DOCSLIB.ORG

Human Parvovirus B19: General Considerations and Impact on Patients with Sickle-Cell Disease and Thalassemia and on Blood Transfusions Svetoslav N

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Human Parvovirus B19: General Considerations and Impact on Patients with Sickle-Cell Disease and Thalassemia and on Blood Transfusions Svetoslav N MINIREVIEW Human parvovirus B19: general considerations and impact on patients with sickle-cell disease and thalassemia and on blood transfusions Svetoslav N. Slavov1, Simone Kashima1,2, Ana Cristina Silva Pinto1 & Dimas Tadeu Covas1 1Regional Blood Center of Ribeira˜ o Preto, Faculty of Medicine in Ribeira˜ o Preto (FMRP), University of Sa˜ o Paulo (USP), SP, Brazil; and 2Faculty of Pharmaceutical Sciences of Ribeira˜ o Preto, University of Sa˜ o Paulo (USP), SP, Brazil Correspondence: Svetoslav N. Slavov, Abstract Regional Blood Center of Ribeira˜ o Preto, Faculty of Medicine in Ribeira˜ o Preto (FMRP), Human parvovirus B19 (B19V) is a small (22–24 nm) nonenveloped DNA virus University of Sa˜ o Paulo (USP), Rua Tenente belonging to the genus Erythrovirus (family Parvoviridae). Although it generally Cata˜ o Roxo 2051, Ribeira˜ o Preto, SP, Brazil. causes self-limiting conditions in healthy people, B19V infection may have a Tel.: 155 16 2101 9309/9680; fax: 155 16 different outcome in patients with inherited hemolytic anemias. In such high-risk 2101 9309; e-mail: svetlyosf@yahoo.com individuals, the high-titer replication may result in bone marrow suppression, triggering a life-threatening drop of hemoglobin values (profound anemia, aplastic Received 31 January 2011; revised 12 April crisis). To date there is no consensus concerning a B19V screening program either 2011; accepted 4 May 2011. for the blood donations used in the hemotherapy or for high-risk patients. Final version published online 15 June 2011. Moreover, questions such as the molecular mechanisms by which B19V produces DOI:10.1111/j.1574-695X.2011.00819.x latency and persistent replication, the primary site (sites) of B19V infection and B19V immunopathology are far from being known. This review summarizes Editor: Alfredo Garzino-Demo general aspects of B19V molecular characteristics, pathogenesis and diagnostic approaches with a focus on the role of this pathogen in blood transfusions and in Keywords patients with some hemoglobinopathies (sickle-cell disease, thalassemia). parvovirus B19; clinical conditions; sickle-cell disease; blood transfusion. hemoglobin values and anemia which could be life-threa- Introduction tening (Heegaard & Brown, 2002; Zaki et al., 2006; Krishna- Human parvovirus B19 (parvovirus B19, B19V) is a small, murti et al., 2007; Toyokawa et al., 2007). nonenveloped DNA virus belonging to the genus Erythro- In 1981, B19V was implicated as the etiologic agent of virus (Parvoviridae family) (International Committee on severe aplastic crises in children with sickle-cell disease Taxonomy of Viruses (ICTV), 2007). Its capsid comprises (SCD), in whom this infection can evolve into various life- 60 capsomers (VP1 and VP2) surrounding a single-stranded threatening conditions (Serjeant et al., 1981) including acute (ss) DNA genome (Kaufman et al., 2004). VP1 protein is a encephalopathy (Bakhshi et al., 2002), nephrotic syndrome dominant target for the neutralizing antibodies and is (Quek et al., 2010), splenic sequestration (Yates et al., 2009) located on the external surface of the virion (Bonsch¨ et al., and fatal bone marrow embolism (Rayburg et al., 2010). This 2008). The mechanism of B19V replication is exceptional: raises important questions related to the safety of transfused DNA is replicated through high-molecular-weight inter- blood and B19V transmission by blood transfusion. B19V mediates linked through hairpin structures because of the infection transmitted by transfusions has already been presence of genomic palindromes (Ozawa et al., 1986). described