences between the CPV viral isolates studied, but antigenic differences were revealed between the CPV isolates and the FPV or MEV. Of 16 mAb produced against CPV, six reacted only with the CPV. The other 10 mAb reacted with all three parvoviruses. Additionally, an antigenic difference was detected by AGP tests between one FPV isolate and the other FPV and MEV isolates. Including both conventional sera and mAb to CPV in a single AGP test with the CPV, MEV and FPV antigens permitted the comparison of results obtained with the different antibodies. The results reported revealed antigenic differences between CPV and FPV or MEV that were most clearly defined using mAb.
Animals↗
Canine parvovirus: relationship to wild-type and vaccine strains of feline panleukopenia virus and mink enteritis virus.
Canine parvovirus (CPV), feline panleukopenia virus (FPLV) and mink enteritis virus (MEV) were compared serologically, by determination of their host range in cell cultures, as well as by restriction enzyme analysis. Maps of the virus genomes were established using seven different restriction enzymes cutting at a total of 56 sites. MEV and FPLV gave maps which were identical except for one restriction site. The map of CPV is closely related to those of FPLV/MEV since their DNAs share about 80% of the restriction sites tested. However, CPV is clearly distinct from FPLV/MEV since either eight (German isolate) or nine (Belgian, Swiss and American isolates) restriction sites are different. The DNAs of six vaccine strains of FPLV and MEV were also analysed. They gave maps which closely resembled those of the respective wild-type strains. CPV and FPLV/MEV also differed with respect to antigenicity, as well as to host range in cell cultures.
Animals↗
Epitope mapping of a monoclonal antibody specific to feline panleukopenia virus and mink enteritis virus.
To obtain monoclonal antibodies (MAbs) specific to feline panleukopenia virus (FPLV) and mink enteritis virus (MEV), 15 hybridomas secreting MAbs against MEV-Abashiri were established and the properties of the MAbs were analyzed. The cross-reactivity of MAbs revealed that one MAb, P2-215 was specific for FPLV and MEV, whereas the remaining fourteen MAbs reacted with canine parvovirus (CPV), FPLV, and MEV. Epitope analyses using various CPV/MEV chimeric viruses revealed that the MAb P2-215 recognized the epitope comprised of amino acid 93-Lys in VP2, which is known to be FPLV and MEV-specific.
Amino Acid Sequence↗
Response of specific-pathogen-free turkeys to vaccines derived from marble spleen disease virus and hemorrhagic enteritis virus.
Tissue-culture-propagated marble spleen disease virus (MSDV-TC) and two preparations of spleen homogenate (MSDV-SH and MSDV-SH-TC) were compared as anti-hemorrhagic enteritis virus (HEV) vaccines in specific-pathogen-free turkeys. Both types of vaccines spread horizontally among turkeys, induced anti-HEV antibodies, and protected turkeys against challenge with virulent HEV. Antibody development and horizontal spread of virus occurred earlier in turkeys given MSDV-SH or MSDV-SH-TC than in those given MSDV-TC. Virulent HEV was serially passed in MDTC-RP19 cells. The 30th passage virus (HEV-P30) was nonpathogenic for turkeys but was immunogenic. Turkeys exposed to HEV-P30 had viral antigen in the spleen, developed neutralizing antibodies, and resisted virulent HEV. The principal difference between MSDV-TC and HEV-P30 vaccines was that MSDV-TC caused well-defined splenomegaly in turkeys, whereas HEV-P30 protected turkeys without causing spleen enlargement.
Animals↗
Some clinical and hematological features of virus enteritis of mink.
Twenty-six, ten-week-old mink were infected by force feeding by pipette 2 ml of a tissue suspension containing a Wisconsin strain of mink enteritis virus. Four days later, diarrhea and partial or complete loss of appetite developed simultaneously in all of the animals. Squinting and occasional vomiting were also observed. By the sixth day after inoculation, all of the mink were anorectic and weak. Anorexia persisted for 48 to 96 hours. Diarrhea and vomiting continued until the eighth to ninth day after exposure. For the first two days after the appearance of diarrhea, the feces contained large quantities of mucus and intestinal casts were seen frequently in the droppings. Thereafter, the feces consisted mostly of yellowish green, watery fluid and contained no casts. Some of the animals died on the eighth day after infection. Those which survived were severely dehydrated and debilitated, but resumed eating and achieved complete clinical recovery within the next five to six days.Leukopenia, i.e., total leukocyte count of less than 5,000 cells per mm(3) of blood, was found in seven of nine mink examined during the height of the disease. Leukopenic animals were deficient in both lymphocytes and neutrophils.
Animals↗
Pathological changes in virus enteritis of mink.
The lesions which characterize viral enteritis of mink (VEM) were studied in twenty-six, ten-week-old mink which had been infected by force feeding a tissue suspension containing a Wisconsin strain of mink enteritis virus. The pathogenesis of the lesions was reconstructed from gross and histopathological changes observed in animals which were selected randomly from the group each day for necropsy during the course of the disease. Alterations were observed in the tissues of all mink examined from post-inoculation day (PID) 4 through 13. The principal macroscopic lesions which consisted of fibrinous enteritis, enlargement and hemorrhage of the spleen and edema of mesenteric and hepatic lymph nodes were most conspicuous on PID 7 and 8. Histopathological changes including necrosis and desquamation of intestinal epithelium, depletion of mature lymphocytes in lymph nodes, thymus and spleen and loss of partly differentiated myeloid and erythroid cells from spleen and bone marrow also reached full development on PID 7 and 8. However, nuclear inclusion bodies which were presumed to be a product of the causative agent and, therefore, of diagnostic significance were most prevalent on PID 3, 4 and 5. The inclusions were observed in mucosal epithelial cells of the intestine, parenchymal cells of the liver and in lymphocyte precursor cells of the spleen, intestinal lymph nodules and masenteric and hepatic lymph nodes.
