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PubMedDate not supplied

Canine parvovirus vaccine elicits protection from the inflammatory and clinical consequences of the disease.

Inflammatory changes following infection are central to the clinical manifestation of disease. However, information regarding such changes in animal disease is limited. In canine parvovirus infected puppies we measured the levels of acute phase proteins and changes in leukocyte phenotypes and cell trafficking by flow cytometry. These parameters correlated with conventional assessment of clinical disease in a vaccine efficacy study. Seropositive (CPV-2) 6-week-old puppies given three doses of a CPV-2 containing vaccine developed significant antibody titers and remained healthy after experimental infection with CPV-2b. Unvaccinated controls developed clinical signs and shed virus. Importantly, acute phase proteins became elevated, and lymphopenia, neutropenia and modulation of neutrophil-CD4 were detected in controls but not in vaccinates.

Animals↗
PubMed1998

Nucleic acid immunization protects dogs against challenge with virulent canine parvovirus.

Nucleic acid vaccines (NAVs) use expression vectors encoding one or more antigen genes to transfect host cells inducing both humoral and cellular immunity against the expressed antigen. NAV offers major advantages over conventional vaccines for the protection of humans and animals. This study shows that a plasmid DNA (pGT36VP1) encoding the full length VP1 region of canine parvovirus (CPV) induces immunity that protects dogs against challenge with virulent virus. Five dogs without anti-CPV antibodies were injected at 9 months of age with increasing doses of pGT36VP1 or saline. NAV vaccinated dogs showed an increase of serum IgG titer starting 1 week post-injection which peaked at week 2 and remained detectable for at least 14 weeks. A second dose of NAV resulted in an anamnestic response within 1 week. IgG titers peaked at week 3 and 4 after the second injection. All pGT36VP1 vaccinated dogs were protected against infection after virulent CPV challenge regardless of dose and the unvaccinated control dog was fully susceptible. This study demonstrated for the first time that a NAV can protect dogs against an infectious disease.

Animals↗
PubMed2002

Antibody responses in parvovirus B19 infected patients.

Parvovirus B19 is the causative agent of erythema infectiosum. In addition, the infection may be associated with other disease manifestations: anemia and aplastic crisis, thrombo- or granulocytopenies; spontaneous abortion or hydrops fetalis in pregnant women; acute and chronic arthritis in adults and children, myocarditis and hepatitis. Both acute and persistent courses of B19-infections have been reported. All patients develop IgG against the capsid proteins VP1 and VP2, the majority of virus neutralizing antibodies that offer life-long protection against reinfections are directed against the VP1-unique region. IgM is mainly directed against VP2-specific epitopes. These antibodies may be present for only a rather short period of two to ten weeks after acute infection. IgG-antibodies against the nonstructural protein NS1 are preferentially found in patients which are unable to eliminate the virus and develop persisting viremia or virus persistence in distinct organs, e.g. synovial fluid, liver, bone marrow.

Antibodies, Viral↗
PubMed2002

Current molecular epidemiology and human parvovirus B19 infection.

Viruses evolve gradually through replication. Therefore, isolates of a virus species can have different genome sequences, albeit slightly, if isolates are epidemiologically unrelated. The difference in virus genome involves difference in virus functions and clinical manifestations of virus infection. Molecular epidemiology of virus infection is a relatively new field directed at infection in humans but not other animals. Analyses are based on genomic differences between virus strains with advances in methodology related to DNA analyses, progress is being made. Classification of virus strains, tracing of transmission of a strain, analyses of outbreaks (including nosocomial infection), and analyses of pathogenesis of virus infection in humans (a natural host) are given attention in molecular epidemiological studies. Human parvovirus B19 is a common human pathogen associated with a wide variety of diseases, including erythema infectiosum, aplastic crisis, hydrops fetalis, and arthritis. B19 is not propagatable in conventional cell lines, hence, molecular cloning of B19 DNA directly from clinical materials has to be done. Events concerning B19 infection were analyzed based on the concept of molecular epidemiology and studies proved to be productive to better understand the pathogenesis of B19 infection.

Cloning, Molecular↗
PubMed2002

Persistence of human parvovirus B19 in human tissues.

Human parvovirus B19 infection causes various clinical symptoms, such as rash, arthropathy, anemias and fetal death, but it can also remain asymptomatic. The arthropathies and anemias can become chronic for several years, not infrequently resembling autoimmune syndromes. B19 replicates only in red blood cell precursors of bone marrow or fetal liver, resulting in high-titred short-lived viremia, but viral DNA is detectable also in cells of several other types. Recently B19 DNA has been found, by very sensitive amplification tests, in certain tissues not only of symptomatic but also of healthy individuals for several years or decades after B19 infection. The mere presence of B19 DNA in these tissues of a symptomatic patient (e.g. joints in chronic arthritis or skin in dermatomyositis) thereby does not prove that the present disease is caused by B19. The diagnosis has to be verified by other innovative means. How and why viral DNA persists in the tissues of healthy individuals is under investigation.