as a cause of chronic anemia (Cohen et al., 1997; The pattern of clinical disease caused by B19V varies and Jordan et al., 1998) as well as transient heart failure (Zanella is influenced by both the hematological and the immunolo- et al., 1995) in affected individuals. Seronegative children gical status of the infected individual. In healthy hosts, B19V with inherited hemolytic diseases are particularly vulnerable IMMUNOLOGY & MEDICAL MICROBIOLOGY generally causes self-limiting subclinical erythroid aplasia to B19V, in whom the introduction of the virus via transfu- followed by a rash or arthralgia. However, in patients with sion can seriously disturb erythropoiesis (Heegaard & diminished production or increased loss of erythrocytes, it is Brown, 2002; Zaki et al., 2006; Yates et al., 2009). However, now clear that B19V infection results in a severe drop of most hematological units worldwide do not carry out FEMS Immunol Med Microbiol 62 (2011) 247–262 c 2011 Federation of European Microbiological Societies Published by Blackwell Publishing Ltd. All rights reserved 248 S.N. Slavov et al. routine screening of donated blood or high-risk patients only one member, the Aleutian mink disease virus, which for B19V, despite the unpredictable infection outcome causes lethal infection among minks. The Bocavirus genus and the lack of treatment options (Prowse et al., 1997; has as a prototype the bovine parvovirus (ICTV, 2007). Blumel et al., 2002). This review summarizes general aspects concerning the molecular, genotypic and pathogenetic features of B19V Viral structure with a focus on its impact on blood transfusion and patients B19V is a nonenveloped virus whose icosahedral virion is with hemoglobinopathies (SCD and thalassemia). composed of two structural proteins (VP1 and VP2) sur- rounding a linear, ssDNA molecule with positive or negative Discovery, brief history and taxonomy of polarity. B19V Viral capsid proteins Discovery and brief history The virion consists of 60 structural subunits, 95% of B19V was discovered accidentally in 1974 in the serum of an which belong to VP2 (58 kDa) and 5% to VP1 (83 kDa) asymptomatic blood donor by Yvonne Cossart’s group in (Kaufman et al., 2004; Bonsch¨ et al., 2008). VP1 and VP2 London (Cossart et al., 1975). The viral name originated originate from overlapping reading frames and are identical from the identification of the tested sample: number 19 of with the exception of 227 additional amino acids at the panel B. The electron microscopy studies which followed N-terminus of VP1, called VP1 ‘unique region’ (VP1u) revealed 23-nm viral particles similar to those of the animal (Kaufman et al., 2004). VP1u exhibits relatively high se- parvoviruses (Heegaard & Brown, 2002; Brown, 2009). quence variability in persistently infected individuals ranging Characterized during 1983–1984, the viral genome of B19V from 3.5% (Heegard et al., 2002) to 6.8/8.2% (Hemauer proved to be a single 5.5 kb DNA molecule (Summers et al., 1996). Such variation could cause nonconservative et al., 1983) surrounded by superficial proteins copurifying amino acid alterations (uncharged amino acid residues are at a density of 1.43 g cmÀ3 (buoyant density for parvoviruses replaced with polar amino acids). This region plays an in CsCl: 1.38–1.45 g cmÀ3) (Clewley, 1984; ICTV, 2007). important role in eliciting immune responses, with this type Description of B19V clinical entities coincided with its of mutations probably leading to a modified viral surface and virological characterization. The first connection between inability of the infected organism to clear B19V, and the B19V and symptomatic disease was made in 1981, when it development of persistent infection (Hemauer et al., 1996). was demonstrated that it causes transient aplastic crisis In contrast to the mammalian parvoviruses and despite (TAC) (Pattison et al., 1981) in patients with SCD. Erythema its low concentration in the virion, VP1u