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PubMed2005

Virulent variants emerging in mice infected with the apathogenic prototype strain of the parvovirus minute virus of mice exhibit a capsid with low avidity for a primary receptor.

The mechanisms involved in the emergence of virulent mammalian viruses were investigated in the adult immunodeficient SCID mouse infected by the attenuated prototype strain of the parvovirus Minute Virus of Mice (MVMp). Cloned MVMp intravenously inoculated in mice consistently evolved during weeks of subclinical infection to variants showing altered plaque phenotypes. All the isolated large-plaque variants spread systemically from the oronasal cavity and replicated in major organs (brain, kidney, liver), in sharp contrast to the absolute inability of the MVMp and small-plaque variants to productively invade SCID organs by this natural route of infection. The virulent variants retained the MVMp capacity to infect mouse fibroblasts, consistent with the lack of genetic changes across the 220-to-335 amino acid sequence of VP2, a capsid domain containing main determinants of MVM tropism. However, the capsid of the virulent variants shared a lower affinity than the wild type for a primary receptor used in the cytotoxic infection. The capsid gene of a virulent variant engineered in the MVMp background endowed the recombinant virus with a large-plaque phenotype, lower affinity for the receptor, and productive invasiveness by the oronasal route in SCID mice, eventually leading to 100% mortality. In the analysis of virulence in mice, both MVMp and the recombinant virus similarly gained the bloodstream 1 to 2 days postoronasal inoculation and remained infectious when adsorbed to blood cells in vitro. However, the wild-type MVMp was cleared from circulation a few days afterwards, in contrast to the viremia of the recombinant virus, which was sustained for life. Significantly, attachment to an abundant receptor of primary mouse kidney epithelial cells by both viruses could be quantitatively competed by wild-type MVMp capsids, indicating that virulence is not due to an extended receptor usage in target tissues. We conclude that the selection of capsid-receptor interactions of low affinity, which favors systemic infection, is a major evolutionary process in the adaptation of parvoviruses to new hosts and in the cause of disease.

Animals↗
PubMed2005

B1 lymphocytes and myeloid dendritic cells in lymphoid organs are preferential extratumoral sites of parvovirus minute virus of mice prototype strain expression.

Due to their oncolytic properties and apathogenicity, autonomous parvoviruses have attracted significant interest as possible anticancer agents. Recent preclinical studies provided evidence of the therapeutic potential of minute virus of mice prototype strain (MVMp) and its recombinant derivatives. In a murine model of hemangiosarcoma, positive therapeutic outcome correlated with high intratumoral expression of MVMp-encoded genes in tumors and lymphoid organs, especially in tumor-draining lymph nodes. The source and relevance of this extratumoral expression, which came as a surprise because of the known fibrotropism of MVMp, remained unclear. In the present study, we investigated (i) whether the observed expression pattern occurs in different tumor models, (ii) which cell population is targeted by the virus, and (iii) the immunological consequences of this infection. Significant MVMp gene expression was detected in lymphoid tissues from infected tumor-free as well as melanoma-, lymphoma-, and hemangiosarcoma-bearing mice. This expression was especially marked in lymph nodes draining virus-injected tumors. Fluorescent in situ hybridization analysis, multicolor fluorescence-activated cell sorting, and quantitative reverse transcription-PCR revealed that MVMp was expressed in rare subpopulations of CD11b (Mac1)-positive cells displaying CD11c+ (myeloid dendritic cells [MDC]) or CD45B (B220+ [B1 lymphocytes]) markers. Apart from the late deletion of cytotoxic memory cells (CD8+ CD44+ CD62L-), this infection did not lead to significant alteration of the immunological profile of cells populating lymphoid organs. However, subtle changes were detected in the production of specific proinflammatory cytokines in lymph nodes from virus-treated animals. Considering the role of B1 lymphocytes and MDC in cancer and immunological surveillance, the specific ability of these cell types to sustain parvovirus-driven gene expression may be exploited in gene therapy protocols.

Animals↗
PubMed1984

Transfection with extracellularly UV-damaged DNA induces human and rat cells to express a mutator phenotype towards parvovirus H-1.

