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Journal articles on the topic 'Human Parvovirus B19'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Qiu, Jianming, Maria Söderlund-Venermo, and Neal S. Young. "Human Parvoviruses." Clinical Microbiology Reviews 30, no. 1 (November 2, 2016): 43–113. http://dx.doi.org/10.1128/cmr.00040-16.

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SUMMARY Parvovirus B19 (B19V) and human bocavirus 1 (HBoV1), members of the large Parvoviridae family, are human pathogens responsible for a variety of diseases. For B19V in particular, host features determine disease manifestations. These viruses are prevalent worldwide and are culturable in vitro, and serological and molecular assays are available but require careful interpretation of results. Additional human parvoviruses, including HBoV2 to -4, human parvovirus 4 (PARV4), and human bufavirus (BuV) are also reviewed. The full spectrum of parvovirus disease in humans has yet to be established. Candidate recombinant B19V vaccines have been developed but may not be commercially feasible. We review relevant features of the molecular and cellular biology of these viruses, and the human immune response that they elicit, which have allowed a deep understanding of pathophysiology.

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2

Ussery, Xilla T., and Gail J. Demmler. "Human parvovirus B19." Seminars in Pediatric Infectious Diseases 7, no. 2 (April 1996): 89–96. http://dx.doi.org/10.1016/s1045-1870(96)81003-x.

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3

Pattison, J. R. "Human parvovirus B19." BMJ 308, no. 6922 (January 15, 1994): 149–50. http://dx.doi.org/10.1136/bmj.308.6922.149.

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4

Igoe, D., B. Gilmer, H. Johnson, and H. J. O'Neill. "Human parvovirus B19." BMJ 308, no. 6933 (April 2, 1994): 918–19. http://dx.doi.org/10.1136/bmj.308.6933.918a.

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5

Heegaard, Erik D., and Kevin E. Brown. "Human Parvovirus B19." Clinical Microbiology Reviews 15, no. 3 (July 2002): 485–505. http://dx.doi.org/10.1128/cmr.15.3.485-505.2002.

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SUMMARY Parvovirus B19 (B19) was discovered in 1974 and is the only member of the family Parvoviridae known to be pathogenic in humans. Despite the inability to propagate the virus in cell cultures, much has been learned about the pathophysiology of this virus, including the identification of the cellular receptor (P antigen), and the control of the virus by the immune system. B19 is widespread, and manifestations of infection vary with the immunologic and hematologic status of the host. In healthy immunocompetent individuals B19 is the cause of erythema infectiosum and, particularly in adults, acute symmetric polyarthropathy. Due to the tropism of B19 to erythroid progenitor cells, infection in individuals with an underlying hemolytic disorder causes transient aplastic crisis. In the immunocompromised host persistent B19 infection is manifested as pure red cell aplasia and chronic anemia. Likewise, the immature immune response of the fetus may render it susceptible to infection, leading to fetal death in utero, hydrops fetalis, or development of congenital anemia. B19 has also been suggested as the causative agent in a variety of clinical syndromes, but given the common nature, causality is often difficult to infer. Diagnosis is primarily based on detection of specific antibodies by enzyme-linked immunosorbent assay or detection of viral DNA by dot blot hybridization or PCR. Treatment of persistent infection with immunoglobulin reduces the viral load and results in a marked resolution of anemia. Vaccine phase I trials show promising results.

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6

Anderson, Larry J., and Thomas J. Török. "Human Parvovirus B19." New England Journal of Medicine 321, no. 8 (August 24, 1989): 536–38. http://dx.doi.org/10.1056/nejm198908243210809.

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7

Anderson, Larry J. "Human Parvovirus B19." Pediatric Annals 19, no. 9 (September 1, 1990): 509–13. http://dx.doi.org/10.3928/0090-4481-19900901-06.

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8

Milosevic, Vesna, Vera Jerant-Patic, Ivana Hrnjakovic-Cvjetkovic, Marija Vukmanovic-Papuga, Jelena Radovanov-Tadic, and Gordana Kovacevic. "The frequency of human parvovirus B19 infections in Vojvodina." Medical review 60, no. 11-12 (2007): 575–79. http://dx.doi.org/10.2298/mpns0712575m.