is the major infectiosum (‘fifth disease’) in children was consequently antigenic target for neutralizing antibodies. It also possesses linked to acute B19V infection (Anderson et al., 1983). phospholipase A (PLA ) motif, which takes part in the Following studies described B19V-induced fetal loss (hy- 2 2 initiation of the infection. VP1u is thought to play an drops fetalis) (Brown et al., 1984) during pregnancy and important role in the induction of autoimmune responses symmetrical arthropathy in adults (Reid et al., 1985; White and chronic inflammation by mechanisms that are not fully et al., 1985). understood (Bonsch¨ et al., 2008). Taxonomy Nonstructural proteins, NS1 B19V is a member of the family Parvoviridae, subdivided into Parvovirinae and Densovirinae depending on the type of B19V possesses several nonstructural (NS) proteins, the the infected host (vertebrate or invertebrate). Parvovirinae is most abundant of which is NS1. It has a molecular mass of further divided into five genera (Amdovirus, Bocavirus, 77 kDa (Sol et al., 1999) and multiple functions, including Dependovirus, Erythrovirus and Parvovirus) due to differ- site-specific DNA-binding, DNA-nicking, helicase function ences in transcription, organization of their terminal repeats and regulation of gene transcription. NS1 trans-regulates the and host range. B19V is an autonomously replicating virus, viral P6 promoter as well as some cellular promoters and as its life cycle is supported only in rapidly dividing thus controls B19V replication (Zhi et al., 2006). This erythroid cells. Therefore, B19V is classified within the protein is highly cytotoxic for erythroid precursors and can genus Erythrovirus as a prototype. The genus Parvovirus induce apoptosis via interaction with caspase 3 (Moffat comprises most of the parvoviruses infecting vertebrates et al., 1998; Morita et al., 2001). Most of the B19V-associated with a prototype member minute virus of mice (MMV). clinical manifestations are thought to be related to damage Dependovirus includes
Load more

Recommended publications
  • Parvovirus B19 Uncoating Occurs in the Cytoplasm Without Capsid Disassembly and It Is Facilitated by Depletion of Capsid-Associated Divalent Cations
    viruses Article Parvovirus B19 Uncoating Occurs in the Cytoplasm without Capsid Disassembly and It Is Facilitated by Depletion of Capsid-Associated Divalent Cations 1 1 1, 1 2 Oliver Caliaro , Andrea Marti , Nico Ruprecht y, Remo Leisi , Suriyasri Subramanian , Susan Hafenstein 2,3 and Carlos Ros 1,* 1 Department of Chemistry and Biochemistry, University of Bern, Freiestrasse 3, 3012 Bern, Switzerland; oliver.caliaro@dcb.unibe.ch (O.C.); andrea.marti@students.unibe.ch (A.M.); nicoolivier.ruprecht@insel.ch (N.R.); remo.leisi@dcb.unibe.ch (R.L.) 2 Department of Medicine, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA; sxs1161@psu.edu (S.S.); suh21@psu.edu (S.H.) 3 Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, PA 16802, USA * Correspondence: carlos.ros@dcb.unibe.ch; Tel.: +41-31-6314331 Present address: Department of Diagnostic, Interventional and Pediatric Radiology, University Hospital, y University of Bern, 3010 Bern, Switzerland. Received: 17 April 2019; Accepted: 9 May 2019; Published: 10 May 2019 Abstract: Human parvovirus B19 (B19V) traffics to the cell nucleus where it delivers the genome for replication. The intracellular compartment where uncoating takes place, the required capsid structural rearrangements and the cellular factors involved remain unknown. We explored conditions that trigger uncoating in vitro and found that prolonged exposure of capsids to chelating agents or to buffers with chelating properties induced a structural rearrangement at 4 ◦C resulting in capsids with lower density. These lighter particles remained intact but were unstable and short exposure to 37 ◦C or to a freeze-thaw cycle was sufficient to trigger DNA externalization without capsid disassembly.
