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PubMed2005

Complete nucleotide sequence and genomic organization of hepatopancreatic parvovirus (HPV) of Penaeus monodon.

We have determined the genome of hepatopancreatic parvovirus (HPV), a minus, single-stranded DNA virus isolated from infected Penaeus monodon in Thailand. Its genome consisted of 6321 nucleotides, representing three large open reading frames (ORFs) and two non-coding termini. The left (ORF1), mid (ORF2), and right (ORF3) ORFs on the complementary (plus) strand may code for 428, 579, and 818 amino acids, equivalent to 50, 68, and 92 kDa, respectively. The 5' and 3' ends of viral genome contained hairpin-like structure length of approximately 222 and 215 bp, respectively. No inverted terminal repeat (ITR) was detected. The ORF2 contained conserved replication initiator motif, NTP-binding and helicase domain similar to NS-1 of other parvoviruses. Therefore, it most likely encoded the major nonstructural protein (NS-1). The ORF1 encoded putative nonstructural protein-2 (NS-2) with unknown function. The ORF3 of the HPV genome encoded a capsid protein (VP) of approximately 92 kDa. This may be later cleaved after arginine residue to produce a 57-kDa structural protein. A phylogenetic tree based on conserved amino acid sequences (119 aa) revealed that it is closely related to Brevidensoviruses, which are shrimp parvovirus (IHHNV) and mosquito densoviruses (AaeDNV and AalDNV). However, the overall genomic organization and genome size of HPV were different from these parvoviruses, for instance, the non-overlapping of NS1 and NS2, the larger VP gene, and the bigger genome size. This suggested that this HPV virus is a new type in Parvoviridae family. We therefore propose to rename this virus P. monodon densovirus (PmDNV).

Amino Acid Sequence↗

PubMed1988

Persistent B19 parvovirus infection as a cause of severe chronic anaemia in children with acute lymphocytic leukaemia.

In two children with acute lymphocytic leukaemia in whom severe anaemia developed, serum samples collected over 9-12 months showed high concentrations of B19 parvovirus, the aertiological agent of fifth disease. In one patient, anaemia recurred with the reappearance of virus in serum; in the other, the anaemia persisted. Smears of bone marrow aspirates obtained during periods of viraemia showed giant pronormoblasts and either absent mature erythroid cells or erythroid hypoplasia. Parvovirus replication in the marrow was detected by Southern blot of cellular DNA. An underlying immune deficit was suggested by low titres of specific antibodies against B19 parvovirus. Treatment of one patient with plasma containing specific antibodies against parvovirus resulted in a transient fall in serum virus levels, the appearance of reticulocytes, and symptoms of fifth disease.

Anemia, Hemolytic↗

PubMed1996

[Severe parvovirus B19 infection in an immunocompetent child with hemophilia A].

BACKGROUND: B19 parvovirus is a widespread virus whose typical manifestations in immunocompetent children are erythema infectiosum, acute erythroblastopenia and fetal anemia. CASE REPORT: An 11 year-old immunocompetent patient with hemophilia A was referred for an hemorrhagic syndrome. Forty days after a pasteurized coagulation factor concentrates treatment, and after 12 days of treatment with solvent/detergent factor VIII concentrates, he developed fever, consciousness disorders, pancytopenia, liver cytolysis and probably minor haemophagocytic syndrome, associated with human parvovirus B19 infection. His clinical state returned to normal within 15 days. A retrospective study revealed that the patient had received every day for 12 days, one parvovirus B19 polymerase chain reaction positive batch before the occurrence of symptoms. CONCLUSION: This case highlights the possibility of severe parvovirus B19 infection transmitted by clotting factors prepared from large pools of plasma. The use of recombinant factors would allow to reduce human virus contamination, even if immune risk has to be more accurately assessed.

Anticoagulants↗

PubMed1987

Human parvovirus infection in pregnancy and hydrops fetalis.