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Introduction. Human parvovirus B19 is found worldwide. It causes various infections, including fifth disease (erythema infectiosum) in small children, acute arthropathy in adults, transient aplastic crisis and chronic anemia in immmunocompromised patients and even fetal infection, which may result in intrauterine fetal death or fetal hydrops. Many of these manifestations of B19 infection are caused by infection of erythroid precursor cells in bone marrow. Material and Methods. The aim of this paper was to establish the frequency of parvovirus B19 infection in the population of Vojvodina, as well as to indicate the significance of further investigations particularly in highly vulnerable population groups such as small children, pregnant women and immune deficient persons. A total of 244 serum samples of out- and in-patients of different age were analyzed using SERION ELISA classic parvovirus B19 IgG/IgM quantitative and qualitative tests for identification of specific antibodies against human parvovirus B19. Results. Acute infection was found in 35% of examinees, whereas parvoviurs B19 was identified in 32% of examined persons. Our tests results proved that 20% of examined pregnant women in our surroundings have acute HPB19 infection. At the same time, 45% of pregnant women have no specific antibodies, so they are at risk of infection during pregnancy. Acute infection was diagnosed in 41 children (43%): 22 samples (23%) were positive only to IgG antibodies and in 32 samples (34%) neither IgM nor IgG antibodies were identified. Acute infection was more frequently found in preschool children, i.e. in children aged 4 to 6 years (29%). Conclusion. In the absence of complete data on the frequency of particular diseases caused by this virus in our population, tests for human parvovirus B19 are strongly recommended.

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9

Weigel-Kelley, Kirsten A., Mervin C. Yoder, and Arun Srivastava. "α5β1 integrin as a cellular coreceptor for human parvovirus B19: requirement of functional activation of β1 integrin for viral entry." Blood 102, no. 12 (December 1, 2003): 3927–33. http://dx.doi.org/10.1182/blood-2003-05-1522.

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Abstract Replication of the pathogenic human parvovirus B19 is restricted to erythroid progenitor cells. Although blood group P antigen has been reported to be the cell surface receptor for parvovirus B19, a number of nonerythroid cells, which express P antigen, are not permissive for parvovirus B19 infection. We have documented that P antigen is necessary for parvovirus B19 binding but not sufficient for virus entry into cells. To test whether parvovirus B19 utilizes a cell surface coreceptor for entry, we used human erythroleukemia cells (K562), which allow parvovirus B19 binding but not entry. We report here that upon treatment with phorbol esters, K562 cells become adherent and permissive for parvovirus B19 entry, which is mediated by α5β1 integrins, but only in their high-affinity conformation. Mature human red blood cells (RBCs), which express high levels of P antigen, but not α5β1 integrins, bind parvovirus B19 but do not allow viral entry. In contrast, primary human erythroid progenitor cells express high levels of both P antigen and α5β1 integrins and allow β1 integrin–mediated entry of parvovirus B19. Thus, in a natural course of infection, RBCs are likely exploited for a highly efficient systemic dissemination of parvovirus B19.

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10

Carlsen, Karen Marie. "Human Parvovirus B19 Erythrovirus ." APMIS 114, s120 (August 2006): 1–121. http://dx.doi.org/10.1111/j.1600-0463.2006.apm_v114_s120.x.

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11

Carper, Elizabeth, and Gary J. Kurtzman. "Human parvovirus B19 infection." Current Opinion in Hematology 3, no. 2 (1996): 111–17. http://dx.doi.org/10.1097/00062752-199603020-00002.

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12

Watanabe, T., M. Satoh, and Y. Oda. "Human parvovirus B19 encephalopathy." Archives of Disease in Childhood 70, no. 1 (January 1, 1994): 71. http://dx.doi.org/10.1136/adc.70.1.71-a.

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13

Parsyan, Armen, Camille Szmaragd, Jean-Pierre Allain, and Daniel Candotti. "Identification and genetic diversity of two human parvovirus B19 genotype 3 subtypes." Journal of General Virology 88, no. 2 (February 1, 2007): 428–31. http://dx.doi.org/10.1099/vir.0.82496-0.

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Three genotypes (1–3) of human parvovirus B19 have been identified. Analysis of 13 nearly full-length genotype 3 sequences from Ghana, Europe and Brazil identified two genetically distinct clusters. The classification of genotype 3 strains into two subtypes (B19/3a and B19/3b) is proposed. The rate of evolutionary change of B19 genotype 3 strains (2×10−4 nucleotide substitutions per site per year) was similar to those of B19 genotype 1 and carnivore parvoviruses, supporting the hypothesis that high mutation rates are characteristic of members of the family Parvoviridae. The estimated divergence time between B19/3a and B19/3b is 525 years. In Ghana, subtype B19/3a is predominant.

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14

Vilmane, Anda, Anna Terentjeva, Paulius L. Tamosiunas, Normunds Suna, Inga Suna, Rasa Petraityte-Burneikiene, Modra Murovska, Santa Rasa-Dzelzkaleja, and Zaiga Nora-Krukle. "Human Parvoviruses May Affect the Development and Clinical Course of Meningitis and Meningoencephalitis." Brain Sciences 10, no. 6 (June 3, 2020): 339. http://dx.doi.org/10.3390/brainsci10060339.

