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• W2052393048 abstract "The article by Sharp and colleagues1 in this issue of TRANSFUSION reports the transmission of human parvovirus 4 (PARV4) by “virus-inactivated” plasma pool-derived clotting factors, demonstrating that infection by non–lipid membrane viruses continues to be a concern for persons with hemophilia and other recipients of such products.1 While the inactivation of lipid-enveloped viruses such as human immunodeficiency virus (HIV) and hepatitis C virus (HCV) by solvent/detergent and/or heating now used in the manufacture of plasma derivatives is highly effective, such treatments (at least as performed before 1992) were not sufficient to prevent the transmission of PARV4. Recipients of nonpooled (from a single or few donors), noninactivated blood products such as plasma or platelets, while at lower risk of receiving a PARV4-containing transfusion, must also be exposed to this recently characterized virus. B19V is the prototypic human parvovirus of concern for recipients of blood component transfusions and plasma derivatives. B19V is a known human pathogen capable of causing fetal hydrops and developmental abnormalities in children, arrest of erythropoiesis in patients with sickle cell anemia or hereditary spherocytosis, and chronic anemia in AIDS patients.2,3 The risk of B19V infection in high-risk recipients of pooled plasma derivatives (e.g., B19V-seronegative pregnant women, patients with chronic anemias, AIDS patients) is currently attenuated by removal of high-viral-load B19V donations (detected by low-sensitivity polymerase chain reaction [PCR] tests) from plasma pools.4,5 Plasma units with low titer of B19V are tolerated with the assumption that infectivity is neutralized in large plasma pools by the anti-B19V present in approximately half of adult donors. The high seroprevalence in the blood donor population results from childhood infections that cause the common minor childhood rash erythema infectiosum or slapped cheek syndrome. B19V transmission through whole blood–derived components, while rare,6 can cause symptoms in recipients;7 however, screening for B19V is not generally performed due to the low risk of transmission and rarity of serious outcomes.4,7,8 PARV4 was initially identified by viral metagenomic analysis of plasma from an injection drug user with symptoms related to those of primary HIV infection but who was found to be HIV RNA negative.9 Related viruses have since been found in chimpanzees,10 baboons,10 bats,11 sheep,12 pigs or boars,13,14 and cows,14 with genetic relationships among them that parallel the phylogeny of their host species consistent with long-term virus–host co-evolution.10 These viruses can be classified into a distinct genus within the Parvoviridae family with a proposed name of Partetravirus.12 Numerous studies have reported PARV4 DNA in human plasma for transfusion,15-18 in plasma pools for the production of blood derivatives,19,20 and in purified coagulation factors.21-23 Viral load, while typically low (often necessitating nested PCR for detection), but can also reach levels as high as 5 × 108 virions/mL during acute infection.24 Beside its detection in plasma, PARV4 has also been reported in marrow,25-27 liver,28 and skin29 as well as other organs.25 PARV4 infections have been reported in the United States,9 United Kingdom,15,16,21,27 Italy,25,26,29 France,30,31 Thailand,17 China,20,32 Ghana,33 Nigeria, and Congo.34 Similar to B19, genetic analyses have revealed the presence of three PARV4 genotypes differing in their amino acids by 2.7% to 2.9% in the nonstructural protein and 1.4% to 2% in their VP1 capsid proteins.33,34 As for B19, where one genotype (B19-gt3) is mostly limited to Africa, the distribution of the PARV4 genotypes also varies geographically with PARV4-gt3 so far restricted to sub-Saharan Africa.33,34 As for B19V,35 the DNA of the different genotypes of PARV4 can be amplified from human tissues even when undetectable in plasma.27,28 PARV4, similar to B19V,36-39 can also be frequently detected at very low level in plasma of immunocompetent subjects indicating that tail-end viremia may be produced for extended periods of time after primary infection.15,29,30 Persistent detection of parvoviral DNA in tissues may reflect ongoing low-level replication or the presence of highly stable viral nucleic acids within capsids deposited in the skin and other tissues.35 Sustained high titers of antibodies and high frequency of T cells responses to PARV4 are consistent with ongoing viral replication40 as previously reported for B19V.39 The genotypes of the B19V and PARV4 persisting in human tissues have also been shown to differ by age, with, for example, B19-gt2 confined to people born before 1973 while B19-gt1 now predominates in younger subjects.27,35 This phenomenon has been dubbed the “bioportfolio,” as