Human parvovirus B19 research concerning the safety of blood and plasma derivatives in China
Review Article

Human parvovirus B19 research concerning the safety of blood and plasma derivatives in China

Junting Jia1, Mengjun Zhang1, Yuyuan Ma1, Jingang Zhang1,2

1Beijing Key Laboratory of Blood Safety and Supply Technologies, Institute of Health Service and Transfusion Medicine, Academy of Military Medical Sciences, Beijing 100850, China; 2School of Biological Sciences, Xinxiang University, Xinxiang 453000, China

Contributions: (I) Conception and design: All authors; (II) Administrative support: All authors; (III) Provision of study materials or patients: All authors; (IV) Collection and assembly of data: All authors; (V) Data analysis and interpretation: All authors; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Yuyuan Ma; Jingang Zhang. Institute of Health Service and Transfusion Medicine, Academy of Military Medical Sciences, No. 27 Taiping Road, Haidian District, Beijing 100850, China. Email:;

Abstract: Human parvovirus B19 (B19V) is a common human pathogen which is associated with a broad spectrum of clinical manifestations. Since B19V can be transmitted via blood and plasma derivatives, it has been considered to pose great risk in transfusion safety. Since the early 21st century, European Pharmacopoeia, the Plasma Protein Therapeutics Association and U.S. Food and Drug Administration have proposed a list of guidelines to reduce the risk of B19V transmission by plasma derivatives. In terms of blood, some countries implement management measures on B19V to maximize the safety of blood transfusion. In China, no related documentation for monitoring B19V has been issued. The aim of this review is to discuss the risk for B19V transmission through blood and plasma derivatives in China. The issues raised with the intention to contribute to further development of risk management measures.

Keywords: Human parvovirus B19 (B19V); blood safety; plasma derivatives; China

Received: 15 October 2018; Accepted: 01 January 2019; Published: 18 January 2019.

doi: 10.21037/aob.2019.01.01

Human parvovirus B19 (B19V) was discovered in the sera of normal blood donors while screening for hepatitis B virus in 1975 (1). Although B19V infection generally runs its course without any problems in healthy individuals, it can result in serious complications in patients with underlying hematological disorders or immunodeficiency (2,3). Due to its pathogenicity and risk of transmission through blood and plasma derivatives, great concerns have been raised on this virus (4). In some countries, guidelines have been developed and proposed for screening tests or eliminating B19V in order to maximize the safety of blood and plasma derivatives. While in China, no regulations or recommendations for monitoring B19V are available at present. However, great efforts have been made to investigate the epidemic status and characterization of B19V circulating in China, thus abundant data are being accumulated for further assessment of the viral safety of blood and plasma derivatives, as well as for policy making. In this report, we reviewed the prevalence and the level of B19V in Chinese blood donors and plasma donations as well as plasma derivatives.

Features of human parvovirus B19

B19V belongs to the Erythroparvovirus genus within the Parvoviridae family. It is a small (around 20 nm diameter), non-enveloped single-stranded DNA virus of approximately 5,600 nucleotides (5,6). The capsid consists of two structural proteins: viral protein 1 (VP1) and 2 (VP2). VP2 is the major capsid protein and constitutes 95% of the capsid composition. VP2 alone can assemble virus-like particles. VP1 is the minor capsid protein and it is not necessary for capsid formation. But VP1 has an additional 227 aa at the N terminus compared with VP2, known as VP1 unique region (VP1u), which contains critical elements for virus entry, especially an original phospholipase A2 (PLA2) domain. B19V also encodes non-structure protein NS1, a multiple functional protein that is essential for the replication of B19V DNA and regulation of gene expression that is cytotoxic to host cells (7,8). In addition, the genome also encodes three smaller nonstructural proteins, i.e., 7.5, 9 and 11 kDa.

B19V is currently classified into 3 genotypes (genotype 1, 2, 3), which were defined as having greater than 10% divergence in overall DNA sequence (9). Within genotypes 1 and 3, two distinct subgroups were identified by phylogenetic analyses, respectively (10,11). All these three genotypes appear to circulate. However, their relative frequencies are strikingly different and their spatial and temporal distribution is not uniform (12). Genotype 1 circulates worldwide and can be found in most parts of the world (13). Genotype 2 is relatively rare. It has only been reported sporadically in several European countries, Brazil and the United States (14-18). Genotype 3 seems to be endemic in Ghana but has also been identified in Brazil, North India, China and the United States (9,19-23). Despite the genome-wide variations among them, these three B19V genotypes are assumed to have similar biological properties, transmission routes, and pathogenic capacities. In the clinical setting, they pose a similar diagnostic challenge (24,25).