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Meningitis and meningoencephalitis are neurological inflammatory diseases, and although routine diagnostics include testing of a wide range of pathogens, still in many cases, no causative agent is detected. Human parvovirus B19 (B19V), human bocaviruses 1–4 (HBoV1–4), and human parvovirus 4 (hPARV4) are members of the Parvoviridae family and are associated with a wide range of clinical manifestations including neurological disorders. The main aim of this study was to determine whether human parvoviruses infection markers are present among patients with meningitis/meningoencephalitis in Latvia as well as to clarify the role of these viruses on the clinical course of the mentioned diseases. Our study revealed HBoV1–4 and B19V genomic sequences in 52.38% and 16.67% of patients, respectively. Furthermore, symptoms such as the presence of a headache and its severity, fatigue, disorientation, and difficulties to concentrate were significantly frequently present in patients with active parvovirus infection in comparison with parvoviruses negative patients, therefore we suggest that HBoV1–4 and B19V infection should be included in the diagnostics to reduce the number of meningitis/meningoencephalitis with unknown/unexplained etiology.

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15

Mihály, Ilona, András Trethon, Zsuzsanna Arányi, Adrienne Lukács, Tímea Kolozsi, Gyula Prinz, Anikó Marosi, et al. "Observations on human parvovirus B19 infection diagnosed in 2011." Orvosi Hetilap 153, no. 49 (December 2012): 1948–57. http://dx.doi.org/10.1556/oh.2012.29447.

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Introduction: The incidence of human parvovirus B19 infection is unknown. Aim: A retrospective analysis of clinical and laboratory findings was carried out in patients diagnosed with human parvovirus B19 infection in 2011 in a virologic laboratory of a single centre in Hungary. Methods: Clinical and laboratory data of patients with proven human parvovirus B19 infection were analysed using in- and out-patient files. Results: In 2011, 72 patients proved to have human parvovirus B19 infection with the use of enzyme immunoassay. The clinical diagnoses of these patients were as follows: human parvovirus B19 infection (30.6%), transient aplastic crisis (16.7%), arthritis (8.3%) and acute hepatitis (4.1%). Symptoms of each of the four phases of the infection occurred in various combinations with the exception of the monophase of cheek exanthema. This occurred without the presence of other symptoms in some cases. Leading symptoms and signs were exanthema (in 74.6% of cases), haematological disorders (in 69% of cases), fever (in 54.9% of cases) and arthritis (in 33.8% of cases). Several atypical dermatological symptoms were also observed. Acute arthritis without exanthema was noted in 8 patients. Of the 72 patients with proven human parvovirus B19 infection there were 7 pregnant women, and one of them had hydrops foetalis resulting spontaneous abortion. In 16 patients (22.5%) human parvovirus B19 IgG was undetectable despite an optimal time for testing. Conclusion: The observations of this study may contribute to a better recognition of clinical symptoms of human parvovirus B19 infection. Orv. Hetil., 2012, 153, 1948–1957.

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16

Söderlund-Venermo, Maria. "Emerging Human Parvoviruses: The Rocky Road to Fame." Annual Review of Virology 6, no. 1 (September 29, 2019): 71–91. http://dx.doi.org/10.1146/annurev-virology-092818-015803.

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Parvoviruses are structurally simple viruses with linear single-stranded DNA genomes and nonenveloped icosahedral capsids. They infect a wide range of animals from insects to humans. Parvovirus B19 is a long-known human pathogen, whereas adeno-associated viruses are nonpathogenic. Since 2005, many parvoviruses have been discovered in human-derived samples: bocaviruses 1–4, parvovirus 4, bufavirus, tusavirus, and cutavirus. Some human parvoviruses have already been shown to cause disease during acute infection, some are associated with chronic diseases, and others still remain to be proven clinically relevant—or harmless commensals, a distinction not as apparent as it might seem. One initially human-labeled parvovirus might not even be a human virus, whereas another was originally overlooked due to inadequate diagnostics. The intention of this review is to follow the rocky road of emerging human parvoviruses from discovery of a DNA sequence to current and future clinical status, highlighting the perils along the way.

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17

Abiodun, Iyanda, Oluyinka Oladele Opaleye, Olusola Ojurongbe, and Ademola Hezekiah Fagbami. "Seroprevalence of parvovirus B19 IgG and IgM antibodies among pregnant women in Oyo State, Nigeria." Journal of Infection in Developing Countries 7, no. 12 (December 15, 2013): 946–50. http://dx.doi.org/10.3855/jidc.3157.