Human parvovirus is the causative agent of erythema infectiosum, a mild epidemic illness. In a recent outbreak in northeast Scotland, six women had serologic evidence of having contracted human parvovirus infection during pregnancy. Two of the women had midtrimester abortions, and both abortuses were grossly hydropic with anemia. They had similar microscopical histopathological features--a pronounced leukoerythroblastic reaction, hepatitis, excessive iron pigment in the liver, and eosinophilic changes in the hematopoietic cell nuclei. Dot hybridization with radiolabeled human parvovirus DNA probes revealed viral DNA in several tissues from both fetuses, indicating that they had been infected by the virus in utero. The remaining four women had uncomplicated pregnancies and delivered apparently healthy babies, none of whom had human parvovirus-specific IgM antibody at delivery. We conclude that this common virus may pose a serious risk to the fetus after maternal infection.

Abortion, Septic↗

PubMed1989

Human parvovirus B19 infection among hospital staff members after contact with infected patients.

In the spring and summer of 1988, two separate outbreaks of an illness with a rash resembling erythema infectiosum occurred among members of the nursing staff of the Children's Hospital of Philadelphia. The sources were two adolescent patients with sickle cell disease and aplastic crisis who had unsuspected parvovirus infection. Tests for IgM and IgG antibodies to parvovirus B19 were positive in both patients, and electron microscopical examination showed parvovirus-like particles in the early serum samples. Of 40 health care workers exposed to infected patients, 12 (30 percent) were infected, 2 (5 percent) were possibly infected, 8 (20 percent) had evidence of a past infection with B19, and 18 (45 percent) remained seronegative. Attack rates among the susceptible contacts were 36 percent in the first outbreak and at least 38 percent in the second. Clinical symptoms began a mean of 12.6 days after exposure and included malaise, rash, and joint pain. We conclude that hospital workers are at risk of contracting nosocomial erythema infectiosum from patients with parvovirus-associated aplastic crisis. We recommend that all patients with hereditary hemolytic anemias who are admitted with a febrile illness be evaluated for aplasia and promptly placed in respiratory and contact isolation if aplastic crisis is suspected.

Adolescent↗

PubMed1988

Parvovirus infections. From benign to life-threatening.

Erythema infectiosum, aplastic crisis, intrauterine fetal demise, and an acute polyarthralgia syndrome can all be caused by human parvovirus B19. The major pathophysiologic effect of infection seems to be cessation of erythropoiesis as a result of cytolytic infection of red cell precursors. Erythema infectiosum is a benign disease that usually occurs in childhood. The acute polyarthralgia syndrome is likewise benign, and patients in whom parvovirus infection has been confirmed by serologic testing can be reassured that their joint symptoms are likely to be self-limited. Parvovirus-induced aplastic crisis in a patient with chronic hemolytic anemia is life-threatening but can be reversed with blood transfusions if recognized promptly. Parvovirus infection during pregnancy clearly increases the risk of fetal demise, and parental anxiety is understandably high. An organized approach using a combination of tests to monitor mother and fetus can provide optimal care in these cases.

Adolescent↗

PubMed1982

A longitudinal serological survey of parvovirus infection in dogs.

Serum samples collected from dogs routinely presented at a clinic between June 1974 and October 1980 were tested for the presence of haemagglutination inhibition (HI) titres to canine parvovirus. The first positive titre (>1:320) was demonstrated in serum collected in October 1979. The first confirmed clinical case of canine parvovirus enteritis was diagnosed by the authors in July 1979. In addition, between 1st December 1980 and 1st March 1981, serum samples were collected from 106 healthy dogs which were presented for canine parvovirus vaccination for the first time. Twenty-four dogs (approx. 23%) showed HI titres >1:320 indicating probable previous canine parvovirus infection. Therefore approx. 80% of dogs in the clinic area were at risk at that time and vaccination should have protected them from infection.

Journal Article↗

PubMed1997

Chronic parvovirus B19 infection resulting in chronic fatigue syndrome: case history and review.

The spectrum of disease caused by parvovirus B19 has been expanding in recent years because of improved and more sensitive methods of detection. There is evidence to suggest that chronic infection occurs in patients who are not detectably immunosuppressed. We report the case of a young woman with recurrent fever and a syndrome indistinguishable from chronic fatigue syndrome. After extensive investigation, we found persistent parvovirus B19 viremia, which was detectable by polymerase chain reaction (PCR) despite the presence of IgM and IgG antibodies to parvovirus B19. Testing of samples from this patient suggested that in some low viremic states parvovirus B19 DNA is detectable by nested PCR in plasma but not in serum. The patient's fever resolved with the administration of intravenous immunoglobulin.