Animals↗
Pathogenicity of a low-virulence duck virus enteritis isolate with apparent immunosuppressive ability.
Duck enteritis virus (DEV) was isolated from commercial 2-to-6-wk-old white Pekin ducks experiencing 25%-30% mortality and high morbidity. Secondary infections with Pasteurella multocida, Riemerella anatipestifer, and Escherichia coli were frequently seen in affected ducks. The isolated virus was identical to the prototype DEV by virus neutralization test but differed from the classic DEV by causing lymphoid organ atrophy and inconsistent hemorrhagic lesions in the intestinal annular bands. Attempts to reproduce the disease in white Pekin ducks were unsuccessful until the virulence of the virus was increased by three passages in Muscovy ducklings. Significant thymic atrophy (P < or = 0.001) was detected during the first 10 days postinfection (DPI), but thymus size returned to normal by 17-24 DPI. However, bursal atrophy increased significantly (P < or = 0.001) from 4 DPI until the end of the experiment (39 DPI). Reduction in body weight was significant (P < or = 0.05) between 4 and 6 DPI. There was massive depletion of thymic and bursal lymphocytes with lymphoid necrosis in the thymus, bursa, spleen, and Harderian gland. Eosinophilic intranuclear inclusions were observed in thymus, bursa, spleen, esophagus, cloaca, liver, conjunctiva, and Harderian gland. Occasional intracytoplasmic inclusions were also found scattered in the epithelial cells of conjunctiva, esophagus, bursa of Fabricius, and cloaca. Virus was recovered from experimentally infected ducks from thymus, bursa, spleen, liver, kidneys, trigeminal ganglion, and cloaca during the first 10 days of infection. These findings suggest that a low-virulent DEV can cause a massive lymphoid atrophy and can sustain immunosuppression as noted by the secondary bacterial infection.
Animals↗
Seminested RT-PCR systems for small round structured viruses and detection of enteric viruses in seafood.
Highly sensitive seminested RT-PCR systems for the specific detection of genotype I and II small round structured viruses (SRSVs) were developed based on the nucleic acid information deposited in the databanks. SRSVs could be detected in 10(7)-fold dilutions of three different stool samples. In addition, a rapid and simple purification protocol for enteric viruses from seafood tissues was elaborated using poliovirus (PV) as model. The virus isolation and viral RNA purification include the following steps: elution of the viruses from the seafood tissue with glycine buffer, their concentration by PEG-precipitation, lysis of viral particles with guanidine hydrochloride and viral RNA isolation using a silica based membrane. The detection limit was 3 to 30 TCID50 of poliovirus in 1.25 g of seeded seafood tissues without marked food matrix differences, whereas SRSV viruses were 10- and 100-fold better detected in mussels than in shrimps and oysters, respectively. The newly developed purification method, which was shown to remove potential RT-PCR inhibitors present in mussel tissue samples, was applied in a small market survey. 15 mussels, 15 oysters and 12 shrimps were examined for the presence of Hepatitis A virus (HAV), Enterovirus (EV), Rotavirus (RV) and SRSV using specific RT-PCR detection systems. The finding of three oyster samples positive for Rotavirus demonstrated the successful application of our method for the detection of enteric viruses in naturally contaminated seafood samples. The rapid isolation method might be suitable for application in routine testing laboratories and will help to improve public health controls for seafood.
Base Sequence↗
Protection of turkeys from hemorrhagic enteritis with a recombinant fowl poxvirus expressing the native hexon of hemorrhagic enteritis virus.
Hemorrhagic enteritis (HE) is an economically important disease of turkeys caused by a type II aviadenovirus, hemorrhagic enteritis virus (HEV). The vaccines currently available to the commercial poultry producer are highly effective in preventing disease outbreaks; however, they are immunosuppressive. A recombinant fowl poxvirus (rFPV) expressing the native hexon of HEV has been shown to induce an anti-HEV humoral immune response in turkeys. In this study, the rFPV expressing the native hexon of HEV was compared with a commercial HEV vaccine (vxHEV) for its ability to protect turkeys from virulent HEV challenge. Complete protection from the enteritis of HE was achieved in experimental groups vaccinated with either the rFPV or the vxHEV. Lymphocyte stimulation was measured in turkeys inoculated with rFPV, vxHEV, or a sublethal dose of HEV or not inoculated. No statistically significant immunodepression was observed in turkeys receiving the rFPV.
Adenoviridae Infections↗
The complete DNA sequence and genome organization of the avian adenovirus, hemorrhagic enteritis virus.
Hemorrhagic enteritis virus (HEV) belongs to the Adenoviridae family, a subgroup of adenoviruses (Ads) that infect avian species. In this article, the complete DNA sequence and the genome organization of the virus are described. The full-length of the genome was found to be 26,263 bp, shorter than the DNA of any other Ad described so far. The G + C content of the genome is 34.93%. There are short terminal repeats (39 bp), as described for other Ads. Genes were identified by comparison of the DNA and predicted amino acid sequences with published sequences of other Ads. The organization of the genome in respect to late genes (52K, IIIa, penton base, core protein, hexon, endopeptidase, 100K, pVIII, and fiber), early region 2 genes (polymerase, terminal protein, and DNA binding protein), and intermediate gene IVa2 was found to be similar to that of other human and avian Ad genomes. No sequences similar to E1 and E4 regions were found. Very low similarity to ovine E3 region was found. Open reading frames were identified with no similarity to any published Ad sequence.
Adenoviridae↗