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Introduction: Human parvovirus B19 causes a wide range of complications in pregnant women including abortion, severe fetal anemia, non-immune hydrops fetalis, and even intrauterine fetal death. However, there is a dearth of information on the prevalence of the virus among pregnant women in southwestern Nigeria. Methodology: Blood samples were collected from 231 pregnant women and screened for antibodies to human parvovirus B19 IgM and IgG using an enzyme immunosorbent assay kits. Results: Of the 231 women, 31 were in their first trimester, 146 were in their second trimester, and 54 were in their third trimester. Forty-five (20%) were positive for parvovirus B19 IgG antibodies, 10 (4%) were positive for parvovirus B19 IgM antibodies, and 176 (76%) had no detectable parvovirus B19 antibodies. Twenty-eight (19%) of the 146 pregnant women in their second trimester were positive for parvovirus B19 IgG antibody while three (2%) of the 146 were positive for parvovirus B19 IgM antibody. Conclusions: It is evident that there is a high prevalence of human parvovirus B19 among pregnant women in south-western Nigeria. This suggests that there is an active transmission of the virus in the community; it is therefore necessary to conduct more studies on the virus in pregnant women in Nigeria to ascertain its effect on the fetus.

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18

M. Matta, Amal, Elsayed M. Abd-Elghany, Abeer A. Aboelazm, Osama Abo. Zaki,, and Doaa Abd. Shaker. "Detection of Human Parvovirus B19 Infection in Children with Chronic Haemolytic Anaemia in Benha University Hospitals." EJMM-Volume 30-Issue 2 30, no. 2 (April 1, 2021): 51–58. http://dx.doi.org/10.51429/ejmm30208.

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Background: Due to the tropism of human parvovirus B19 to erythroid progenitor cells, infection in patients with an underlying hemolytic disorder such as thalassemia, hereditary spherocytosis, sickle cell disease and Glucose-6-phosphate dehydrogenase deficiency leads to suppression of erythrocyte formation, referred to as transient aplasia crisis (TAC), which may be life-threatening. Objectives: Detection of parvovirus B19 DNA and its IgG antibodies in the serum of children with chronic hemolytic anemia and in apparently healthy children in Benha University Hospitals. Methodology: The study was conducted on 80 children. Forty of them with chronic hemolytic anemia, they were subdivided into 2 groups, Group (1a) included 20 patients without history of aplastic crisis, Group (Ib) included 20 patients with a history of aplastic crisis and 40 age and sex-matched apparently healthy children representing control (Group II). All patients were subjected to full history taking, clinical examination and laboratory investigations. Parvovirus B19 IgG was measured using anti-parvovirus B19 ELISA kits (SUNRED), and parvovirus B19 DNA was detected by using nestedpolymerase chain reaction. Results: The seroprevalence of parvovirus B19 IgG was significantly higher (P value =0.016) in Group Ia (50%) (10 out of 20) and Group Ib (45%) (9 out of 20) than the control group (Group II) (17.5%) (7 out of 40). There was a significant positive correlation between anti-parvovirus B19 IgG and age of all patients, frequency of blood transfusion. The prevalence of parvovirus B19 DNA was 10% (2 out of 20) in group Ia and 30% (6 out of 20) in group Ib and no viral DNA was detected in the controls (P value=0.001). Although 42.3% (11 out of 26) of children with β thalassemia major had a detectable level of antiparvovirus B19 virus IgG antibodies, only (23.1%) (6 out of 26) of them had B19 DNA. Anti-parvovirus B19 IgG antibodies were detected in 4 children out of 5 children of sickle cell anemia (80%) but the the prevalence of Parvovirus B19 DNA was 20% among them. Conclusion: Measures to keep away from iatrogenic and nosocomial infection transmission should be implemented including screening of donated blood for parvovirus B19 especially blood given to patients with blood disorders. Recommendation: Data from this study support the need for introduction of an approved vaccine that mainly protects children with chronic hemolytic anemia against that infection.

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19

Bock, Claus-Thomas, Karin Klingel, and Reinhard Kandolf. "Human Parvovirus B19–Associated Myocarditis." New England Journal of Medicine 362, no. 13 (April 2010): 1248–49. http://dx.doi.org/10.1056/nejmc0911362.

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20

Anderson, Larry J., and Eugene S. Hurwitz. "Human Parvovirus B19 and Pregnancy." Clinics in Perinatology 15, no. 2 (June 1988): 273–86. http://dx.doi.org/10.1016/s0095-5108(18)30712-7.

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21

Yoto, Yuko, Tooru Kudoh, Keiji Haseyama, and Hiroyuki Tsutsumi. "Human parvovirus B19 and meningoencephalitis." Lancet 358, no. 9299 (December 2001): 2168. http://dx.doi.org/10.1016/s0140-6736(01)07199-9.

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22

Brown, MD, K. E., and N. S. Young, MD. "PARVOVIRUS B19 IN HUMAN DISEASE." Annual Review of Medicine 48, no. 1 (February 1997): 59–67. http://dx.doi.org/10.1146/annurev.med.48.1.59.

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23

Weigel-Kelley, Kirsten A., and Arun Srivastava. "Recombinant human parvovirus B19 vectors." Pathologie Biologie 50, no. 5 (June 2002): 295–306. http://dx.doi.org/10.1016/s0369-8114(02)00310-3.