Human and rat cells transfected with UV-irradiated linear double-stranded DNA from calf thymus displayed a mutator activity. This phenotype was identified by growing a lytic thermosensitive single-stranded DNA virus (parvovirus H-1) in those cells and determining viral reversion frequencies. Likewise, exogenous UV-irradiated closed circular DNAs, either double-stranded (simian virus 40) or single-stranded (phi X174), enhanced the ability of recipient cells to mutate parvovirus H-1. The magnitude of mutator activity expression increased along with the number of UV lesions present in the inoculated DNA up to a saturation level. Unirradiated DNA displayed little inducing capacity, irrespective of whether it was single or double stranded. Deprivation of a functional replication origin did not impede UV-irradiated simian virus 40 DNA from providing rat and human cells with a mutator function. Our data suggest that in mammalian cells a trans-acting mutagenic signal might be generated from UV-irradiated DNA without the necessity for damaged DNA to replicate.

Animals↗
PubMed1986

Nonhomologous recombination in the parvovirus chromosome: role for a CTATTTCT motif.

The mechanism of nonhomologous recombination in murine cells infected with the parvovirus minute virus of mice (MVM) has been investigated by analysis of DNA sequences at recombination junctions in naturally occurring deletion variants of the virus. We report here that nonhomologous recombination in the MVM chromosome is characterized by short homologies, by insertion at recombination junctions of foreign DNA sequences that are enriched for preferred eucaryotic topoisomerase I cleavage sites, and by an association with a common DNA sequence motif of the type 5'-CTATTTCT-3'. Additional analyses of broken MVM chromosomes provided evidence for specific enzymatic cleavage within 5'-CTTATC-3' and 5'-CTATTC-3' sequences. The results indicate that the 5'-CTATTTCT-3' motif is an important genetic element for nonhomologous recombination in the parvovirus chromosome.

Animals↗
PubMed1987

Replication of DNA containing apurinic sites in human and mouse cells probed with parvoviruses MVM and H-1.

We studied the effect of apurinic sites on DNA replication in mouse and human cells, using parvoviruses MVM (minute virus of mice) and H-1 as probes. Although apurinic sites are efficient blocks to the replication of these single-stranded DNA viruses in vivo, depurinated parvoviruses can be reactivated if host cells have been preexposed to a subtoxic dose of UV light. The target of this conditional reactivation process is the conversion of depurinated input DNA into double-stranded replicative forms; the concomitant increase in viral mutagenesis strongly suggests that apurinic sites can be bypassed in mammalian cells.

Animals↗
PubMed1987

Parvovirus associated aplastic crisis in homozygous sickle cell disease.

Aplastic crises in homozygous sickle cell disease in Jamaica predominantly affect children and occur in epidemics. Of 67 cases in a cohort study of 314 children with homozygous sickle cell disease, 62 were attributable to human parvovirus infection. Affected children were aged 0.5-12.5 years, and the incidence rose to 28% by 10 years. No recurrences were seen. Symptoms and signs on presentation were attributable to the viraemia and acute anaemia. Asymptomatic thrombocytopenia was common. Blood transfusion was given in 54 cases (87%). Thirty eight children (61%) were admitted to hospital, 16 of whom were extremely ill on presentation and one of whom died soon after admission. Twenty four (39%) were managed as outpatients, 16 of whom were transfused. Parvovirus associated aplastic crisis is a self limited condition with excellent prognosis if diagnosed promptly and managed appropriately.

Anemia, Aplastic↗
PubMed1996

Effect of HLA type and hypocomplementaemia on the expression of parvovirus arthritis: one year follow up of an outbreak.

OBJECTIVES: To determine the effect of HLA type and hypocomplementaemia on the duration and severity of joint involvement in parvovirus infection (HPV). METHODS: Forty seven patients were selected on a geographical basis from 83 with proven HPV infection during an outbreak that occurred in Oxfordshire in 1993. They were contacted by questionnaire a year later. Thirty five patients were available for examination and blood sampling. Subjects were typed for HLA-DRB1 alleles and HLA-B27 status. Immunological profiles, including C3 and C4 complement components, were determined. RESULTS: Joint symptoms occurred in all patients. They resolved within a week in 12 patients and persisted beyond one year in 19. On review, none had a picture of rheumatoid arthritis, but three patients had developed carpal tunnel syndrome. Decreased C4 was found in four. The HLA frequencies were similar to those in controls; however, joint symptoms persisted for more than one week in all HLA-DR4 positive patients (p = 0.009). There was no relation between the severity of joint symptoms and either HLA type, or hypocomplementaemia. CONCLUSIONS: Joint symptoms are common in parvovirus infection and the presence of HLA-DR4 may be associated with persistence of joint symptoms beyond one week. This study revealed no evidence of progression to rheumatoid arthritis.

