Comparison of the viral proteins of canine parvovirus-2, mink enteritis virus and feline panleukopenia virus

Canine parvovirus-2 (CPV-2), Mink enteritis virus (MEV) and feline panleukopenia virus (FPV) were produced using identical cell culture and purification techniques. The distributions of the haemagglutinating activity of the three different parvoviruses in a CsCl gradient were similar with haemagglutinating peaks identified at 1.48–1.49, 1.42, 1.36 and 1.30–1.31 g cm^?3. The number and distribution of the viral proteins and the equivalent protein molecular weights are similar for all three viruses in SDS-polyacrylamide gels (10%). Four viral proteins were identified and their molecular weights were determined: protein A (77 500–79 500), protein B (63 000–63 500), protein C (61 500–63 000) and protein D (50 000–55 000). The viral protein D although reported for some other parvoviruses has not previously been demonstrated in CPV-2, MEV or FPV.     

Comparisons of feline panleukopenia virus, canine parvovirus, raccoon parvovirus, and mink enteritis virus and their pathogenicity for mink and ferrets

Parvoviruses from mink (mink enteritis virus [MEV]), cats (feline panleukopenia virus [FPV]), raccoons (raccoon parvovirus [RPV]), and dogs (canine parvovirus [CPV]) were compared. Restriction enzyme analysis of the viral replicative-form DNA revealed no consistent differences between FPV and RPV isolates, but CPV and MEV isolates could be distinguished readily from other virus types. Feline panleukopenia virus, RPV, and MEV, but not CPV, replicated to high titers in mink. However, on the first passage, disease and microscopic lesions were observed only in mink inoculated with MEV. Feline panleukopenia virus and RPV isolates replicated in ferrets, but disease or microscopic lesions were not observed. Feline panleukopenia virus and RPV isolates could be passaged repeatedly in mink and ferrets. Virulence of FPV and RPV isolates was low compared with that of MEV, and only a single mink inoculated with FPV or with RPV developed clinical disease on the sixth passage of virus.     

The propagation of feline panleukopenia virus in micro-carrier cell culture and use of the inactivated virus in the protection of mink against viral enteritis

Using microcarrier cell culture for the production of virus antigen, a formalin-inactivated feline panleukopenia virus vaccine was evaluated for protection of mink against specific mink enteritis virus infection. The vaccine showed a good immunogenic effect in mink when used either alone or in combination with Clostridium botulinum type C-toxoid and/or Pseudomonas aeruginosa vaccine. A single vaccination induced persistent immune responses for periods of at least 1 year, as evaluated by ELISA and challenge tests. Neither immunological interference between vaccine constituents nor adverse reactions were observed.     

Apoptosis in feline panleukopenia and canine parvovirus enteritis

Tissue samples of cats and dogs with panleukopenia and parvovirus enteritis, respectively, were examined for the presence of viral antigen-positive cells and apoptotic cells by immunohistochemistry and by TUNEL assay (Terminal Transferase-Mediated dUTP Nick End Labelling). Compared to control animals, infected cats and dogs generally had more TUNEL-positive cells. Cell types positive for parvovirus antigen, for example digestive tract epithelial and mesenchymal cells, and lymphocytes and macrophages in lymphoid tissues were also positive for TUNEL signals. Occasionally, TUNEL signal and viral antigen were present in the same tissue areas, suggesting a direct viral trigger of apoptosis. More frequently, however, there was no complete overlap of antigen and TUNEL-positive areas. The results of this study indicate that apoptotic cell death contributes significantly to the widespread tissue damage of parvovirus infection in cats and dogs.     

The growth of attenuated strains of canine parvovirus, mink enteritis virus, feline panleukopenia virus, and rabies virus on various types of cell cultures