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24

Finch, Catherine M. "Human Parvovirus B19 in Pregnancy." Journal of Obstetric, Gynecologic & Neonatal Nursing 24, no. 6 (July 1995): 495–98. http://dx.doi.org/10.1111/j.1552-6909.1995.tb02386.x.

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25

ROGO, L. D., T. MOKHTARI-AZAD, M. H. KABIR, and F. REZAEI. "Human parvovirus B19: A review." Acta virologica 58, no. 03 (2014): 199–213. http://dx.doi.org/10.4149/av_2014_03_199.

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26

Brennand, JE, and AD Cameron. "Human parvovirus B19 in pregnancy." Hospital Medicine 61, no. 2 (February 2000): 93–96. http://dx.doi.org/10.12968/hosp.2000.61.2.1288.

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27

Ueno, Yukio, Hiroshi Umadome, Mutsuro Shimodera, Ikuo Kishimoto, Kozo Ikegaya, and Toshiyasu Yamauchi. "Human parvovirus B19 and arthritis." Lancet 341, no. 8855 (May 1993): 1280. http://dx.doi.org/10.1016/0140-6736(93)91183-m.

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28

Lynch, Catherine M., Douglas A. Holt, and John T. Sinnott. "Human parvovirus B19 and pregnancy." Infectious Diseases Newsletter 10, no. 10 (October 1991): 84–85. http://dx.doi.org/10.1016/0278-2316(91)90017-t.

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29

Servant-Delmas, Annabelle, Jean-Jacques Lefrère, Frédéric Morinet, and Sylvie Pillet. "Advances in Human B19 Erythrovirus Biology." Journal of Virology 84, no. 19 (July 14, 2010): 9658–65. http://dx.doi.org/10.1128/jvi.00684-10.

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ABSTRACT Since its discovery, human parvovirus B19 (B19V), now termed erythrovirus, has been associated with many clinical situations (neurological and myocardium infections, persistent B19V DNAemia) in addition to the prototype clinical manifestations, i.e., erythema infectiosum and erythroblastopenia crisis. In 2002, the use of new molecular tools led to the characterization of three different genotypes of human B19 erythrovirus. Although the genomic organization is conserved, the geographic distribution of the different genotypes varies worldwide, and the nucleotidic divergences can impact the molecular diagnosis of B19 virus infection. The cell cycle of the virus remains partially unresolved; however, recent studies have shed light on the mechanism of cell entry and the interactions of B19V proteins with apoptosis pathways.

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30

Tokarska-Rodak, Małgorzata. "Seroprevalence of Toxoplasma gondii, varicella zoster virus and human parvovirus B19 among women in the Biała Podlaska District of Eastern Poland." Medical Science Pulse 13, no. 3 (January 10, 2020): 1–6. http://dx.doi.org/10.5604/01.3001.0013.7160.

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Background: Infections in pregnant women or women planning pregnancy caused by the protozoan Toxoplasma gondii and the viruses varicella zoster virus (VZV) and human parvovirus B19 can be a danger to the fetus. Aim of the study: The aim of the study was to determine the serological status of women of childbearing age in relation to T. gondii, VZV and human parvovirus B19 in a region of Eastern Poland (Biała Podlaska District). Material and methods: The study group consisted of 174 women aged 19 to 35 (average 23, SD 3.68) from the Biała Podlaska District. Anti-T. gondii IgM/IgG antibodies, anti-VZV IgG and anti-human parvovirus B19 IgG were detected by ELISA. Results: Serological screening revealed that the most common antibodies were anti-VZV and anti-parvovirus B19 (in 96% and 60.9% of women, respectively). Anti-T. gondii antibodies were found in 28.6%. No correlation was found between the presence of anti-T. gondii, human parvovirus B19, and VZV antibodies and the age of the examined women, their place of residence, and their education. Conclusions: About 4%, 39% and 71.2% of women participating in this study were still susceptible to infection with VZV, human parvovirus B19, and T. gondii, respectively. It is therefore important to address health education primarily in women of childbearing age in order to help them undertake relevant measures for prevention of T. gondii, human parvovirus B19 and VZV infection.

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Shackelton, Laura A., and Edward C. Holmes. "Phylogenetic Evidence for the Rapid Evolution of Human B19 Erythrovirus." Journal of Virology 80, no. 7 (April 1, 2006): 3666–69. http://dx.doi.org/10.1128/jvi.80.7.3666-3669.2006.

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ABSTRACT Human B19 erythrovirus is a ubiquitous viral pathogen, commonly infecting individuals before adulthood. As with all autonomous parvoviruses, its small single-stranded DNA genome is replicated with host cell machinery. While the mechanism of parvovirus genome replication has been studied in detail, the rate at which B19 virus evolves is unknown. By inferring the phylogenetic history and evolutionary dynamics of temporally sampled B19 sequences, we observed a surprisingly high rate of evolutionary change, at approximately 10−4 nucleotide substitutions per site per year. This rate is more typical of RNA viruses and suggests that high mutation rates are characteristic of the Parvoviridae.