B19V is a common virus that spreads worldwide. It is normally transmitted through the respiratory route. It can also be transmitted vertically and through bone marrow and organ transplantations as well as via transfused blood and plasma derivatives (26-28). Viremia occurs 1 week after exposure to the virus and virus titers peak within the first 2 days. Viremia usually lasts about 5 days. In acute infection, the virus titer could reach 1014 IU/mL in peripheral blood (29). B19V specific IgM antibodies are detectable 10 to 14 days after infection and can generally persist for 5 months. However, in some patients, the IgM antibodies can last even longer. IgG antibodies against B19V usually appear about 15 days after infection, remain high for several months and persist long-term. The seroprevalence of B19V is age dependent, increasing from 15% in preschool children to 50% in younger adults and to about 85% in the elderly (30).

B19V is the first parvovirus demonstrated to be pathogenic in humans. It causes diverse clinical manifestations, whose characteristics and outcomes mostly depend on the immune and physiological status of the infected individuals: asymptomatic or just some self-limiting illnesses in the normal population, transient aplastic crisis in patients with hematological problems, chronic anemia in immunodeficient patients, and abortion or non-immune hydrops fetalis in pregnant women. B19V could be also involved in the induction or pathogenesis of numerous autoimmune diseases, notably rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) (3).

Human parvovirus B19: relevance with transfusion safety

B19V can be transmitted through blood and plasma derivatives. In fact, B19V transmission by transfusion of blood is rare due to its low prevalence in blood donors. Thus, screening of blood donors for B19V infection is not routine. Some countries including Japan, Germany, and Netherland implemented relative measures to mitigate the risk of B19V transmission so as to make blood transfusions as safe as possible.

In September 1997, Japanese Red Cross (JRC) introduced a receptor-mediated hemagglutination assay as a screening test for B19V. This assay has been used for all donated blood until 2007. Since 2008, with an aim to improve assay sensitivity, the hemagglutination test has been replaced by chemiluminescent enzyme immunoassay, with the sensitivity of approximately 106.3 IU/mL with the genotype samples and 106.4 IU/mL with B19V DNA-positive donor samples, respectively (31).

In Germany, screening for B19V DNA in blood donors began in the year 2000. Minipool real-time NAT (testing in a minipool format of up to 96 donations) was introduced to do such screening. Blood products with B19V DNA virus load ≥105 IU/mL were discarded. In contrast, minipools with B19V DNA virus load <105 IU/mL were not resolved, and all blood products contained were released. In any case, donors were not informed about their B19V infection and were allowed to give subsequent donations (32).

In Netherlands, Health Council proposed a high-risk-group approach for cellular blood products, meaning that “B19V safe” cellular blood products (ones from a donor in which B19V specific IgG antibodies have been detected in two separate blood samples, one taken at least 6 months after the other) be administered to risk groups: pregnant women (except in the case of transfusions given during birth), patients with congenital or acquired hemolytic anemia who have no detectable B19V specific antibodies and patients with cellular immunodeficiency who have no detectable B19V specific antibodies (33).

Since source plasma pools for manufacturing plasma derivatives are consisted of thousands of plasma derivatives, even one donation with B19V could contaminate the entire pool. In some cases, acutely infected blood donors, with extremely high viremic levels of B19V but without symptoms, are not recognized and thus allowed to donate blood or plasma, resulting in a considerable risk of B19V transmission via plasma derivatives. What’s more, because of its small size and lack of envelope, B19V is difficult to be completely inactivated and/or removed. Therefore, limiting the viral load of B19V in the source plasma pools is crucial for reducing the risk of B19V transmission via plasma derivatives (34,35).

In order to counteract the transmission of B19V via plasma derivatives, since the early 21st century, U.S. Food and Drug Administration (FDA), European Pharmacopoeia (Ph. Eur.) and the Plasma Protein Therapeutics Association (PPTA) have issued a list of guidelines, proposing a limit of 104 IU/mL for levels of B19V DNA in manufacturing pools destined for making some or all kinds of plasma derivatives (36-39). Since all B19V genotype variants can be contaminants, the NAT assay for screening B19V DNA is required to be able to detect all three genotypes of B19V (40,41).

In China, neither specific documentation nor technical guidelines for monitoring B19V have been issued.

Human parvovirus B19 in Chinese blood donors

To our knowledge, Cai et al. presented the first report on the detection of B19V infection among Chinese blood donors in Zhaoqing in 1999 (42). Since then, abundant data with respect to the prevalence of B19V are being accumulated in different parts of China, especially in Southwest China, South China and Central China.