    [Show full text]
  • Infection Status of Human Parvovirus B19, Cytomegalovirus and Herpes Simplex Virus-1/2 in Women with First-Trimester Spontaneous
    Gao et al. Virology Journal (2018) 15:74 https://doi.org/10.1186/s12985-018-0988-5 RESEARCH Open Access Infection status of human parvovirus B19, cytomegalovirus and herpes simplex Virus- 1/2 in women with first-trimester spontaneous abortions in Chongqing, China Ya-Ling Gao1, Zhan Gao3,4, Miao He3,4* and Pu Liao2* Abstract Background: Infection with Parvovirus B19 (B19V), Cytomegalovirus (CMV) and Herpes Simplex Virus-1/2 (HSV-1/2) may cause fetal loses including spontaneous abortion, intrauterine fetal death and non-immune hydrops fetalis. Few comprehensive studies have investigated first-trimester spontaneous abortions caused by virus infections in Chongqing, China. Our study intends to investigate the infection of B19V, CMV and HSV-1/2 in first-trimester spontaneous abortions and the corresponding immune response. Methods: 100 abortion patients aged from 17 to 47 years were included in our study. The plasma samples (100) were analyzed qualitatively for specific IgG/IgM for B19V, CMV and HSV-1/2 (Virion\Serion, Germany) according to the manufacturer’s recommendations. B19V, CMV and HSV-1/2 DNA were quantification by Real-Time PCR. Results: No specimens were positive for B19V, CMV, and HSV-1/2 DNA. By serology, 30.0%, 95.0%, 92.0% of patients were positive for B19V, CMV and HSV-1/2 IgG respectively, while 2% and 1% for B19V and HSV-1/2 IgM. Conclusion: The low rate of virus DNA and a high proportion of CMV and HSV-1/2 IgG for most major of abortion patients in this study suggest that B19V, CMV and HSV-1/2 may not be the common factor leading to the spontaneous abortion of early pregnancy.
    [Show full text]
  • Guillain–Barré Syndrome—The Challenge of Unrecognized Triggers
    Neurological Sciences (2019) 40:2403–2404 https://doi.org/10.1007/s10072-019-03926-z LETTER TO THE EDITOR Guillain–Barré syndrome—the challenge of unrecognized triggers Rodrigo de Andrade da Silva1 & Renata Carvalho Cremaschi1,2 & Joao Renato Rebello Pinho3 & João Bosco de Oliveira3 & Fernando Morgadinho Coelho1,2,4 Received: 16 February 2019 /Accepted: 7 May 2019 /Published online: 16 May 2019 # Fondazione Società Italiana di Neurologia 2019 Dear editor, and Mycoplasma pneumoniae were prevalent in GBS patients. Giordano and col. published excellent work describing the Other less common triggers for GBS are infections for epidemiology and seasonal characteristics of Guillain–Barré Haemophilus influenzae, hepatitis E virus, and Parvovirus B19. syndrome (GBS) in the USA. This study designated epidemi- In São Paulo, Brazil, we investigated possible infection triggers ology and seasonal aspects of GBS in this USA population- in 11 adult patients hospitalized after GBS diagnosis, between based study, and possible relationship with possible triggers 2016 and 2017, in a university. Six patients (54.5%) were female are discussed [1]. and the mean age of the patients was 60.27 ± 11.05 years. The GBS is a rare disease, with an incidence of 1.1 cases per real-time blood polymerase chain reaction (RT-PCR) technique 100,000 person-years, more common in elderly men. The most was used to detect Herpes simplex viruses 2, 6, and 7, important triggers are previous infections, mainly of the airways Cytomegalovirus, Epstein-Barr, Varicella zoster, Enterovirus, and gastrointestinal tract [2]. In China, there is an increased Parechovirus, Parvovirus B19, Adenovirus, Zika virus, incidence of GBS during the summer, possibly related to the chikungunya virus, and dengue.