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Harada, Tomoya, Yuriko Sueda, Kensaku Okada, Tsuyoshi Kitaura, Kosuke Yamaguchi, Haruhiko Makino, Masaki Nakamoto, Hiroki Chikumi, and Akira Yamasaki. "Splenic Infarction in Acute Cytomegalovirus and Human Parvovirus Concomitant Infection." Case Reports in Infectious Diseases 2018 (December 3, 2018): 1–5. http://dx.doi.org/10.1155/2018/7027656.

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We present a case report of a 35-year-old woman who had splenic infarction. She had persistent high fever, systemic joint pain, and abnormal liver function. She was diagnosed with cytomegalovirus and human parvovirus B19 concomitant infection. Her coagulopathy test revealed no abnormal results. She was treated with intravenous ganciclovir for 13 days; consequently, her splenic infarction improved after 7 weeks. As per our knowledge, this is the first case of cytomegalovirus and parvovirus B19 coinfection complicated by splenic infarction. Cytomegalovirus and parvovirus B19 may induce a hypercoagulation state during the acute phase.

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Tolfvenstam, T., A. Oxenius, D. A. Price, B. L. Shacklett, H. M. L. Spiegel, K. Hedman, O. Norbeck, et al. "Direct Ex Vivo Measurement of CD8+T-Lymphocyte Responses to Human Parvovirus B19." Journal of Virology 75, no. 1 (January 1, 2001): 540–43. http://dx.doi.org/10.1128/jvi.75.1.540-543.2001.

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ABSTRACT Parvovirus B19 is a common human pathogen which can cause severe syndromes, including aplastic anemia and fetal hydrops. The mapping of the first parvovirus B19-derived CD8+ T-lymphocyte epitope is described. This HLA-B35-restricted peptide derives from the nonstructural (NS1) protein and is strongly immunogenic in B19 virus-seropositive donors.

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Oliveira, Maria Isabel de, Ana Maria Sardinha Afonso, Suely Pires Curti, Patrícia Evelin Silva, Tamyris Fernanda Barbosa, Elian Reis Silva Junior, and Cristina Adelaide Figueiredo. "Genotype 1 of human parvovirus B19 in clinical cases." Revista da Associação Médica Brasileira 63, no. 3 (March 2017): 224–28. http://dx.doi.org/10.1590/1806-9282.63.03.224.

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Summary Introduction: Virus surveillance strategies and genetic characterization of human parvovirus B19 (B19V) are important tools for regional and global control of viral outbreak. In São Paulo, Brazil, we performed a study of B19V by monitoring the spread of this virus, which is an infectious agent and could be mistakenly reported as a rash and other types of infection. Method: Serum samples were subjected to enzyme immunoassay, real time polymerase chain reaction, and sequencing. Results: From the 462 patients with suspected cases of exanthematic infections, the results of the 164 serum samples were positive for B19V immunoglobulin M. Among these cases, there were 38 patients with erythema infections and B19-associated with other infections such as encephalitis, hydrops fetalis, chronic anemia, hematological malignancies. These samples were sequenced and identified as genotype 1. Conclusion: This study showed patients with infections caused by B19V and sequencing genotype 1. Continuous monitoring is necessary to detect all known genotypes, and the emergence of new genotypes of these viruses for case management in public health control activities.

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35

Ducloux, Céline, Bruno You, Amandine Langelé, Olivier Goupille, Emmanuel Payen, Stany Chrétien, and Zahra Kadri. "Enhanced Cell-Based Detection of Parvovirus B19V Infectious Units According to Cell Cycle Status." Viruses 12, no. 12 (December 18, 2020): 1467. http://dx.doi.org/10.3390/v12121467.

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Human parvovirus B19 (B19V) causes various human diseases, ranging from childhood benign infection to arthropathies, severe anemia and fetal hydrops, depending on the health state and hematological status of the patient. To counteract B19V blood-borne contamination, evaluation of B19 DNA in plasma pools and viral inactivation/removal steps are performed, but nucleic acid testing does not correctly reflect B19V infectivity. There is currently no appropriate cellular model for detection of infectious units of B19V. We describe here an improved cell-based method for detecting B19V infectious units by evaluating its host transcription. We evaluated the ability of various cell lines to support B19V infection. Of all tested, UT7/Epo cell line, UT7/Epo-STI, showed the greatest sensitivity to B19 infection combined with ease of performance. We generated stable clones by limiting dilution on the UT7/Epo-STI cell line with graduated permissiveness for B19V and demonstrated a direct correlation between infectivity and S/G2/M cell cycle stage. Two of the clones tested, B12 and E2, reached sensitivity levels higher than those of UT7/Epo-S1 and CD36+ erythroid progenitor cells. These findings highlight the importance of cell cycle status for sensitivity to B19V, and we propose a promising new straightforward cell-based method for quantifying B19V infectious units.