it is thought to reflect a subject's prior infectious history.35 At the population level, the bioportfolio may result from epidemics of different parvovirus genotypes spreading in temporal waves, with virus becoming deposited for life in the tissues of contemporaneously infected populations.35 The limited genetic diversity within PARV4-gt1, which dominates in the younger European and US populations indicates that PARV4-gt1 may have been only recently introduced into these populations.41 It is well documented that highly infectious parvovirus can rapidly spread and infect new animal hosts worldwide, as happened with canine parvovirus 2 (CPV2) in the late 1970s and with subsequent CPV2 variants displacing earlier strains.42,43 Serologic assays for PARV4 have been developed and serosurveys have shown that infections in developed countries are strongly associated with HIV and HCV infections. The much higher prevalence observed specifically in injection drug users (IDUs) indicates that blood–blood contact is the principal cause of PARV4 transmission.17,26,27,32,44-47 Outside of Western countries, other parenteral transmission routes are suspected; for example, elderly Cameroonians are frequently seropositive for PARV4 but in this case infections were associated with injections of antimalarial drugs, streptomycin, or contraceptives.48 PARV4 was also shown to be transmitted through the placenta,49 and seropositivity was high in hemodialysis and hepatitis B virus–infected patients.31,32 Seroprevalence of past PARV4 infection was not higher in homosexuals who did not inject drugs than in heterosexuals in the same populations.41 It is possible that the current global distribution of PARV4 is a recent phenomenon associated with some of the same demographic factors that facilitated the spread of HIV and HCV.27,41,45 Blood-borne transmission is an unusual mode of transmission for parvoviruses, which are more typically transmitted by aerosol (e.g., B19V and HBoV1) or by the oral–fecal route for animal parvoviruses such as CPV2 (18, 44) and possibly for human HBoVs 2 to 4, which are detected almost exclusively in feces.50 HBoV1 also has a short viremic phase associated with respiratory symptoms.51 However, in contrast to the restriction of PARV4 infection to those exposed to parenteral routes of transmission in developed countries, PARV4 exposure was extremely high in the general population in several African countries (Cameroon, Burkina Faso, and Democratic Republic of Congo, respectively, showed PARV4 seroprevalence of 25, 37, and 35%), observations that strongly suggest a different mode of transmission.52 Furthermore, infants from Ghana showed a PARV4 viremia frequency of 8% (all gt3), higher in older than younger children indicative of a different mode of transmission.33 Although PARV4 can be transmitted through exposure to blood and plasma-derived products, whether this virus is a human pathogen that needs to be excluded from plasma pools or even nonpooled blood components remains uncertain. PARV4's original detection in an IDU with symptoms typical of many viral infections (fatigue, night sweats, pharyngitis, neck stiffness, vomiting, diarrhea, arthralgias, and confusion).9 Nested PCR testing of a larger set of such patients with related symptoms (suspected acute HIV infection but HIV RNA and antibody negative) showed a PARV4 DNA prevalence of 6%. Using the same nested PCR, 2% of healthy blood donors from California (a significantly lower prevalence) were also PARV4 DNA positive.15 The higher prevalence of PARV4 DNA in symptomatic individuals indicated that PARV4 infections may be pathogenic but could also simply reflect a higher rate of exposure to blood-borne viruses resulting in more frequent chronic viral infections including with PARV4. In the article by Sharp and colleagues,1 two of nine persons with hemophilia undergoing primary PARV4 infection showed exacerbation of their hepatitis. PARV4 was also detected in Taiwanese newborns with hydrops, where four of five mothers were positive for anti-PARV4 IgM and PARV4 gt2 DNA was found in four out of five newborns.49 Also worrisome was the detection of PARV4 using viral metagenomics in the cerebral spinal fluid of 2 of 12 Indian children with encephalitis of unknown etiology where one PARV4 DNA–positive patient tested was also anti-PARV4 IgM positive and IgG negative indicating a recent infection.53 Arguing against common and severe pathogenicity for PARV4 is the absence of recalled symptoms in two HCV-infected IDUs undergoing PARV4 seroconversion,54 and the frequent detection of PARV4 in healthy blood donors and plasma pools (all collected from nonfebrile, asymptomatic donors).15-17,19-22,29 The detection of PARV4 DNA in healthy children from Ghana also argues against severe symptomatic infection, at least in a large fraction of recently infected subjects.33 PARV4 is frequently