Adult↗
PubMed1982

Occurrence of infection with a parvovirus-like agent in children with sickle cell anaemia during a two-year period.

The occurrence of infection with a parvovirus-like agent during the period April 1979-May 1981 in children attending a single sickle cell clinic in London was investigated. Virus was detected in serum by counter-current immunoelectrophoresis (CIE) and immunoelectron microscopy (IEM). Viral antibody was detected by CIE and specific IgM antibody by an IgM-antibody capture assay. Of the 68 children studied nine presented in aplastic crisis and evidence of infection with the parvovirus-like agent at the time of the crisis was found in all nine. Eighteen of the other children were antibody-positive at some time during the study. In 11 children there was no evidence of recent infection; however, two of these had a history of aplastic crisis in previous years. The other seven seroconverted during the course of the study but did not show any haematological effects. Five of these had a primary infection, one appeared to have reinfection and in the seventh there were insufficient data to distinguish between the two. Possible explanations for the difference between those presenting with aplastic crisis and those with asymptomatic seroconversion are discussed.

Anemia, Sickle Cell↗
PubMed1986

Parvovirus infection associated with aplastic crisis in a patient with HEMPAS.

An aplastic crisis associated with parvovirus infection occurred in a patient suffering from hereditary erythrocytic multinuclearity associated with a positive acidified (Hams) test (HEMPAS). This case emphasises that any patient who has a shortened red cell survival is susceptible to an aplastic crisis induced by parvovirus.

Adult↗
PubMed1990

Parvovirus infection and anaemia in a patient with AIDS: case report.

Opportunistic infections such as Pneumocystis carinii pneumonia are well-recognised in patients with the acquired immune deficiency syndrome (AIDS). Anaemia due to a variety of causes also occurs in AIDS. Persistent infection with parvovirus (B19) causing severe anaemia has been reported in patients with leukaemia and congenital immunodeficiency. A case is now reported of parvovirus infection and anaemia, in an adult with AIDS, which responded dramatically to immunoglobulin therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Canine parvovirus enteritis 3: Scanning electron microscopical features of experimental infection.

A group of 10-week-old puppies was orally inoculated with canine parvovirus of faecal origin. Scanning electron microscopy was used to study and compare the surface topography in both control and inoculated animals. In control dogs the villi were tall and finger-like in shape and numerous irregular transverse circumferential grooves were present on the surface. At higher magnification, the outlines of individual epithelial cells and depressions, interpreted as goblet cells, could be discerned. In the inoculated dogs, scanning electron microscopy changes were first seen at six days after inoculation. The small intestinal mucosa was covered by a thick layer of mucus. The underlying villi were stunted and had lost their surface features. In some instances there was loss of the luminal epithelium, exposing the lamina propria. In addition, there was dilation of the circumvillar basins and the crypt mouths. There appeared to be regenerative changes by day 7 after inoculation. The surface of the small intestinal mucosa was still covered by a thick layer of mucus. Where villi could be discerned, they were short and pointed and transverse grooves could be seen on their surface. There was some hypertrophy of the intervillus ridges. The changes in the surface topography of the small intestinal mucosa following canine parvovirus infection are compared to those seen in enteric infections in other species and the similarity of the lesion to that seen following sublethal irradiation is discussed.

Animals↗
PubMed1986

Observations on the use of an inactivated canine parvovirus vaccine.

Data are presented on studies of field and experimental use of a formalin-inactivated canine parvovirus vaccine. There was an absolute correlation between a single successful vaccination and subsequent protection against clinical disease. Unsuccessful vaccinations were consistently associated with the presence of maternal antibody at the time of vaccination. The vaccine induced an antibody response within two days and anamnestic responses within 24 hours. It is suggested that a single successful vaccination probably protects against clinical parvovirus disease for life.