Autoimmune Diseases↗
PubMed2002

Parvovirus B19 and erythroid cells.

Parvovirus B19 is a human erythrovirus, i.e. which induces the death of erythroid progenitors. In such cells, until now only ubiquitous transcription factors have been described to regulate promoter driven gene expression. Their possible interactions with erythroid specific transcription factors merit further investigations. Effectively, the high level of replication of B19 in erythroid cells is not well understood. In addition to apoptosis, necrosis or inhibition of cell growth, the death of B19 infected erythroid progenitors has been never clearly reported as the result of immunological attack: this mecanism will merit further investigations. The interactions with other cell types in vitro remain at present not well defined but many obstacles have been mentioned which counteract B19 expression.

Cell Death↗
PubMed1999

Use of a recombinant parvovirus to facilitate screening for human melanoma cell clones expressing tetracycline-responsive transactivators.

The tetracycline regulatory (TET) system provides a useful means of controlling foreign gene expression in mammalian cells. Exploiting this system in cultured cells requires the prior isolation, from the cells of interest, of transfectant clones expressing the necessary TET transactivator, tTA, or reverse transactivator, rtTA. We describe a simple screening procedure for identifying transfectant clones expressing a properly regulated transactivator, and the application of this method to isolating clones of human melanoma cells expressing either tTA or rtTA. Clones in multi-well plates are transduced by exposure to a recombinant parvovirus containing a luciferase reporter, under control of a promoter responsive to the TET system transactivators. Transactivation of reporter expression in the presence or absence of doxycycline (DOXY) is determined after one to two days, using a rapid luciferase assay. Screening is easier and more reproducible with this transduction method than with conventional transient transfection of analogous reporter plasmids. Clones of two human melanoma cell lines showing >100-200-fold transactivation after transfection with either tTA or rtTA were readily identified using this method.

Clone Cells↗
PubMed2001

Contact rates between wild and domestic canids: no evidence of parvovirus or canine distemper virus in crab-eating foxes.

Evaluating the risk of disease spill-over from domestic dogs to wildlife depends on knowledge of inter-specific contact rates and/or exposure to aetiological agents in dog environments. Here, contact rates of crab-eating foxes (Cerdocyon thous) with sympatric domestic dog populations were measured over 25months in Amazon Brazil. Foxes and dogs were serologically and clinically monitored for exposure to canine parvovirus (CPV-2) and canine distemper virus (CDV), pathogens known to have caused wildlife population declines elsewhere. Twenty-two of 24 (92%) tagged foxes visited one or more houses in a median 2 (range 1-3) villages per night where dog densities ranged from 7.2 to 15.4 per km(2) (mean 9.5 per km(2)). Foxes spent an average 6.4% (0-40.3%) of their 10h nocturnal activity period in villages, the equivalent of 38m (range 0-242) per night. The rate of potential exposure to disease agents was thus high, though varied by 3 orders of magnitude for individual foxes. Overall, 46% of the fox population was responsible for 80% of all contacts. None of the 37 monitored foxes however showed serological or clinical evidence of infection with CPV-2 or CDV. Seroprevalences for CPV-2 and CDV antibodies in the local domestic dog population were 13% (3/23) and 9% (2/23), respectively, and 89% of 97 monitored pups born during the study presented clinical signs consistent with active CPV-2 infection (haemorrhagic diarrhoea, vomiting, rapid morbidity and emaciation). Although there was no evidence for infection with either virus in foxes, the high level of contact of foxes with peridomestic habitats suggests that the probability of potential spill-over infections from dogs to foxes is high.

Age Factors↗
PubMed1997

Detection of antibodies against porcine parvovirus nonstructural protein NS1 may distinguish between vaccinated and infected pigs.