The growth characteristics were studied in the attenuated strains of canine parvovirus CPVA-BN 80/82, mink enteritis virus MEVA-BN 63/82 and feline panleucopenia virus FPVA-BN 110/83 on the stable feline kidney cell line FE, and in the attenuated canine distemper virus CDV-F-BN 10/83 on chicken embryo cell cultures (KEB) and cultures of the stable cell line VERO. When the FE cultures were infected with different parvoviruses in cell suspension at MOI 2-4 TKID50 per cell, the first multiplication of the intracellular virus was recorded 20 hours p. i. In the canine parvovirus, the content of intracellular and extracellular virus continued increasing parallelly until the fourth day; then, from the fourth to the sixth day, the content of extracellular virus still increased whereas that of intracellular virus fell rapidly. In the case of the mink enteritis virus the release of the virus into the culture medium continued parallelly with the production of the cellular virus until the sixth day. In the case of the feline panleucopenia virus the values concerning free virus and virus bound to cells were lower, starting from the second day p. i. When KEB or VERO cultures were infected in cell suspension with the canine distemper virus at MOI about 0.004 per 1 cell, the replicated intracellular virus was first recorded in the KEB cultures five hours after infection but in the VERO cultures only 20 hours after infection, with a timely release of the virus into the culture medium in both kinds of tissue. In the KEB and VERO cultures the highest values of infection titres were recorded on the fourth day p. i., the course of virus multiplication on the cells being parallel with its release into the culture medium.     

Evaluation of a killed feline panleukopenia virus vaccine against canine parvoviral enteritis in dogs

Immunogenic potency of a killed feline panleukopenia virus vaccine against canine parvoviral enteritis in dogs was examined. The vaccine elicited hemagglutination-inhibition antibodies to canine parvovirus (CPV) in all of the 72 dogs which were vaccinated. The vaccine was protective in dogs against both experimentally induced and naturally occurring CPV-induced disease. By statistical analysis, 4 weeks was found to be the optimal spacing between 2 vaccinal doses resulting in hemagglutination-inhibition antibody titers up to 1:5,120. Adverse reactions to the vaccine were not observed. Atypical lymphocytes were found consistently in the CPV-infected control dogs.     

Response of mink, skunk, red fox and raccoon to inoculation with mink virus enteritis, feline panleukopenia and canine parvovirus and prevalence of antibody to parvovirus in wild carnivores in Ontario.

Mink virus enteritis, feline panleukopenia and canine parvovirus-2 were inoculated separately into groups of raccoon, mink, red fox and striped skunk. Raccoons were highly susceptible to mink virus enteritis and feline panleukopenia, with animals developing clinical illness, and several dying within six to ten days of inoculation with lesions typical of parvovirus infection. Both viruses were shed in high titre in the feces of infected raccoons, and high antibody titres were stimulated. Raccoons inoculated with canine parvovirus-2 showed no signs; shedding of virus was sporadic though moderate titres of antibody developed. Mink inoculated with mink virus enteritis and feline panleukopenia developed signs and lesions of early parvovirus infection. No signs or significant lesions followed canine parvovirus-2 inoculation. Shedding of virus was heavy (mink virus enteritis) or sporadic (feline panleukopenia and canine parvovirus-2), though good serological responses were elicited to all three viruses. Red fox showed no signs of infection, shed all three viruses only sporadically, and the serological response was strong only to feline panleukopenia. Skunks developed low antibody titres, but no signs, and did not shed virus. Antibody to parvovirus was found in 79.2% of 144 wild red foxes; 22.3% of 112 wild raccoons; 1.3% of 157 wild skunks and 6/7 coyotes in southern Ontario. The likely significance of these viruses to wild and captive individuals and populations of these carnivores is discussed.     

A non-haemagglutinating isolate of mink enteritis virus

A virus was isolated from mink showing clinical and pathological signs of mink enteritis. This virus was identified as mink enteritis virus (MEV) from results of serological tests, determination of its density in CsCl (1.415 g cm^?3), and morphology, including size (20 nm in diameter). The isolate was designated MEV-S. In contrast to other known MEV strains, the MEV-S isolate has no haemagglutinating (HA) activity with swine red blood cells (RBCs) at 4°C and pH 6.8.Neither was there any HA at other pH values and temperatures, or when worse, bovine and rhesus monkey RBC's were used.     