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36

Zhi, Ning, Zhihong Wan, Xiaohong Liu, Susan Wong, Dong Joo Kim, Neal S. Young, and Sachiko Kajigaya. "Codon Optimization of Human Parvovirus B19 Capsid Genes Greatly Increases Their Expression in Nonpermissive Cells." Journal of Virology 84, no. 24 (October 13, 2010): 13059–62. http://dx.doi.org/10.1128/jvi.00912-10.

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ABSTRACT Parvovirus B19 (B19V) is pathogenic for humans and has an extreme tropism for human erythroid progenitors. We report cell type-specific expression of the B19V capsid genes (VP1 and VP2) and greatly increased B19V capsid protein production in nonpermissive cells by codon optimization. Codon usage limitation, rather than promoter type and the 3′ untranslated region of the capsid genes, appears to be a key factor in capsid protein production in nonpermissive cells. Moreover, B19 virus-like particles were successfully generated in nonpermissive cells by transient transfection of a plasmid carrying both codon-optimized VP1 and VP2 genes.

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37

Izquierdo-Blasco, Jaume, María Teresa Salcedo Allende, Maria Gemma Codina Grau, Ferran Gran, Elena Martínez Sáez, and Joan Balcells. "Parvovirus B19 Myocarditis: Looking Beyond the Heart." Pediatric and Developmental Pathology 23, no. 2 (July 23, 2019): 158–62. http://dx.doi.org/10.1177/1093526619865641.

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Human parvovirus B19 represents the most common etiology of myocarditis in the pediatric population. Although it usually causes a benign exanthematic viral infection, parvovirus B19 may also present as disseminated disease with tropism for the myocardium, causing heart failure with high mortality. We present the case of a 2-year-old patient with fulminating acute myocarditis in whom the histological, immunophenotypic, and microbiological findings in necropsy showed multiorgan involvement caused by parvovirus B19. The autopsy revealed changes due to infection with parvovirus B19 as well as hypoxic-ischemic and secondary autoimmune changes. Medullary aplasia was observed, transmural lymphocyte myocarditis, lymphocytosis in the dermis with endothelial cells positive for parvovirus B19 in immunohistochemistry, cholestatic hepatitis due to ischemia and autoimmune hepatitis, lymphadenitis, and signs of hemophagocytosis. We also found hypoxic-ischemic encephalopathy.

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38

Srivastava, A., E. Bruno, R. Briddell, R. Cooper, C. Srivastava, K. van Besien, and R. Hoffman. "Parvovirus B19-induced perturbation of human megakaryocytopoiesis in vitro." Blood 76, no. 10 (November 15, 1990): 1997–2004. http://dx.doi.org/10.1182/blood.v76.10.1997.1997.

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Abstract Parvovirus B19 infection leads to transient aplastic crises in individuals with chronic hemolytic anemias or immunodeficiency states. An additional unexplained sequela of B19 infection is thrombocytopenia. Because B19 is known to have a remarkable tropism for human erythropoietic elements, and is not known to replicate in nonerythroid cells, the etiology of this thrombocytopenia is uncertain. We sought to define the pathobiology of B19-associated thrombocytopenia by examining the role of B19 on in vitro megakaryocytopoiesis. B19 infection of normal human bone marrow cells significantly suppressed megakaryocyte (MK) colony formation compared with mock-infected cells. No such inhibition was observed with a nonpathogenic human parvovirus, the adeno-associated virus 2 (AAV). The B19-MK cell interaction was also studied at the molecular level. Whereas low-density bone marrow cells containing erythroid precursor cells supported B19 DNA replication, no viral DNA replication was observed in B19-infected MK-enriched fractions as determined by the presence of viral DNA replicative intermediates on Southern blots. However, analysis of total cytoplasmic RNA isolated from B19-infected MK fractions showed a low-level expression of the B19 genome as detected by quantitative RNA dot blots as well as by Northern analysis. Furthermore, a frame-shift mutation in a recombinant AAV-B19 hybrid genome segment that encodes the viral nonstructural (NS1) protein significantly reduced the observed inhibition of MK colony formation. These studies indicate tissue- tropism of B19 beyond the erythroid progenitor cell, and lend support to the hypothesis that B19 genome expression may be toxic to cell populations that are nonpermissive for viral DNA replication.

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39

Srivastava, A., E. Bruno, R. Briddell, R. Cooper, C. Srivastava, K. van Besien, and R. Hoffman. "Parvovirus B19-induced perturbation of human megakaryocytopoiesis in vitro." Blood 76, no. 10 (November 15, 1990): 1997–2004. http://dx.doi.org/10.1182/blood.v76.10.1997.bloodjournal76101997.