Adolescent↗

PubMed1985

The genome structure of a new chicken virus identifies it as a parvovirus.

The nucleic acid of chicken parvovirus-like particles showed sensitivity to DNase and S1 nuclease treatment and resistance to digestion with RNase. Viral DNA readily served as a template for self-primed conversion in vitro into a double-stranded form of about 5200 base pairs. There was no evidence for encapsidation of strands of opposite polarities. These findings confirm the taxonomic classification of chicken parvovirus-like particles as fowl parvovirus type 1 within the Parvovirus genus of the Parvoviridae.

Animals↗

PubMed1986

Antigenic relationships among autonomous parvoviruses.

The antigenic relatedness of minute virus of mice (MVM), Kilham rat virus (KR), H-1 virus (H-1), haemorrhagic encephalopathy of rats virus (HER), porcine parvovirus (PPV), canine parvovirus (CPV), feline panleukopenia virus (FPV), goose parvovirus (GPV) and bovine parvovirus (BPV) was studied by immunofluorescence microscopy (FA) and by serum neutralization (SN). An antigenically related group comprising MVM, KR, HER, PPV, CPV and FPV was recognized by FA and most reactions within the group were reciprocal. Antigenic relatedness was less evident when the same viruses and antisera were tested by SN. Only CPV and FPV were closely and reciprocally related. Other cross-reactions by SN were quantitatively minor and included neutralization of CPV and FPV by pig anti-PPV serum and neutralization of H-1 and HER by rat anti-KR serum. Neither FA nor SN revealed any antigenic relationship of BPV and GPV either with each other or with any of the other viruses tested.

Animals↗

PubMed1989

The possible enhancement of parvovirus vaccination on the mortality rate of diseased dogs.

A survey was conducted by using questionnaires dealing with morbidity and mortality of young dogs. Seventy-one clinical evaluations of diseased dogs were included in this survey. The cases were divided into 3 groups according to their vaccination history: 1. dogs vaccinated with the parvovirus and distemper live modified vaccine; 2. dogs vaccinated with the killed parvovirus vaccine; 3. non-vaccinated dogs. Statistical analysis of the information obtained by analyzing the questionnaires gave the following results: The survival rate of the non-vaccinated and killed parvovirus vaccine-vaccinated dogs was significantly higher than that of the dogs which were vaccinated by the live modified vaccine. No such difference was encountered between groups 2 and 3. This finding, once more, supports the notion that the live modified parvovirus vaccine may have an immunosuppressive property.

Animals↗

PubMed1984

Characterization and molecular cloning of a human parvovirus genome.

The genome of the small human virus serologically associated with erythrocyte aplasia and erythema infectiosum (fifth disease) is shown to be a linear, nonpermuted, single-stranded DNA molecule with self-priming hairpin termini, properties which are characteristic of the genomes of the family Parvoviridae. This human parvovirus chromosome was molecularly cloned into bacterial plasmid vectors and the cloned DNA was used to explore its relatedness to other mammalian parvovirus serotypes by DNA:DNA hybridization. It is not related to the human adeno-associated viruses but does show a distant evolutionary relationship to genomes of the helper-independent parvoviruses of rodents. This strongly suggests that it is an autonomous parvovirus, and as such is the first example of a member of this group of common animal pathogens to cause disease in man.

Base Sequence↗

PubMed2002

Serodiagnosis of mice minute virus and mouse parvovirus infections in mice by enzyme-linked immunosorbent assay with baculovirus-expressed recombinant VP2 proteins.