The humoral antibody response against the nonstructural protein NS1 and the structural protein VP2 of porcine parvovirus (PPV) was evaluated by immuno-peroxidase test (IPT) and enzyme linked immuno sorbent assay (ELISA) using recombinant PPV antigens. The coding sequence for NS1 and VP2 was inserted into the baculovirus. Autographa californica nuclear polyhedrosis virus (AcNPV) genome resulting in two recombinant baculoviruses AcNPV-NS1 and AcNPV-VP2, respectively. Sf9 cells (Spodoptora frugidiperda) inoculated with AcNPV-NS1 producing recombinant nonstructural protein (rNS1) and AcNPV-VP2 producing recombinant virion protein (rVP2) were used in IPT and ELISA to analyse serum antibodies. Pigs vaccinated with an inactivated whole virus vaccine and experimentally infected pigs were studied. Significant titers against rVP2 were obtained in both vaccinated and infected pigs. Specific antibodies against rNS1 could only be detected in infected pigs and NS1 may in this way allow the specific detection of infected animals. Analysis of serum samples collected up to 18 days post infection (p.i.) from four pigs experimentally infected with PPV showed that antibodies against rNS1 and rVP2 could in all cases be detected on day 9 p.i. Two individual pigs were inoculated twice with PPV and the antibody response was followed 89 days after second inoculation. Serum antibodies against both rVP2 and rNS1 could be detected for this period of time.

Animals↗
PubMed1998

Asymptomatic bacteriuria in puppies with canine parvovirus infection: a cohort study.

This study aimed to investigate the possible association between canine parvoviral enteritis and asymptomatic bacteriuria. Forty-three puppies that were admitted to the outpatient service of the Animal Medical Clinic with clinical signs compatible with parvoviral enteritis formed the exposed group. The clinical diagnosis was subsequently confirmed by a positive fecal ELISA test (CITE test: IDDEX Lab., Westbrook, ME). Twenty-three (53.5%) of these puppies were males and 20 (46.5%) were females. Their age ranged from 1.5 to 5.5 months. Forty-eight clinically normal and age-matched puppies, that had been admitted to the clinic for vaccinations and had a negative result in the aforementioned ELISA test, were randomly selected to form the unexposed group. Urine samples were collected by antebupic cystocentesis from all puppies and submitted for bacterial culture. In the parvovirus exposed group, 11 of 43 puppies had detectable bacteriuria. The isolates were Escherichia coli alone (8/11-72.7%) Staphylococcus aureus alone (1/11-9.1%) and mixed cultures of E. coli and S. epidermitis (2/11-18.2%). In the unexposed group there were three puppies with detectable bacteriuria, one isolate each of E. coli, Enterococcus durans and Corynebacterium spp. Puppies with parvoviral enteritis had five (95% CI: 1.3-19.8) times higher odds of developing asymptomatic bacteriuria than puppies without the disease. The observed increased risk of asymptomatic bacteriuria among puppies with parvoviral enteritis was probably due to the fecal contamination of the external genitalia and the neutropenia these puppies exhibited.

Animals↗
PubMed1999

Host range relationships and the evolution of canine parvovirus.

Canine parvovirus (CPV) is an example of an unusual class of emerging virus-those that gain an altered host range through genetic variation and subsequently become widespread pathogens of their new and previously resistant host species. CPV was first detected in 1978 as the cause of new diseases in dogs throughout the world, when it rapidly spread throughout domestic populations, as well as becoming widespread in wild dogs. CPV was soon shown to be a variant of the long recognized feline panleukopenia virus (FPV), from which it differed in less than 1% at the nucleotide sequence level. Genetic analysis showed that virtually all of the biological differences between CPV and FPV, including the canine host range, were determined by three or four sequence differences in the viral capsid protein gene. Analysis of the atomic structures of the CPV and FPV capsids showed that the differences controlling host range were located within two different structural regions and were exposed on the capsid surface. The CPV which first emerged in 1978 appeared to be derived from a single ancestral sequence, which has allowed the ready analysis of the subsequent evolution of the virus in nature. Sequence analysis has also revealed that CPV strains have undergone a series of evolutionary selections in nature which have resulted in the global distribution of new virus variants. This was first seen in the global replacement between 1979 and 1981 of the original (1978) strain of the virus by a genetically and antigenically variant strain, and the subsequent widespread selection of other variants which have also become globally distributed. The genetic and antigenic variation in the virus strains was also correlated with changes in the host range of the virus, in particular in the ability to replicate in cats, and in canine host range differences seen in tissue culture cells.

Amino Acid Sequence↗
PubMed1999

Emergence and recent evolution of canine parvovirus.

This review summarizes the current knowledge about the emergence of canine parvovirus from an ancestor virus similar to feline panleukopenia virus most likely from a wild carnivore host. The recent evolution of CPV, namely the emergence of new antigenic types, their biological properties and global distribution are also discussed.

Animals↗
PubMed2000

The effect of porcine parvovirus and porcine reproductive and respiratory syndrome virus on porcine reproductive performance.