用PCR法检测东北虎感染猫细小病毒的研究

根据GenBank中已发表的猫细小病毒基因组中的保守序列 ,利用Goldkey软件设计了一对能扩增 750bp片段大小的引物 ,对某动物园 1只病死东北虎的脾脏样品进行了PCR检测。结果得到了与设计大小完全相符且与标准猫细小病毒扩增产物大小一致的特异核酸带 ,同时对犬瘟热、犬腺病毒、轮状病毒的核酸扩增结果均为阴性。敏感性试验表明 ,此法可检出血凝价为 1 2 8×脾脏匀浆液上清 1 0 - 5倍稀释的模板 ,远高于血凝试验的敏感性 ,为虎、狮、熊猫等野生动物细小病毒病的快速诊断提供了一个有效的方法     

Comparison of feline parvovirus subspecific strains using monoclonal antibodies against a feline panleukopenia virus

Four monoclonal antibodies (mAb) against a feline panleukopenia virus (FPLV) TU 1 strain, one of the host range variants of feline parvovirus (FPV), were produced and applied for antigenic analysis of FPLV, canine parvovirus (CPV) and mink enteritis virus (MEV). All mAbs were considered to be directed at epitopes on the virus capsid surface because they neutralized the infectivity and inhibited the hemagglutination (HA) of the homologous virus as well as other FPV strains. They were of the mouse IgG1 type. High antigenic homogeneity among FPLV strains was confirmed by HA-inhibition (HI) test with the mAbs and polyclonal immune sera against FPLV or CPV. But the TU 11 strain of FPLV was antigenically distinguished from the remaining 14 FPLV strains by both the HI test and the micro-neutralization test with one of the mAbs produced. MEV Abashiri strain was found to be antigenically indistinguishable from FPLV. Most of the CPV strains isolated after 1981 were considered to be antigenically different from earlier CPV isolates when some mAbs were applied in the serological tests, confirming the replacement of CPV by an antigenic variant in Japan. However, antigenically different CPVs were detected at the end of 1984 from unrelated epizootics occurred a month apart in the same area.     

Three-year duration of immunity in cats following vaccination against feline rhinotracheitis virus, feline calicivirus, and feline panleukopenia virus

Forty-two seronegative cats received an initial vaccination at 8 weeks of age and a booster vaccination at 12 weeks. All cats were kept in strict isolation for 3 years after the second vaccination and then were challenged with feline calicivirus (FCV) or sequentially challenged with feline rhinotracheitis virus (FRV) followed by feline panleukopenia virus (FPV). For each viral challenge, a separate group of 10 age-matched, nonvaccinated control cats was also challenged. Vaccinated cats showed a statistically significant reduction in virulent FRV-associated clinical signs (P = .015), 100% protection against oral ulcerations associated with FCV infection (P < .001), and 100% protection against disease associated with virulent FPV challenge (P < .005). These results demonstrated that the vaccine provided protection against virulent FRV, FCV, and FPV challenge in cats 8 weeks of age or older for a minimum of 3 years following second vaccination.     

动物园猫瘟热净化的新手段—聚合酶链式反应

猫泛白细胞减少症病毒 (FPV)又名猫细小病毒、猫传染性肠炎病毒、猫瘟病毒。该病以高热、呕吐、白细胞严重减少和肠炎为特征。 1 957年 (Bilin)病毒首次被分离培养成功。通过对多种动物类似疾病的病原学研究 ,证明 FPV在自然条件下感染猫科和鼬科多种动物 ,如虎、豹、狮子和浣熊 ,但以体型较小的猫科动物 ,包括水貂最为易感。FPV是目前本属病毒中感染范围最宽、致病性最强的一种。由FPV引起的猫泛白细胞减少症 ,可能存在于世界各地。在欧洲和北美已被认为是猫的重要传染病之一。我国张振兴和李刚等人 (1 982— 1 984)报道 ,我国许多省…     

Dog response to inactivated canine parvovirus and feline panleukopenia virus vaccines

Inactivated canine parvovirus (CPV) and inactivated feline panleukopenia virus (FPV) vaccines were evaluated in dogs. Maximal serologic response occurred within 1-2 weeks after vaccination. Antibody titers then declined rapidly to low levels that persisted at least 20 weeks. Immunity to CPV, defined as complete resistance to infection, was correlated with serum antibody titer and did not persist longer than 6 weeks after vaccination with inactivated virus. However, protection against generalized infection was demonstrated 20 weeks after vaccination. In unvaccinated dogs, viremia and generalized infection occurred after oronasal challenge with virulent CPV. In contrast, viral replication was restricted to the intestinal tract and gut-associated lymphoid tissue of vaccinated dogs. Canine parvovirus was inactivated by formalin, beta-propiolactone (BPL), and binary ethylenimine (BEI) in serum-free media; inactivation kinetics were determined. Formalin resulted in a greater loss of viral HA than either BEI of BPL, and antigenicity was correspondingly reduced.