Data regarding the prevalence of B19V specific IgG and IgM among Chinese blood donors are shown in Table 1. The rate of B19V IgG-positive blood donors serves for the assessment of the rate of donors who have had a past infection.

Table 1

The prevalence of human parvovirus B19 reported in blood donors

Region Province City/county Yr(s) of sample collection Seroprevalence of B19V Reference
IgG (%) IgM (%) IgM and IgG (%) No of investigated donors
Northwest China Xinjiang Urumqi Apr. 2008–Aug. 2009 24.78 7.96 2.65 113 (43)
Jan. 2013–Feb. 2014 22.41 1.72 58 (44)
Southwest China Yunnan Kunming Apr. 2008–Aug. 2009 20.87 1.74 0 115 (43)
Sichuan Chengdu et al. 2009 32.61 7.61 2.17 92 (45)
Mianyang Jan. 2013–Feb. 2014 0 1.72 58 (44)
Guizhou 52.50 15.00 40 (46)
Chongqing Oct. 2012–Sep. 2013 36.68 5.07 1.90 1,104 (47)
Oct. 2012–Sep. 2013 36.70 5.59 1.86 752 (47)
Jan. 2013–Feb. 2014 41.67 0 60 (44)
Central China Henan Luoyang Apr. 2008–Aug. 2009 43.40 10.38 5.66 106 (43)
Jan. 2013–Feb. 2014 13.79 1.72 58 (44)
Zhengzhou Mar. 2015–Mar. 2016 32.98* 1,046 (48)
Hubei Wuhan 47.69 10.65 216 (46)
Yichang et al. Sep. 2013–Nov. 2013 43.36 2.46 934 (49)
South China Guangxi Liuzhou Apr. 2008–Aug. 2009 10.53 7.89 1.75 114 (43)
Jan. 2013–Feb. 2014 41.38 3.45 58 (44)
Guangdong Guangzhou Mar. 2004–Feb. 2005 38.58 1.88 0.28 1,760 (50)
Foshan 25.00 0.54 368 (51)
Lianshan and Liannan 29.26 (52)
East China Fujian Xiamen May 2013–Nov. 2013 16.79 4.64 1,078 (53)
38.10 3.57 56 (54)
Shandong Jining 2013–2014 36.15 5.94 4.69 960 (55)
North China Tianjin 31.60 7.36 326 (46)
Northeast China Jilin Changchun Mar. 2005–Apr. 2005 55.43 (56)
Liaoning Shenyang 24.28 15.22 276 (46)

*, positive samples were B19V IgG or IgM positive.

The seroprevalence differs between 10.53% and 55.43% in different cities with the lowest incidence been found in Liuzhou (43) and the highest incidence in Changchun (56). However, Hou et al. detected B19V IgG in 41.38% of 58 blood donors in Liuzhou (44), showing significantly different incidence rate in the same city. There was the same scenario for Luoyang: Ke et al. detected B19V IgG in 43.40% of 106 blood donors (43), while Hou et al. detected only in 13.79% of 58 (44). Since testing for B19V specific antibodies was performed with the same commercial assay kit of parvovirus IgG/IgM in these studies, the significant different incidence rate in the same city might be partly due to the differences in the size of the study population and the years of sample collection. In Chinese blood donors, the prevalence of IgG antibodies against B19V increases with age (47,49,53,57). In most studies, approximately 30% of 18- to 30-year-old subjects have detectable IgG, while about 60% of around 50-year-old subjects are seropositive (57). However, the B19V IgG prevalence of blood donors in Xiamen seems lower than that of blood donors at the same age in other cities (53).

The rate of B19V IgM-positive blood donors serves for the assessment of the rate of donors who were infected with B19V recently. In China, the prevalence of B19V IgM in healthy blood donors varies from 0.54% (51) to 15.22% (46) in different cities, except Chongqing in Hou Y’s study (none of 60 samples tested was B19V IgM positive) (44), with the lowest incidence found in Foshan and the highest incidence in Shenyang. The current studies showed an insignificant effect of age on the incidence of seropositive IgM.

Studies have also been carried out to determine the prevalence of B19V DNA in blood donors. An overview about the prevalence and levels of B19V DNA in blood donations are provided in Table 2. In most studies, the prevalence of B19V DNA is usually very low, varies from 0.02% (58) to 6.80% (52), except in Wuhan study (20.91%, 23/110) (60); and DNA concentration in these positive samples has been detected to be low (<4.89×105 IU/mL plasma). Acute B19V infections with high DNA concentrations in Chinese blood donors seemed to be rarely detectable. Using phylogenetic analysis, Ke et al. demonstrated the circulation of B19V Genotype 1 in Chinese blood donors. Genotype 2 and 3 have not been detected in their study (43).

