Chapter 29 : Human Parvoviruses

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The family is divided into two subfamilies: the , which infect insects, and the , which infect vertebrates. The members of the that infect humans are the focus of this chapter. The parvoviruses known to infect humans include B19 parvovirus in the genus , adeno-associated viruses (AAVs) in the genus , human bocavirus (HBoV) in the genus , and PARV4 and PARV5, not yet placed into a genus. With the appropriate helper virus, AAVs can replicate in a variety of tissue culture systems. If a helper virus is not present, AAV integrates into the host cell genomic DNA in a site-specific fashion. Nosocomial transmission can, however, occur, and standard precautions are recommended for all B19-infected patients and droplet precautions are recommended for those most likely to have high-titer infection, i.e., those with chronic B19 infection and those with transient aplastic crisis. The occurrence of rash in an immunocompromised patient after treatment with immune globulin and again after the patient mounts an antibody response suggests that anti-B19 antibody is important to the pathogenesis of the rash. The majority of recent studies of AAVs and studies of PARV4 and PARV5 and HBoV have been based on a variety of PCR assays to detect the viral DNA. A serologic assay for HBoV has recently been described based on cloned expressed capsid proteins forming empty capsids.

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29

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Image of FIGURE 1

Phylogenetic relationships between NS genes of selected members of the subfamily Shown is an estimated-maximum-parsimony tree generated with PAUP* software showing clustering of different parvovirus genera and ungrouped parvoviruses. The parvoviruses that infect humans are indicated with lighter gray shading. aa, amino acids; AAV, adeno-associated virus; CMV, canine minute virus; BPV, bovine parvovirus; PPV, porcine parvovirus; KRV, Kilham rat virus; MPV, mouse parvovirus; LuIIIV, LuIII virus; RPV, rat parvovirus; CPV, canine parvovirus; MEV, mink enteritis virus; AMDV, Aleutian mink disease virus; MDPV, muscovy duck parvovirus; GPV, goose parvovirus; ChPV, chipmunk parvovirus; RmPV, rhesus macaque parvovirus; PmPV, pig-tailed macaque parvovirus. B19, V9, and A6 are human parvovirus B19 strains; PARV4 and PARV5 are human parvovirus strains.

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Image of FIGURE 2

Electron micrograph of B19 empty particles in a serum specimen from a patient with transient aplastic crisis. Magnification, ×170,000. (Courtesy of G. William Gary, CDC, Atlanta, GA.)

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Image of FIGURE 3

Schematic of B19 mRNA produced in erythroid progenitor cells. The thin line represents introns, and the thick line represents the nontranslated portion of exons. The solid boxes represent translated portions of exons. The numbers below the line indicate the start or end of the respective exon. All mRNAs are initiated at the same promoter (P6). The NS protein (first mRNA) is encoded in one reading frame; the 7.5-kDa, VP1, and VP2 proteins are encoded in a second reading frame (–1 relative to the NS protein); and the 11.0-kDa protein is encoded in the third reading frame. (Based on data from references and .)

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Image of FIGURE 4

Schematic of replication of B19 virion DNA. Replication is initiated at the 3′-terminal hairpin by host DNA polymerases and proceeds to form monomer duplex DNA and then dimer duplex DNA. The dimer duplex DNA is cleaved by cellular endonucleases into positive- and negative-sense single-stranded DNAs (ssDNAs), which are packaged with equal frequencies into B19 virions. (Reprinted from reference with permission of the American Association for the Advancement of Science.)

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Image of FIGURE 5

(A) Wright-Giemsa stain of a bone marrow aspirate from a patient with B19 infection. Note the giant pronormoblasts (arrow) with multiple vacuoles in the darkly stained (basophilic) cytoplasm, high nucleus-to-cytoplasm ratio, and prominent nucleoli. (B) Hematoxylin and eosin stain of bone marrow biopsy section from a patient with B19 infection. Note the prominent nuclear inclusions, marginated chromatin, and high nucleus-to-cytoplasm ratio in erythroid precursor cells (arrow). (C) Hematoxylin and eosin stain of placental tissue from a fetus that died with B19 infection. Note the ground-glass-appearing nuclear inclusions and marginated chromatin in erythroid precursor cells within fetal vessels. Magnifications, ×625. (All panels courtesy of Sherif R. Zaki, CDC, Atlanta, GA.)

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Image of FIGURE 6

Rates of B19 IgG antibody positivity by age. (Adapted from reference .)

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Image of FIGURE 7

Schematic of clinical and laboratory findings during the course of B19 infection in adult volunteers. Note the drop in reticulocyte (Retic) and platelet counts and the presence of symptoms (fever, myalgias, and malaise) associated with peak viremia (days 6 to 12). During this period, there is also a transient drop in neutrophil and lymphocyte counts. Associated with the drop in reticulocyte counts, there is a progressive drop in hemoglobin levels to about 90% of normal by days 14 to 16. The timing of the drop in hemoglobin levels corresponds to the time of anemia in patients with transient aplastic crisis. Note the second period of symptoms (rash, arthritis, and arthralgias) on days 18 to ≥22. This second period of illness corresponds to symptoms of erythema infectiosum. (Data from reference .)

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29
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Proteins of human parvovirus B19

Citation: Anderson L, Erdman D. 2009. Human Parvoviruses, p 645-661. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch29

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