    [Show full text]
  • Human Parvovirus B19: a Mechanistic Overview of Infection and DNA Replication
    REVIEW For reprint orders, please contact: reprints@futuremedicine.com Human parvovirus B19: a mechanistic overview of infection and DNA replication Yong Luo1 & Jianming Qiu*,1 ABSTRACT Human parvovirus B19 (B19V) is a human pathogen that belongs to genus Erythroparvovirus of the Parvoviridae family, which is composed of a group of small DNA viruses with a linear single-stranded DNA genome. B19V mainly infects human erythroid progenitor cells and causes mild to severe hematological disorders in patients. However, recent clinical studies indicate that B19V also infects nonerythroid lineage cells, such as myocardial endothelial cells, and may be associated with other disease outcomes. Several cell culture systems, including permissive and semipermissive erythroid lineage cells, nonpermissive human embryonic kidney 293 cells and recently reported myocardial endothelial cells, have been used to study the mechanisms underlying B19V infection and B19V DNA replication. This review aims to summarize recent advances in B19V studies with a focus on the mechanisms of B19V tropism specific to different cell types and the cellular pathways involved in B19V DNA replication including cellular signaling transduction and cell cycle arrest. Human parvovirus B19 (B19V) was discovered in 1975 by Cossart and colleagues when screening KEYWORDS for hepatitis B virus in a panel of human serum samples [1] . The virus was described as 23 nm in • B19V • cell cycle • DDR diameter, a typical capsid size of a parvovirus. The virus came from the serum sample coded as • DNA damage response panel B number 19, and thereafter was named ‘Parvovirus B19.’ Most commonly, B19V infection • DNA replication causes erythema infectiosum or fifth disease (also named ‘slapped cheek syndrome’), which was first • Epo/EpoR signaling identified by Anderson et al.
    [Show full text]
  • Fifth Disease)
    Parvovirus B19 (Fifth Disease) What is "fifth disease?" Fifth disease is a mild rash illness that occurs most commonly in children. The ill child typically has a "slapped-cheek" rash on the face and a lacy red rash on the trunk and limbs. Occasionally, the rash may itch. An ill child may have a low-grade fever, malaise, or a "cold" a few days before the rash breaks out. The child is usually not very ill, and the rash resolves in 7 to 10 days. What causes fifth disease? Fifth disease is caused by infection with human parvovirus B19. This virus infects only humans. Pet dogs or cats may be immunized against "parvovirus," but these are animal parvoviruses that do not infect humans. Therefore, a child cannot "catch" parvovirus from a pet dog or cat, and a pet cat or dog cannot catch human parvovirus B19 from an ill child. Can adults get fifth disease? Yes, they can. An adult who is not immune can be infected with parvovirus B19 and either have no symptoms or develop the typical rash of fifth disease, joint pain or swelling, or both. Usually, joints on both sides of the body are affected. The joints most frequently affected are the hands, wrists, and knees. The joint pain and swelling usually resolve in a week or two, but they may last several months. About 50% of adults, however, have been previously infected with parvovirus B19, have developed immunity to the virus, and cannot get fifth disease. Is fifth disease contagious? Yes. A person infected with parvovirus B19 is contagious during the early part of the illness, before the rash appears.
    [Show full text]
  • Parvovirussatoko Ugai, MD,​A Yuta Aizawa, MD, Phd,B19:​B Tetsuya Kanayama, a Cause MD,A​ Akihiko Saitoh, of MD, Phdb
    ParvovirusSatoko Ugai, MD, a Yuta Aizawa, MD, PhD,B19: b Tetsuya Kanayama, A Cause MD, a Akihiko Saitoh, of MD, PhDb Sepsislike Syndrome in anabstract Infant Parvovirus B19 (PB19) is an important human pathogen that results in a wide spectrum of clinical outcomes, from mild, self-limiting erythema infectiosum in immunocompetent children and arthralgia in adults to lethal cytopenia in immunocompromised patients and intrauterine – fetal death.‍ However, there have been few reports of PB19 infection in neonates or young infants (aged 28 90 days), and no previous reports contained descriptions of PB19 infection as a cause of sepsislike syndrome in this age group.‍ We report a case of sepsislike syndrome caused by PB19 infection in a 56-day-old infant whose mother had polyarthralgia at the time of his admission.‍ PB19 infection was diagnosed on the basis aDepartment of Pediatrics, Tokamachi Prefectural Hospital, of positive polymerase chain reaction results for PB19 DNA in the Tokamachi, Niigata, Japan; and bDepartment of Pediatrics, serum and cerebrospinal fluid.‍ Positive immunoglobulin M and negative Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan immunoglobulin G for PB19 suggested acute infection.‍ He was admitted to the ICU because of poor peripheral circulation, but fully recovered without Dr Ugai conceived and designed the study and antibiotic administration.‍ After excluding other possible pathogens, PB19 drafted the initial manuscript; Drs Aizawa and Kanayama critically reviewed the manuscript; should be suspected as a cause of sepsislike syndrome in young infants, Dr Saitoh supervised the study and revised and especially those who have close contact with PB19-infected individuals.‍ critically reviewed the manuscript; and all authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.