Table 2

The prevalence of human parvovirus B19 DNA reported in blood donors

Region Province City/county Yr(s) of sample collection Prevalence of B19V DNA (%) No of investigated donations Viral load among positive samples Reference
Northwest China Xinjiang Urumqi Apr. 2008–Aug. 2009 0.72 836 2.13×103–4.93×104 IU/mL (43)
Jan. 2013–Feb. 2014 2.42 413 2.66×102–7.20×104 copies/mL (44)
Southwest China Yunnan Kunming Apr. 2008–Aug. 2009 0.28 1,075 7.90×102–1.56×104 IU/mL (43)
Sichuan Chengdu et al. 2009 0 92 (45)
Mianyang Jan. 2013–Feb. 2014 0 479 0 (44)
Jul. 2012–Dec. 2012 0.02 5,030 4.89×105IU/mL (58)
Chongqing Oct. 2012–Sep. 2013 0.40 752 1.10×102–2.80×103 copies/mL (47)
Jan. 2013–Feb. 2014 0.37 1,611 3.73×102–1.59×103 copies/mL (44)
South China Guangdong Foshan 4.26 94 (51)
Lianshan and Liannan 6.80 147 (52)
Zhaoqing Nov. 1996–Dec. 1997 5.08 374 (42)
Dec. 2013–Dec. 2014 0.27 6,000 (59)
Guangxi Liuzhou Apr. 2008–Aug. 2009 0.28 1,075 7.90×102–1.56×104 IU/mL (43)
Jan. 2013–Feb. 2014 0.60 667 3.68×102–1.45×103 copies/mL (44)
Central China Hubei Wuhan Mar. 2000 20.91 110 (60)
Henan Luoyang Jan. 2013–Feb. 2014 0.16 624 2.72×102 copies/mL (44)
Apr. 2008–Aug. 2009 1.24 1,051 2.48×102–4.65×104 IU/mL (43)
North China Jiangsu Jul. 2001 2.67 600 (61)
Fujian Xiamen May 2013–Nov. 2013 0.06 10,452 3.59×102–1.07×104 IU/mL (53)
East China Shandong Jining 2013–2014 2.23* 359 (55)
Linyi Jan. 2009–Jun. 2009 6.65 632 (62)
Oct. 2006–Oct. 2007 6.33 300 (63)

*, prevalence of B19V DNA in B19V IgG or IgM positive blood donors.

The prevalence of B19V IgM and B19V DNA in blood donors is usually lower than that of IgG in these studies, suggesting that acute B19V infection in Chinese blood donors is in the minority.

Human parvovirus B19 in Chinese pooled plasmas and plasma derivatives

In China, all the plasma for manufacturing into plasma derivatives are collected from plasma donors. The plasma recovered from the whole blood collected from blood donors are not allowed for manufacturing. Data about the prevalence of B19V in Chinese plasma donors are lacking. However, the prevalence of B19V in plasma donors seems to be similar to that in blood donor population. Han et al. compared the prevalence of B19V between plasma donors and blood donors, and results showed that the prevalence of B19V DNA was 0.06% in blood donors and 0.079% in source plasma donors, respectively and there was no significant difference between them (58).

There are 29 manufacturers for plasma derivatives in China. NAT screening of source plasma pools for B19V has not yet been implemented in the manufacturing. According to the reports listed in Table 3, there were great differences among the positive rates of industrial plasma pools in China, ranging from 5.45% (9/165) (59) to 100% (10/10) (64). Such diversities are likely to reflect geographic differences in the circulation of B19V in diverse parts of China, methodological differences in screening procedures, differences in sample size, or differences in number of plasma units within each pool sample.

Table 3

The prevalence of B19V DNA in plasma donors, plasma pool samples for fractionation, and plasma derivatives

Study author and year of publication Prevalence of B19V DNA
Plasma donors Plasma pools F VIII PCC IVIG Fibrinogen Thrombin Albumin
Wu Y, 2009 (64) 100% (10/10) 75% (12/16)
Hou JF, 2012 (65) 0.09% (6/6,505) 82.41% (89/108) 67.86% (38/56) 78.79% (26/33) 0 (0/84) 45.83% (11/24)
Zhang W, 2012 (66) 54.23% (77/142) 54.29% (19/35)b 70.59% (12/17)b 6.45% (10/155)a, 38.9% (21/54)b 85.71% (6/7)b 30% (3/10)a, 0 (0/50) b
Zheng RB, 2015 (59) 5.45% (9/165) 7.41% (4/54) 10.34% (6/58) 0(0/55) 5.66% (3/53)
Han T, 2015 (58) 0.04% (2/5,040)
Zeng FX, 2015 (67) 0.03% (3/10,150) 23.73% (14/59) 0 (0/4)c, 0 (0/16) 0 (0/4)c, 0 (0/15)
Jia JT, 2015 (68) 59.49% (116/195) 93.55% (29/31) 88.89% (8/9) 100% (10/10) 85.71% (6/7)
Jia JT, 2015 (34) 71.91% (169/235)

a, samples collected in the period 1993–1995; b, samples collected in the period 2009–2011; c, samples were produced from pooled plasma with B19V DNA positive plasma pools sample.