Animals↗
PubMed1998

Detection of feline parvovirus in dying pedigree kittens.

Feline parvovirus (FPV) was detected in the intestinal tract contents of 13 pedigree kittens which were fading or died suddenly by the use of a new chromatographic test strip for canine parvovirus (CPV) and FPV. The test appeared to be sensitive and specific for the detection of FPV and was a useful diagnostic aid. In three cases in which virus was grown in cell culture, the isolates were characteristic of FPV and not CPV. Cats in the households in which the kittens were reared were regularly immunised with FPV vaccines. The most likely explanation for the occurrence of FPV-associated disease was exposure of the young kittens to large doses of virus contaminating the environment.

Animals↗
PubMed1990

Human parvovirus infections.

The B19 strain of parvovirus causes several distinct and important clinical diseases in humans. Aplastic crisis in patients with chronic hemolytic anemia, persistent bone marrow depression in immunocompromised individuals, and hydrops fetalis all result from direct infection of hematopoietic cells by the virus. Erythema infectiosum, arthritis, and purpuric vasculitis are postinfectious manifestations of B19 parvovirus infection.

Female↗
PubMed1993

Primary infection by human parvovirus B19.

We describe a case of primary infection by human parvovirus B19 in a 20-year-old woman; it manifested as erythemato-maculo-papular lesions, pharyngotonsillitis, lymphadenopathy, fever, arthralgia and myalgia, asthenia and anorexia. Laboratory tests revealed anaemia, leucopenia, thrombocytopaenia and a rise in some inflammatory indices. Elisa test was positive for anti-human parvovirus B19 IgM. Clinical symptoms spontaneously regressed in 2 weeks. Thirty days after hospital admission all the laboratory tests returned to normal values; furthermore, specific IgM and IgG were detectable.

Adult↗
PubMed1984

Direct demonstration of the human parvovirus in erythroid progenitor cells infected in vitro.

The human parvovirus (HPV), the cause of transient aplastic crisis of hereditary hemolytic anemia, has been shown to be cytotoxic for erythroid progenitor cells and its presence in these cells demonstrated by morphologic techniques. A relatively pure population of progenitors, isolated by removal of immature erythroid bursts from primary culture, was the target of the virus infection. Infected cells failed to proliferate in secondary culture. Using a monoclonal antibody to HPV, specific fluorescence was demonstrated in a minority of cells 24-48 h after infection with virus. Infected cells examined by electron microscopy showed marked toxic ultrastructural alterations and parvovirus-like particles in crystalline arrays in the nucleus.

Antibodies, Monoclonal↗
PubMed1985

Pathogenesis of canine parvovirus enteritis: sequential virus distribution and passive immunization studies.

After oral inoculation, the sequential distribution of canine parvovirus was studied in 14 nine-week-old seronegative beagle dogs. Two or three dogs were necropsied on days 1 through 6 after inoculation. Tissues were collected for virus isolation, immunofluorescence testing, and light microscopy. Virus was isolated from, and fluorescent cells were seen in the tonsil, retropharyngeal and mesenteric lymph nodes one and two days after inoculation. Virus infection of systemic and intestinal lymphoid tissues occurred as early as three days after inoculation and was associated with viremia. Intestinal epithelial infection was first seen four days after oral inoculation. All dogs were viremic before intestinal epithelial infection was found. Fecal virus excretion first occurred four days after oral virus inoculation. Intestinal virus infection and lesions became progressively more severe between four and six days after inoculation. The severity of intestinal lesions was variable and related to the severity of systemic lymphoid tissue lesions and the magnitude and duration of viremia. Four littermates of virus-infected dogs were passively immunized against canine parvovirus with convalescent canine serum 24 hours after oral virus inoculation. Neither clinical signs, lymphopenia, nor fecal virus excretion occurred in passively immunized dogs. Intestinal epithelial infection was not demonstrable by immunofluorescence testing when passively immunized dogs were necropsied four, five, and six days after virus inoculation.

Animals↗