    [Show full text]
  • RASH in INFECTIOUS DISEASES of CHILDREN Andrew Bonwit, M.D
    RASH IN INFECTIOUS DISEASES OF CHILDREN Andrew Bonwit, M.D. Infectious Diseases Department of Pediatrics OBJECTIVES • Develop skills in observing and describing rashes • Recognize associations between rashes and serious diseases • Recognize rashes associated with benign conditions • Learn associations between rashes and contagious disease Descriptions • Rash • Petechiae • Exanthem • Purpura • Vesicle • Erythroderma • Bulla • Erythema • Macule • Enanthem • Papule • Eruption Period of infectivity in relation to presence of rash • VZV incubates 10 – 21 days (to 28 d if VZIG is given • Contagious from 24 - 48° before rash to crusting of all lesions • Fifth disease (parvovirus B19 infection): clinical illness & contagiousness pre-rash • Rash follows appearance of IgG; no longer contagious when rash appears • Measles incubates 7 – 10 days • Contagious from 7 – 10 days post exposure, or 1 – 2 d pre-Sx, 3 – 5 d pre- rash; to 4th day after onset of rash Associated changes in integument • Enanthems • Measles, varicella, group A streptoccus • Mucosal hyperemia • Toxin-mediated bacterial infections • Conjunctivitis/conjunctival injection • Measles, adenovirus, Kawasaki disease, SJS, toxin-mediated bacterial disease Pathophysiology of rash: epidermal disruption • Vesicles: epidermal, clear fluid, < 5 mm • Varicella • HSV • Contact dermatitis • Bullae: epidermal, serous/seropurulent, > 5 mm • Bullous impetigo • Neonatal HSV • Bullous pemphigoid • Burns • Contact dermatitis • Stevens Johnson syndrome, Toxic Epidermal Necrolysis Bacterial causes of rash
    [Show full text]
  • Evidence of Human Parvovirus B19 Infection in the Post-Mortem Brain Tissue of the Elderly
    viruses Article Evidence of Human Parvovirus B19 Infection in the Post-Mortem Brain Tissue of the Elderly Sandra Skuja 1,*, Anda Vilmane 2, Simons Svirskis 2, Valerija Groma 1 and Modra Murovska 2 1 Institute of Anatomy and Anthropology, R¯ıga Stradin, š University, Kronvalda blvd 9, Riga LV-1010, Latvia; Valerija.Groma@rsu.lv 2 Institute of Microbiology and Virology, R¯ıga Stradin, š University, Riga LV-1067, Latvia; Anda.Vilmane@rsu.lv (A.V.); ssvirskis@latnet.lv (S.S.); Modra.Murovska@rsu.lv (M.M.) * Correspondence: Sandra.Skuja@rsu.lv; Tel.: +371-673-20421 Received: 23 October 2018; Accepted: 24 October 2018; Published: 25 October 2018 Abstract: After primary exposure, the human parvovirus B19 (B19V) genome may remain in the central nervous system (CNS), establishing a lifelong latency. The structural characteristics and functions of the infected cells are essential for the virus to complete its life cycle. Although B19V has been detected in the brain tissue by sequencing PCR products, little is known about its in vivo cell tropism and pathogenic potential in the CNS. To detect B19V and investigate the distribution of its target cells in the CNS, we studied brain autopsies of elderly subjects using molecular virology, and optical and electron microscopy methods. Our study detected B19V in brain tissue samples from both encephalopathy and control groups, suggesting virus persistence within the CNS throughout the host’s lifetime. It appears that within the CNS, the main target of B19V is oligodendrocytes. The greatest number of B19V-positive oligodendrocytes was found in the white matter of the frontal lobe.