In previous reports, we investigated the prevalence and genotypic characterization of B19V in plasma pools used in the manufacture of plasma derivatives. By using an in-house qPCR assay for simultaneous detection of all three genotypes of B19V, 71.91% (169/235) of plasma pools were confirmed to be contaminated by B19V DNA, with the concentrations of 5.18×102–1.05×109 IU/mL. Approximately 31.95% of the B19V DNA-positive samples were <104 IU/mL, while 68.05% contained >104 IU/mL (34). Further phylogenetic analysis of B19V DNA derived from source plasma pool samples showed that there were B19V 1a, 1b and 3b, putative 1a/3b recombinants and unclassified strains circulating in China (23).

Because of the resistance of B19V to most viral inactivation procedures used in manufacturing of plasma derivatives, B19V DNA can always be detected in various plasma derivatives, particularly in coagulation factors.

Table 3 summarizes the prevalence of B19V DNA in Chinese plasma derivatives. In most reports, factor VIII, prothrombin complex concentrate (PCC), fibrinogen and thrombin were found to be highly contaminated with B19V DNA, with the prevalence rates of 54.29–93.55%, 70.59–88.89%, 45.83–100%, and 85.71%, respectively. However, an extremely lower prevalence in factor VIII, PCC, and fibrinogen produced by 2 manufactures located in South China has been reported by Zheng et al. This unexpected finding might be attributed to the lower prevalence of B19V DNA in these regions (59).

Intravenous immunoglobulin (IVIG) and albumin are comparatively safe, and B19V DNA is less frequently detected in these products and, when detected, the levels are usually low. In Zhang W’s study, low levels of B19V DNA were detected in 3 of 10 batches of albumin produced during 1993 to 1995, while no B19V DNA was detected in 50 batches of albumin produced during 2009 to 2011. For IVIG, although the ratio of B19V DNA positive IVIG produced during 2009 to 2011 was significantly higher than that produced during 1993 to 1995, IVIG were moderately contaminated with low levels of B19V DNA (66).

Future and perspective

Despite the frequent detection of B19V DNA in blood donors and pooled plasmas, as well as plasma derivatives, there is no suspected transfusion-transmitted B19V infections in China. This could be explained by the fact that most recipients already have B19V specific antibodies due to previous infections and that many B19V DNA-positive plasma derivatives were also positive for the presence of B19V specific antibodies, resulting in neutralization of the virus. Another possible explanation is that B19V infections were underreported, because many of the infections are clinically inapparent, or because the role of B19V infection in the etiology of some diseases was not recognized. Thus, the risk for B19V transmission through blood and plasma derivatives in China should not be neglected.

Despite abundant data regarding the prevalence of B19V in Chinese blood donors and plasma derivatives have been reported, continued evaluation of the incidence and genotypic characterization of B19V are also required to support decision making on whether limit for blood and plasma derivatives should be proposed in China.

In the case of blood, it might cost much time and money to test all blood donors for the presence of B19V. According to Netherland’s measure (33), a less expensive option is the risk-group approach, in which “B19V safe” blood would only be given to those patients for whom infection with B19V would pose a serious health risk. Adoption of this differentiated approach would obviate the need to test all blood donors for infection with B19V.

In the case of plasma derivatives, the implementation of a universal B19V NAT screening as an in-process test for source plasma is highly recommended. If the introduction of screening for B19V is under consideration or required by a national authority regulating blood program, it is necessary to establish a cutoff level for screening. In addition, since the co-existence of B19V 1a, 1b and 3b, as well as putative B19V 1a/3b recombinants in Chinese plasma donations, B19V NAT assay used in the manufacturing of plasma derivatives must be able to detect all B19V variants circulating in China.


Funding: This work was funded by the National Natural Science Foundation of China (NSFC) (Grant No. 81570169), Beijing Municipal Natural Science Foundation (Grant No. 7132144 and 7162147), and National High-tech R&D Program of China (863 Program) (Grant No. 2012AA021902).


Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See:


  1. Cossart YE, Field AM, Cant B, et al. Parvovirus-like particles in human sera. Lancet 1975;1:72-3. [Crossref] [PubMed]
  2. Young NS, Brown KE. Parvovirus B19. N Engl J Med 2004;350:586-97. [Crossref] [PubMed]
  3. Brown KE. The expanding range of parvoviruses which infect humans. Rev Med Virol 2010;20:231-44. [Crossref] [PubMed]
  4. Juhl D, Hennig H. Parvovirus B19: What Is the Relevance in Transfusion Medicine? Front Med (Lausanne) 2018;5:4. [Crossref] [PubMed]
  5. Cotmore SF, Tattersall P. Characterization and molecular cloning of a human parvovirus genome. Science 1984;226:1161-5. [Crossref] [PubMed]
  6. Shade RO, Blundell MC, Cotmore SF, et al. Nucleotide sequence and genome organization of human parvovirus B19 isolated from the serum of a child during aplastic crisis. J Virol 1986;58:921-36. [PubMed]
  7. Ozawa K, Ayub J, Kajigaya S, et al. The gene encoding the nonstructural protein of B19 (human) parvovirus may be lethal in transfected cells. J Virol 1988;62:2884-9. [PubMed]
  8. Raab U, Beckenlehner K, Lowin T, et al. NS1 protein of parvovirus B19 interacts directly with DNA sequences of the p6 promoter and with the cellular transcription factors Sp1/Sp3. Virology 2002;293:86-93. [Crossref] [PubMed]
  9. Servant A, Laperche S, Lallemand F, et al. Genetic diversity within human erythroviruses: identification of three genotypes. J Virol 2002;76:9124-34. [Crossref] [PubMed]
  10. Toan NL, Duechting A, Kremsner PG, et al. Phylogenetic analysis of human parvovirus B19, indicating two subgroups of genotype 1 in Vietnamese patients. J Gen Virol 2006;87:2941-9. [Crossref] [PubMed]
  11. Parsyan A, Szmaragd C, Allain JP, et al. Identification and genetic diversity of two human parvovirus B19 genotype 3 subtypes. J Gen Virol 2007;88:428-31. [Crossref] [PubMed]
  12. Gallinella G. Parvovirus B19 Achievements and Challenges. ISRN Virol 2013;2013:898730 [Crossref]
  13. Hübschen JM, Mihneva Z, Mentis AF, et al. Phylogenetic analysis of human parvovirus b19 sequences from eleven different countries confirms the predominance of genotype 1 and suggests the spread of genotype 3b. J Clin Microbiol 2009;47:3735-8. [Crossref] [PubMed]
  14. Bock CT, Duchting A, Utta F, et al. Molecular phenotypes of human parvovirus B19 in patients with myocarditis. World J Cardiol 2014;6:183-95. [Crossref] [PubMed]
  15. Nguyen QT, Wong S, Heegaard ED, et al. Identification and characterization of a second novel human erythrovirus variant, A6. Virology 2002;301:374-80. [Crossref] [PubMed]
  16. Grabarczyk P, Kalinska A, Kara M, et al. Identification and characterization of acute infection with parvovirus B19 genotype 2 in immunocompromised patients in Poland. J Med Virol 2011;83:142-9. [Crossref] [PubMed]
  17. Corcioli F, Zakrzewska K, Rinieri A, et al. Tissue persistence of parvovirus B19 genotypes in asymptomatic persons. J Med Virol 2008;80:2005-11. [Crossref] [PubMed]
  18. Hokynar K, Soderlund-Venermo M, Pesonen M, et al. A new parvovirus genotype persistent in human skin. Virology 2002;302:224-8. [Crossref] [PubMed]
  19. Candotti D, Danso K, Parsyan A, et al. Maternal-fetal transmission of human parvovirus B19 genotype 3. J Infect Dis 2006;194:608-11. [Crossref] [PubMed]
  20. Sanabani S, Neto WK, Pereira J, et al. Sequence variability of human erythroviruses present in bone marrow of Brazilian patients with various parvovirus B19-related hematological symptoms. J Clin Microbiol 2006;44:604-6. [Crossref] [PubMed]
  21. Jain P, Jain A, Prakash S, et al. Prevalence and genotypic characterization of human parvovirus B19 in children with hemato-oncological disorders in North India. J Med Virol 2015;87:303-9. [Crossref] [PubMed]
  22. Rinckel LA, Buno BR, Gierman TM, et al. Discovery and analysis of a novel parvovirus B19 Genotype 3 isolate in the United States. Transfusion 2009;49:1488-92. [Crossref] [PubMed]