Mice minute virus (MMV) and mouse parvovirus (MPV) type 1 are the two parvoviruses known to naturally infect laboratory mice and are among the most prevalent infectious agents found in contemporary laboratory mouse colonies. Serologic assays are commonly used to diagnose MMV and MPV infections in laboratory mice; however, highly accurate, high-throughput serologic assays for the detection of MMV- and MPV-infected mice are needed. To this end, the major capsid viral protein (VP2) genes of MMV and MPV were cloned and MMV recombinant VP2 (rVP2) and MPV rVP2 proteins were expressed by using a baculovirus system. MMV rVP2 and MPV rVP2 spontaneously formed virus-like particles that were morphologically similar to empty parvovirus capsids. These proteins were used as antigens in enzyme-linked immunosorbent assays (ELISAs) to detect anti-MMV or anti-MPV antibodies in the sera of infected mice. Sera from mice experimentally infected with MMV (n = 43) or MPV (n = 35) and sera from uninfected mice (n = 30) were used to evaluate the ELISAs. The MMV ELISA was 100% sensitive and 100% specific in detecting MMV-infected mice, and the MPV ELISA was 100% sensitive and 98.6% specific in detecting MPV-infected mice. Both assays outperformed a parvovirus ELISA that uses a recombinant nonstructural protein (NS1) of MMV as antigen. The MMV rVP2 and MPV rVP2 proteins provide a ready source of easily produced antigen, and the ELISAs developed provide highly accurate, high-throughput assays for the serodiagnosis of MMV and MPV infections in laboratory mice.

Animals↗

PubMed1988

Nucleotide sequence and genome organization of canine parvovirus.

The genome of a canine parvovirus isolate strain (CPV-N) was cloned, and the DNA sequence was determined. The entire genome, including ends, was 5,323 nucleotides in length. The terminal repeat at the 3' end of the genome shared similar structural characteristics but limited homology with the rodent parvoviruses. The 5' terminal repeat was not detected in any of the clones. Instead, a region of DNA starting near the capsid gene stop codon and extending 248 base pairs into the coding region had been duplicated and inserted 75 base pairs downstream from the poly(A) addition site. Consensus sequences for the 5' donor and 3' acceptor sites as well as promotors and poly(A) addition sites were identified and compared with the available information on related parvoviruses. The genomic organization of CPV-N is similar to that of feline parvovirus (FPV) in that there are two major open reading frames (668 and 722 amino acids) in the plus strand (mRNA polarity). Both coding domains are in the same frame, and no significant open reading frames were apparent in any of the other frames of both minus and plus DNA strands. The nucleotide and amino acid homologies of the capsid genes between CPV-N and FPV were 98 and 99%, respectively. In contrast, the nucleotide and amino acid homologies of the capsid genes for CPV-N and CPV-b (S. Rhode III, J. Virol. 54:630-633, 1985) were 95 and 98%, respectively. These results indicate that very few nucleotide or amino acid changes differentiate the antigenic and host range specificity of FPV and CPV.

Amino Acid Sequence↗

PubMed1988

Transformation of human fibroblasts by ionizing radiation, a chemical carcinogen, or simian virus 40 correlates with an increase in susceptibility to the autonomous parvoviruses H-1 virus and minute virus of mice.

Morphologically altered and established human fibroblasts, obtained either by 60Co gamma irradiation, treatment with the carcinogen 4-nitroquinoline 1-oxide, or simian virus 40 (SV40) infection, were compared with their normal finite-life parental strains for susceptibility to the autonomous parvoviruses H-1 virus and the prototype strain of minute virus of mice (MVMp). All transformed cells suffered greater virus-induced killing than their untransformed progenitors. The cytotoxic effect of H-1 virus was more severe than that of MVMp. Moreover, the level of viral DNA replication was much (10- to 85-fold) enhanced in the transformants compared with their untransformed parent cells. Thus, in this system, cell transformation appears to correlate with an increase in both DNA amplification and cytotoxicity of the parvoviruses. However, the accumulation of parvovirus DNA in the transformants was not always accompanied by the production of infectious virus. Like in vitro-transformed fibroblasts, a fibrosarcoma-derived cell line was sensitive to the killing effect of both H-1 virus and MVMp and amplified viral DNA to high extents. The results indicate that oncogenic transformation can be included among cellular states which modulate permissiveness to parvoviruses under defined growth conditions.

4-Nitroquinoline-1-oxide↗

PubMed1991

Assembly of empty capsids by using baculovirus recombinants expressing human parvovirus B19 structural proteins.