    [Show full text]
  • New Insights of Human Parvovirus B19 in Modulating
    Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 16 October 2019 doi:10.20944/preprints201910.0179.v1 1 1 New Insights of Human Parvovirus B19 in Modulating Erythroid 2 Progenitor Cells Differentiation 3 4 Shuwen Feng, Dongxin Zeng, Junwen Zheng*, Dongchi Zhao* 5 Pediatrics Department, Children Digital and Health Data Research Center, Zhongnan Hospital of 6 Wuhan University 7 Authors: Shuwen Feng fengshuwen@whu.edu.cn 8 Dongxin Zeng zengdongxin@163.com 9 *Correspondence Authors: Junwen Zheng* zhengjunwen@whu.edu.cn 10 Dongchi Zhao* zhao_wh2004@hotmail.com; 11 Abstract 12 Background 13 Human parvovirus B19, a human pathogen of the erythroparvovirus genus, is responsible for 14 a variety of diseases. Despite less symptoms caused by B19 infection in healthy individuals, this 15 pathogen can not be neglected in specific groups who exhibit severe anemia. 16 Main body of abstract 17 Transient aplastic crisis and pure red cell aplasia are two kinds of anemic hemogram 18 respectively in acute phase and chronic B19 infection, especially occur in individuals with a 19 shortened red cell survival or immunocompromised patients. In addition, B19 infected pregnant 20 women may suffer risks of hydrops fetalis secondary to severe anemia and fetal loss. B19 21 possesses high affinity to bone marrow and fetal liver due to its extremely restricted cytotoxicity 22 to erythroid progenitor cells mediated by viral proteins. The nonstructural protein NS1 is 23 considered to be the major pathogenic factor, which takes parts in differentiational inhibition and 24 apoptosis of erythroid progenitor cells through inducing viral DNA damage responses and cell 25 cycle arrest.
    [Show full text]
  • List of Biological Agents and Toxins
    CORRESPONDING AVS PRODUCT DESCRIPTION MOH PRODUCT CODE CODE FIRST SCHEDULE PART I BACTERIA 1. BRUCELLA CANIS MOHHP3BBRUCCAN01 2. CHLAMYDIA PSITTACI (AVIAN STRAINS)1 MOHHP3BCHLAPSI01 VVP0B3CHLPSIB 3. MYCOBACTERIUM CANETTII MOHHP3BMYCOCAN01 4. MYCOBACTERIUM AFRICANUM MOHHP3BMYCOAFR01 5. MYCOBACTERIUM BOVIS (NON-BCG STRAINS)1 MOHHP3BMYCOBOV01 VVP0B3MYCBOVB 6. MYCOBACTERIUM MICROTI MOHHP3BMYCOMIC01 7. MYCOBACTERIUM TUBERCULOSIS MOHHP3BMYCOTUB01 8. ANY BIOLOGICAL AGENT THAT IS A CONSTRUCTED OR SEE CORRESPONDING CODE FOR THE RECONTRUCTED REPLICATION-COMPETENT FORM OF ANY MOHHP3BCNSTRCT01 AGENT, IF APPLICABLE BACTERIUM SET OUT IN THIS PART FUNGI 1. BLASTOMYCES DERMATITIDIS MOHHP3FBLASDER01 2. COCCIDIOIDES IMMITIS MOHHP3FCOCCIMM01 3. COCCIDIOIDES POSADASII, EXCEPT FOR THE FOLLOWING ATTENUATED STRAINS MOHHP3FCOCCIPO01 (A) ∆CHS5; AND (B) ∆CTS2/∆ARD1/∆CTS3 4. HISTOPLASMA CAPSULATUM VAR. CAPSULATUM1 MOHHP3FHISTCAP01 VVP0F3HISCAPC 5. HISTOPLASMA CAPSULATUM VAR. DUBOISII1 MOHHP3FHISTCAP01 VVP0F3HISCAPD 6. PARACOCCIDIOIDES BRASILIENSIS MOHHP3FPARABRA01 7. ANY BIOLOGICAL AGENT THAT IS A CONSTRUCTED OR SEE CORRESPONDING CODE FOR THE RECONSTRUCTED REPLICATION-COMPETENT FORM OF ANY MOHHP3FCNSTRCT01 AGENT, IF APPLICABLE FUNGUS SET OUT IN THIS PART 1 AVS Approval required 1 CORRESPONDING AVS PRODUCT DESCRIPTION MOH PRODUCT CODE CODE VIRUSES 1. ARENAVIRIDAE (A) FLEXAL VIRUS MOHHP3VARENFLE01 (B) LCM-LASSA COMPLEX VIRUSES (EXCEPT LASSA VIRUS) MOHHP3VARENOTH01 (C) LYMPHOCYTIC CHORIOMENINGITIS VIRUS1 MOHHP3VARENLYM01 VVP0V3ARELCVV (D) MOPEIA VIRUS MOHHP3VARENMOP01
    [Show full text]
  • Fifth Disease (Parvovirus B19)