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Abstract:

Parvovirus B19 infection leads to transient aplastic crises in individuals with chronic hemolytic anemias or immunodeficiency states. An additional unexplained sequela of B19 infection is thrombocytopenia. Because B19 is known to have a remarkable tropism for human erythropoietic elements, and is not known to replicate in nonerythroid cells, the etiology of this thrombocytopenia is uncertain. We sought to define the pathobiology of B19-associated thrombocytopenia by examining the role of B19 on in vitro megakaryocytopoiesis. B19 infection of normal human bone marrow cells significantly suppressed megakaryocyte (MK) colony formation compared with mock-infected cells. No such inhibition was observed with a nonpathogenic human parvovirus, the adeno-associated virus 2 (AAV). The B19-MK cell interaction was also studied at the molecular level. Whereas low-density bone marrow cells containing erythroid precursor cells supported B19 DNA replication, no viral DNA replication was observed in B19-infected MK-enriched fractions as determined by the presence of viral DNA replicative intermediates on Southern blots. However, analysis of total cytoplasmic RNA isolated from B19-infected MK fractions showed a low-level expression of the B19 genome as detected by quantitative RNA dot blots as well as by Northern analysis. Furthermore, a frame-shift mutation in a recombinant AAV-B19 hybrid genome segment that encodes the viral nonstructural (NS1) protein significantly reduced the observed inhibition of MK colony formation. These studies indicate tissue- tropism of B19 beyond the erythroid progenitor cell, and lend support to the hypothesis that B19 genome expression may be toxic to cell populations that are nonpermissive for viral DNA replication.

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40

Sato, Hiroyuki. "Human parvovirus B19 and related diseases." Journal of the Japan Society of Blood Transfusion 42, no. 3 (1996): 74–82. http://dx.doi.org/10.3925/jjtc1958.42.74.

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41

SATO, HIROYUKI. "Donor screening of human parvovirus B19." Journal of the Japan Society of Blood Transfusion 44, no. 3 (1998): 352–55. http://dx.doi.org/10.3925/jjtc1958.44.352.

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42

Franciosi, Ralph A., and Peter Tattersall. "Fetal infection with human parvovirus B19." Human Pathology 19, no. 4 (April 1988): 489–91. http://dx.doi.org/10.1016/s0046-8177(88)80505-7.

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43

ANDERSON, M. "HUMAN PARVOVIRUS B19 AND HYDROPS FETALIS." Lancet 331, no. 8584 (March 1988): 535. http://dx.doi.org/10.1016/s0140-6736(88)91331-1.

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44

Sebire, NJ. "Human parvovirus B19 and fetal death." Lancet 358, no. 9288 (October 2001): 1180. http://dx.doi.org/10.1016/s0140-6736(01)06277-8.

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45

Tolfvenstam, Thomas, Nikos Papadpgoammalos, Oscar Norbeck, Karin Peterson, and Kristina Broliden. "Human parvovirus B19 and fetal death." Lancet 358, no. 9288 (October 2001): 1180. http://dx.doi.org/10.1016/s0140-6736(01)06278-x.

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46

Crowly, Brendan, George Kokai, and Bernard Cohen. "Human parvovirus B19 and fetal death." Lancet 358, no. 9288 (October 2001): 1180–81. http://dx.doi.org/10.1016/s0140-6736(01)06279-1.

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47

Schwarz, TinoF, M. Roggendorf, Barbara Hottenträger, Friedrich Deinhardt, Gisela Enders, KarlP Gloning, Thomas Schramm, and Manfred Hansmann. "HUMAN PARVOVIRUS B19 INFECTION IN PREGNANCY." Lancet 332, no. 8610 (September 1988): 566–67. http://dx.doi.org/10.1016/s0140-6736(88)92684-0.

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48

Shiraishi, Hiroyuki, Takeshi Sasaki, Masataka Nakamura, Nobuo Yaegashi, and Kazuo Sugamura. "Laboratory infection with human parvovirus B19." Journal of Infection 22, no. 3 (May 1991): 308–10. http://dx.doi.org/10.1016/s0163-4453(05)80026-x.

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49

Nocton, James J., Laurie C. Miller, Lori B. Tucker, and Jane G. Schaller. "Human parvovirus B19-associatedarthritis in children." Journal of Pediatrics 122, no. 2 (February 1993): 186–90. http://dx.doi.org/10.1016/s0022-3476(06)80111-3.

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50

WOERNLE, C. H., L. J. ANDERSON, P. TATTERSALL, and J. M. DAVISON. "Human Parvovirus B19 Infection during Pregnancy." Obstetrical & Gynecological Survey 43, no. 2 (February 1988): 96–98. http://dx.doi.org/10.1097/00006254-198843020-00011.

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