Empty parvovirus B19 capsids were isolated from insect cells infected with a recombinant baculovirus expressing parvovirus B19 VP2 alone and also with a double-recombinant baculovirus expressing both VP1 and VP2. That VP2 alone can assemble to form capsids is a phenomenon not previously observed in parvoviruses. The stoichiometry of the capsids containing both VP1 and VP2 was similar to that previously observed in parvovirus B19-infected cells. The capsids were similar to native capsids in size and appearance, and their antigenicity was demonstrated by immunoprecipitation and enzyme-linked immunosorbent assay with B19-specific antibodies.

Animals↗

PubMed1999

Three-dimensional structure of Aleutian mink disease parvovirus: implications for disease pathogenicity.

The three-dimensional structure of expressed VP2 capsids of Aleutian mink disease parvovirus strain G (ADVG-VP2) has been determined to 22 A resolution by cryo-electron microscopy and image reconstruction techniques. A structure-based sequence alignment of the VP2 capsid protein of canine parvovirus (CPV) provided a means to construct an atomic model of the ADVG-VP2 capsid. The ADVG-VP2 reconstruction reveals a capsid structure with a mean external radius of 128 A and several surface features similar to those found in human parvovirus B19 (B19), CPV, feline panleukopenia virus (FPV), and minute virus of mice (MVM). Dimple-like depressions occur at the icosahedral twofold axes, canyon-like regions encircle the fivefold axes, and spike-like protrusions decorate the threefold axes. These spikes are not present in B19, and they are more prominent in ADV compared to the other parvoviruses owing to the presence of loop insertions which create mounds near the threefold axes. Cylindrical channels along the fivefold axes of CPV, FPV, and MVM, which are surrounded by five symmetry-related beta-ribbons, are closed in ADVG-VP2 and B19. Immunoreactive peptides made from segments of the ADVG-VP2 capsid protein map to residues in the mound structures. In vitro tissue tropism and in vivo pathogenic properties of ADV map to residues at the threefold axes and to the wall of the dimples.

Aleutian Mink Disease↗

PubMed2001

Genome replication and postencapsidation functions mapping to the nonstructural gene restrict the host range of a murine parvovirus in human cells.

The infection outcome of the Parvoviridae largely relies on poorly characterized intracellular factors modulated by proliferation, differentiation, and transformation of host cells. We have studied the interactions displayed by the highly homologous p and i strains of the murine parvovirus minute virus of mice (MVM), with a series of transformed cells of rat (C6) and human (U373, U87, SW1088, SK-N-SH) nervous system origin, seeking for molecular mechanisms governing parvovirus host range. The MVMp infection of C6 and U373 cells was cytotoxic and productive, whereas the other nervous cells behaved essentially as resistant to this virus. In contrast, MVMi did not complete its life cycle in any of the human nervous cells, though it efficiently killed the astrocytic tumor cells by two types of nonproductive infections: (i) normal synthesis of all viral macromolecules with a late defect in infectious virion maturation and release to the medium in U373; and (ii) high levels of accumulation of the full set of viral messenger RNAs and of both nonstructural (NS-1) and structural (VP-1 and VP-2) proteins, under a very low viral DNA amplification, in U87 and SW1088 cells. Further analyses showed that U87 was permissive for nuclear transport of MVMi proteins, leading to efficient assembly of empty viral capsids with a normal phosphorylation and VP1-to-VP2 ratio. The DNA amplification blockade in U87 occurred after conversion of the incoming MVMi genome to the monomeric replicative form, and it operated independently of the delivery pathway used by the viral particle, since it could not be overcome by transfection with cloned infectious viral DNA. Significantly, a chimeric MVMi virus harboring the coding region of the nonstructural (NS) gene replaced with that of MVMp showed a similar pattern of restriction in U87 cells as the parental MVMi virus, and it attained in U373 cultures an infectious titer above 100-fold higher under equal levels of DNA amplification and genome encapsidation. The results suggest that the activity of complexes formed by the NS polypeptides and recruited cellular factors restrict parvovirus DNA amplification in a cell type-dependent manner and that NS functions may in addition determine MVM host range acting at postencapsidation steps of viral maturation. These data are relevant for understanding the increased multiplication of autonomous parvovirus in some transformed cells and the transduction efficacy of nonreplicative parvoviral vectors, as well as a general remark on the mechanisms by which NS genes may regulate viral tropism and pathogenesis.

Animals↗