  23. Jia J, Ma YY, Zhao X, et al. Existence of various human parvovirus B19 genotypes in Chinese plasma pools: genotype 1, genotype 3, putative intergenotypic recombinant variants and new genotypes. Virol J 2016;13:155. [Crossref] [PubMed]
  24. Ekman A, Hokynar K, Kakkola L, et al. Biological and immunological relations among human parvovirus B19 genotypes 1 to 3. J Virol 2007;81:6927-35. [Crossref] [PubMed]
  25. Chen Z, Guan W, Cheng F, et al. Molecular characterization of human parvovirus B19 genotypes 2 and 3. Virology 2009;394:276-85. [Crossref] [PubMed]
  26. Anand A, Gray ES, Brown T, et al. Human parvovirus infection in pregnancy and hydrops fetalis. N Engl J Med 1987;316:183-6. [Crossref] [PubMed]
  27. Broliden K. Parvovirus B19 infection in pediatric solid-organ and bone marrow transplantation. Pediatr Transplant 2001;5:320-30. [Crossref] [PubMed]
  28. Jordan J, Tiangco B, Kiss J, et al. Human parvovirus B19: prevalence of viral DNA in volunteer blood donors and clinical outcomes of transfusion recipients. Vox Sang 1998;75:97-102. [Crossref] [PubMed]
  29. Anderson MJ, Higgins PG, Davis LR, et al. Experimental parvoviral infection in humans. J Infect Dis 1985;152:257-65. [Crossref] [PubMed]
  30. Anderson LJ, Tsou C, Parker RA, et al. Detection of antibodies and antigens of human parvovirus B19 by enzyme-linked immunosorbent assay. J Clin Microbiol 1986;24:522-6. [PubMed]
  31. Sakata H, Matsubayashi K, Ihara H, et al. Impact of chemiluminescent enzyme immunoassay screening for human parvovirus B19 antigen in Japanese blood donors. Transfusion 2013;53:2556-66. [Crossref] [PubMed]
  32. Schmidt M, Themann A, Drexler C, et al. Blood donor screening for parvovirus B19 in Germany and Austria. Transfusion 2007;47:1775-82. [Crossref] [PubMed]
  33. Health Council of the Netherlands. Blood Products and Parvovirus B19. Health Council of the Netherlands: The Hague, 2002; publication no. 2002/07E.
  34. Jia J, Ma YY, Zhao X, et al. Prevalence of human parvovirus B19 in Chinese plasma pools for manufacturing plasma derivatives. Virol J 2015;12:162. [Crossref] [PubMed]
  35. Geng Y, Wu CG, Bhattacharyya SP, et al. Parvovirus B19 DNA in Factor VIII concentrates: effects of manufacturing procedures and B19 screening by nucleic acid testing. Transfusion 2007;47:883-9. [Crossref] [PubMed]
  36. Guidance for industry: nucleic acid testing (NAT) to reduce the possible risk of parvovirus B19 transmission by plasma-derived products. U.S. Department of Health and Human Services, Food and Drug Administration, Center for Biologics Evaluation and Research. July 2009. Available online:
  37. Human anti-D immunoglobulin. European Pharmacopoeia (version 5.0). France 2015:1732-3.
  38. Human plasma (pooled and treated for virus inactivation). European Pharmacopoeia (version 5.0). France 2005:1747-8.
  39. QSEAL NAT Testing Standard (Version 2.0). The PPTA QSEAL Standards Committee. June 2013. Available online:
  40. Baylis SA. Standardization of nucleic acid amplification technique (NAT)-based assays for different genotypes of parvovirus B19: a meeting summary. Vox Sang 2008;94:74-80. [PubMed]
  41. Modrow S, Wenzel JJ, Schimanski S, et al. Prevalence of nucleic acid sequences specific for human parvoviruses, hepatitis A and hepatitis E viruses in coagulation factor concentrates. Vox Sang 2011;100:351-8. [Crossref] [PubMed]
  42. Cai DB, Guo L, Xian BP, et al. Human parvovirus B19 infection in blood donors. Guangdong Med 1999;20:661-2.
  43. Ke L, He M, Li C, et al. The prevalence of human parvovirus B19 DNA and antibodies in blood donors from four Chinese blood centers. Transfusion 2011;51:1909-18. [Crossref] [PubMed]
  44. Hou Y, He M, Chen LM. A study of rates of human parvovirus B19 cytomegalovirus and herpes simplex virus among Chinese blood donors. 2016:29-40. Available online:
  45. He M, Zhu J, Yin H, et al. Human immunodeficiency virus/human parvovirus B19 co-infection in blood donors and AIDS patients in Sichuan, China. Blood Transfus 2012;10:502-14. [PubMed]