    Fifth Disease (parvovirus B19) This fact sheet talks about fifth disease during pregnancy and while breastfeeding. This information should not take the place of medical care and advice from your healthcare provider. What is fifth disease? Fifth disease, also called erythema infectiosum, is a viral illness caused by human parvovirus B19. It usually affects children ages 4 to 14 (is more common in children than adults). The infection often starts with mild fever, headache, sore throat, and flu-like symptoms. Children can also develop a bright red rash on the face that looks like “slapped cheeks”, along with a lacy or bumpy rash on the body, arms, and legs. In adults, joint aches are a common symptom. Rash and joint symptoms may develop several weeks after infection. A pregnant woman who develops symptoms of fifth disease may or may not develop a facial or body rash and can pass the virus to her baby. Some adults (about 20 to 30%) infected with parvovirus B19 will not have symptoms. Is fifth disease contagious? Yes, fifth disease is very contagious. The virus is spread through contact with respiratory secretions of the nose (nasal mucus), saliva, and lungs (sputum / mucus) and through contact with blood. When an infected person coughs or sneezes, the virus can travel several feet. The time between infection and the development of the illness (incubation period) is usually between 4 and 14 days. Individuals with fifth disease are most infectious before the onset of symptoms and are unlikely to be contagious after the development of the rash. This makes efforts to prevent exposure difficult.
    [Show full text]
  • Human Parvovirus B19 Common Human Exposure Routes
    APPENDIX 2 Human Parvovirus B19 Common Human Exposure Routes: Disease Agent: • Respiratory (droplet infection) • In utero (transplacental) from acutely infected • Human parvovirus B19 (B19V) mother Disease Agent Characteristics: Likelihood of Secondary Transmission: • High in day-care centers, schools, and household • Family: Parvoviridae; Genus: Erythrovirus; Species: contacts through the respiratory route human parvovirus B19 (B19V) • Virion morphology and size: Nonenveloped, icosahe- At-Risk Populations: dral nucleocapsid symmetry, spherical particles, 23-26 nm in diameter • Children (because of lack of immunity) • Nucleic acid: Linear, negative-sense, single-stranded • Populations at most risk for serious complications by DNA, ~5.6 kb in length transfusion route include patients who have short- • Physiochemical properties: Heat resistant (56°C for ened RBC survivals, patients who are immunocom- 60 min), relatively susceptible to inactivation by pas- promised, and women who are pregnant (because of teurization at 60°C for 10 hours and to dry heat in a transmission of infection to the fetus). freeze-dried state (1.5% moisture) at 80°C for 72 hours; stable in lipid solvents; acid stable at pH 3-9; Vector Involved: inactivated by other solvents • None Disease Name: Blood Phase: • Erythema infectiosum (fifth disease) in children • Virus is tropic for erythroid progenitor cells. • Extremely high-titer viremia (up to 1014 IU/mL) Priority Level: occurs approximately 1 week following infection and • Scientific/Epidemiologic evidence regarding blood persists for approximately 5 days. safety: Blood components: Very low/Low: In the US • IgM antibody develops 10-14 days postinfection and there is a higher level of concern for immunocompro- viremia subsequently declines rapidly, usually disap- mised patients, patients with chronic anemia (sickle pearing within weeks of IgM development.
    [Show full text]