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

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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: [email protected] 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
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