From a worldwide perspective, porcine parvovirus (PPV) and porcine reproductive and respiratory syndrome virus (PRRSV) are the most common viral causes of porcine reproductive failure. A typical epidemic of PPV-induced reproductive failure is presented as an increased number of mummified fetuses and sometimes, entire litters are mummified. If infection with PPV is very early in gestation, the number of liveborn pigs may be further reduced as a result of embryonic death and resorption. During the acute stage of infection gilts and sows have few, if any, clinical signs, and it is unlikely that PPV is ever the direct cause of abortion. In contrast, a typical epidemic of PRRSV-induced reproductive failure is presented as a broader spectrum of clinical features including abortions, late-term dead fetuses, stillborn pigs, and weakborn pigs. In the later stages of an epidemic, there may also be an increase in the number of mummified fetuses, but their prevalence is likely to be far less than during an epidemic of PPV-induced reproductive failure. During the acute stage of infection with PRRSV, gilts and sows may have few, if any, clinical signs, or they may be severely affected and even die. This difference largely reflects the relative virulence of the strain of PRRSV causing the epidemic. A timely and reliable laboratory diagnosis of either disease can be made when appropriate tests are performed with appropriate samples. Vaccines are available for prevention of both diseases.

Animals↗
PubMedDate not supplied

Estimation of serum concentration of parvovirus B19 DNA by PCR in patients with chronic anaemia.

Parvovirus B19 DNA was detected in serum samples from 10 out of 42 patients with chronic anaemia, the majority of whom suffered from aplastic anaemia, haemolytic anaemia, pure red cell anaemia or myelodysplastic syndrome. Nested PCR methods with sensitivities of 0.005-0.05 fg DNA were developed. In nine patients, B19 DNA could only be detected by nested PCR. Conventional PCR with a sensitivity of 50 fg B19 DNA could only detect B19 DNA in one patient. In the majority of B19-DNA-positive patients, the DNA concentration was estimated at 0.005-0.05 fg per 5 microliters serum.

Adolescent↗
PubMed1994

A recombinant immunoblot and ELISA for detection of acute parvovirus B19 infection.

Laboratory diagnosis of parvovirus B19 (B19) infection has been hampered by the limited availability of B19 virus. Recombinant viral proteins are now available for use as antigen in serological assays. We compared detection of anti-B19 IgM by "mu-capture assay" using viral B19 particles to a recombinant (rec.) immunoblot and a rec. enzyme-immunoassay (ELISA) using viral structural proteins as antigens expressed in E. coli. The rec. immunoblot was 94.3% sensitive and 96.4% specific for anti-B19 IgM, and the sensitivity of the rec. ELISA was 94.3% and the specificity, only 72.7%. There was an agreement between the "mu-capture assay" and the rec. immunoblot in 87.8% and the rec. ELISA in only 74.4%. For detection of anti-B19 IgG in patients with acute B19 infection, the rec. immunoblot was 94.3% and the rec. ELISA 85.7% sensitive. The rec. immunoblot is more reliable for detection of acute B19 infection than the rec. ELISA.

Antibodies, Viral↗
PubMed1992

Prevalence of antibodies to parvovirus B19 in selected groups of patients and healthy individuals.

The prevalence of antibodies to parvovirus B19 in sera (n = 745) of various groups of patients and healthy individuals was determined by the enzyme immunoassay, using viral particles as antigen. Among healthy individuals, anti-B19 IgG prevalence was highest in nurses (65.4% (17/26)); in medical students it was 34.1% (47/138) and in pregnant females, 24.4% (48/197). 37.0% (44/119) of HIV-negative haemophiliac patients and 91.7% (33/36) of haemophilic patients with HIV infection were anti-B19 IgG-positive. 45.8% (55/120) of dialysis patients and 27.5% (30/109) of patients with asymptomatic HIV infection were positive for anti-B19 IgG. With the exception of HIV-infected haemophiliac patients, no specific "risk group" for B19 infection could be identified.

Adolescent↗
PubMed1992

Heat stability of parvovirus B19: kinetics of inactivation.

Heat inactivation of parvovirus B19 (B19) was studied in a culture of hematopoietic progenitor cells generated in vitro from peripheral human blood. After inoculating cell cultures with identical volumes of plasma (MII) containing B19 (B19-MII) heat-treated (60 degrees C) for various periods of time, a time-dependent inactivation of the input virus was determined by a decrease of viral DNA replication. No B19 DNA was detected after infection with B19-MII heat-treated for 20 min or more by Southern blot. Viral B19 protein production decreased time-dependently and was not detected after infection with samples treated for 12 min at 60 degrees C or more determined by the enzyme immunoassay. This study indicates that infectivity of B19 virus in plasma can be reduced in vitro by heat-treatment (60 degrees C). However, this does not mean that the heat treatment completely inactivated B19 virus.

Cells, Cultured↗