detected in HCV and/or HIV-infected donors (1-8) and its impact on the pathologies caused by these coinfections has begun to receive attention. HCV infection outcome was not affected by PARV4 seropositivity.46 The emergence of early HIV-related symptoms was significantly associated with anti-PARV4 detection,46,55 although the large fraction of PARV4-HIV-HCV coinfections and injection drug usage in that group complicated a definitive link of PARV4 to HIV disease acceleration.46 It seems clear that blood product transfusions frequently expose recipients to highly prevalent viruses such as the ubiquitous and highly genetically diverse anelloviruses and the flavivirus GBV-C, resulting in chronic infections.56 Such transfusion events are tolerated because of the lack of demonstrated pathogenicity of these viruses and the very high frequency of viremic donors and for anelloviruses the recognition that nearly universal infection occurs in infants and young children.57,58 Although transfusion-transmitted B19V infections continue to occur from blood components, evidence of its pathogenicity led to the exclusion of high B19V titer donations from plasma pools used in the manufacture of derivatives. It took 6 years after its initial discovery in 197559 to uncover B19V's first association with disease when its role in causing hypoplastic crisis in sickle cell anemia was revealed.60,61 Potential disease associations for PARV4 currently include encephalitis,53 fetal hydrops,49 and hepatitis.1 Decisions on whether to initiate steps to reduce or exclude PARV4 from blood components and manufactured products are dependent on the outcome of future studies to investigate these links or reveal new ones. For example, epidemiologic studies of encephalitis could test unexplained cases for PARV4 DNA and anti-PARV4 to determine if recent seroconversions occurred at higher frequencies in cases versus matched controls. Similar studies could also be applied to individuals with unexplained fever or hepatitis and with chronic arthritis (a condition linked with B19V infection).62 Given its widespread distribution, it seems likely that any disease associations with PARV4 infection will be restricted to a small subset of highly susceptible individuals, perhaps those with overt immunologic deficiencies or genetic polymorphisms in innate and intrinsic viral defense pathways that are increasingly recognized as underlying much of the variability in outcomes of infectious diseases.63 Severe cases of PARV4-associated diseases may therefore benefit from in-depth host genetic analyses, particularly of loci associated with innate immune responses. There are no cell lines currently known to amplify PARV4. Quantitation of PARV4 infectivity in antibody-positive and -negative samples, after different virus-inactivating treatments used for the manufacture of plasma products or to generically inactivate all viruses in blood products for transfusion,64-66 therefore currently remains unfeasible. The ability to culture PARV4 or to express infectious particles for infectivity measurements would greatly facilitate PARV4 inactivation studies and determine its susceptibility to cross-neutralization by antibodies to different genotypes in plasma pools. For the immediate future PARV4 is likely to remain under suspicion as a potential etiologic agent for different symptoms in subsets of infected individuals. Determining what disease association exists, if any, and for what susceptible populations will determine whether costly measures testing and excluding PARV4-positive donations from the blood supplies should be implemented. Further progress in virus discovery will continue to yield previously unrecognized viral genomes whose risks to the safety of the blood supply will be initially unknown. The ability to rapidly test large numbers of banked blood samples or plasma pools for viral nucleic acids and antibodies in people of different age strata, geographic origins, and high levels of exposure to blood (IDUs, persons with hemophilia and thalassemia) will facilitate evaluation of the potential risks of these viruses to the safety of the blood supply. Coordination and collaborations between blood banks, clinical researchers, epidemiologists, and laboratory scientists worldwide will be required for a rapid and balanced response to the detection of novel blood-borne viruses.67-72" @default.
• W2052393048 created "2016-06-24" @default.
• W2052393048 creator A5073063058 @default.
• W2052393048 date "2012-07-01" @default.
• W2052393048 modified "2023-10-16" @default.
• W2052393048 title "Human parvovirus 4 in the blood supply and transmission by pooled plasma-derived clotting factors: does it matter?" @default.
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• W2052393048 doi "https://doi.org/10.1111/j.1537-2995.2012.03721.x" @default.
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