  46. Fan JP, Lin L, Li SC, et al. Epidemiological investigation of human parvovirus B19 in 6 provinces and cities in China. 2011:195-6. Available online:
  47. Qing WF, Liao HM, Tan QQ, et al. Study on the infection status of human parvovirus B19 among unpaid blood donors in Chongqing. Chongqing Med 2015;44:4969-71.
  48. Zhou YJ, Zhang Y, Xu XL, et al. Prevalence of human herpesvirus 8 cytomegalovirus and parvovirus B19 infection among unpaid blood donors. Chin J Nosocomiol 2017;27:514-6.
  49. Bao HE, Yang BJ, Pan XY, et al. A survey of human parvovirus B19 prevalence among blood donors in Three Gorges Region. J Clin Hematol 2015;28:289-90.
  50. Zheng YR, Li ZP, Liang HJ, et al. Analysis of human parvovirus B19 infection and viral load in blood donors in Guangzhou. Chin J Blood Transfusion 2009;22:550-1.
  51. Yan JX, Wu WJ, Zhou JX, et al. Human parvovirus B19 detection in voluntary blood donors of foshan city. Int J Lab Med 2016;37:1039-43.
  52. Guo J, Yu HL, Liu YB, et al. HPV B19, HBV, HCV and HGV infection among blood donors of Yao ethnic group in Guangdong. J Trop Med 2014;14:1431-2.
  53. Ou SH, Xie JZ, Zhang YL, et al. Prevalence of parvovirus B19 infection in Chinese Xiamen area blood donors. Zhongguo Shi Yan Xue Ye Xue Za Zhi 2016;24:1572-6. [PubMed]
  54. Li SQ, Yan YS, Chen R, et al. Serological investigation on human parvovirus B19 infections in Fujian. Strai J Prev Med 2000;6:1-2.
  55. Wang ZX, Zhou BB, Zhang N, et al. Research on human parvovirus B19 infection among blood donors in Jining. J Pub Health Prev Med 2015;26:4-6.
  56. Wei Q, Li Y, Wang JW, et al. Prevalence of anti-human parvovirus B19 IgG antibody among blood donors in Jilin province. Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi 2006;20:60-2. [PubMed]
  57. Zheng YR, Li ZP, Liang HJ, et al. Investigation on the infection of human parvovirus B19 in blood donors In Guangzhou. Mod Hospi 2008;8:14-5.
  58. Han T, Li C, Zhang Y, et al. The prevalence of hepatitis A virus and parvovirus B19 in source-plasma donors and whole blood donors in China. Transfus Med 2015;25:406-10. [Crossref] [PubMed]
  59. Zheng RB, Yu Y. Testing and analysis of human bocavirus B19 gene in blood products. Chin Med Sci 2015;5:151-2.
  60. Yang ZX, He HJ, Dai F, et al. Investigation on HPV B19 infection in 110 blood donors. J Huazhong Univ Sci Tech 2003;32:344-5.
  61. Wang R, Wu MH, Xue M, et al. Analysis of the results of PCR screening for human parvovirus B19 in blood donors. Jiangsu Health Care 2002;4:14.
  62. Li BD, Xie SG, Ning Y. The status investigation of blood donors who infect the human parvovirus B19 in Linyi City. Med Lab Sci Clin 2010;21:58-60.
  63. Zhang NH, Du ZL, Zhao YH, et al. Epidemiological investigation of the human parvovirus B19 among part blood donors in LuXi region of Shandong. Mod Prev Med 2009;36:17-8.
  64. Wu Y, Geng YS, Wang JZ, et al. Preliminary study on the contamination and genotype of human parvovirus B19 in Chinese blood products. Chin J Microbiol Immunol 2009;29:1031-4.
  65. Hou JF, Wang M, Ma QP. Determination of human parvovirus B19 DNA in source plasma and blood products. Chin J Biol Prod 2012;25:1043-4.
  66. Zhang W, Ke L, Li CQ, et al. Parvovirus B19V DNA contamination in Chinese plasma and plasma derivatives. J Transl Med 2012;10:194. [Crossref] [PubMed]
  67. Zeng FX, He PD, Li YJ, et al. Investigation on the prevalence of human parvovirus B19 in raw plasma. Chin J Blood Transfusion 2015;28:162-4.
  68. Jia JT, Ma YY, Guo Y, et al. Contamination of human parvovirus B19 in source plasma and coagulation factor products. Mil Med Sci 2015;39:169-71.
doi: 10.21037/aob.2019.01.01
Cite this article as: Jia J, Zhang M, Ma Y, Zhang J. Human parvovirus B19 research concerning the safety of blood and plasma derivatives in China. Ann Blood 2019;4:2.

Download Citation