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We investigated the role that erythroviruses (parvovirus B19 and erythrovirus genotypes 2 and 3) play in the lives of immunosuppressed HIV-infected patients with chronic anemia. We screened the serum samples of 428 patients by specific ultrasensitive real-time polymerase chain reaction assay. Sixteen patients had circulating DNA, with no apparent clinical impact. Erythrovirus-associated anemia is an extremely rare event in HIV-infected patients.

The presence of erythrovirus infections was investigated by PCR with bone marrow samples of patients with various parvovirus B19-related hematological symptoms. Erythrovirus DNA was found in 17.3% (12/69) of patients. Phylogenetic analysis revealed that five strains cluster with genotype 1, one clusters with genotype 2, and six cluster with genotype 3. Our study is the first to document the presence of the three erythrovirus genotypes in Brazil.

Introduction: Simian parvovirus (SPV) causes severe anemia in immunocompromised macaques. The closely related erythrovirus, parvovirus B19, causes anemia in susceptible humans and can be grown in human bone marrow mononuclear cells in vitro. We hypothesized that SPV may infect humans and replicate in human bone marrow mononuclear cells., Methods: Serum samples from handlers of an SPV-seropositive macaque colony were tested by Western blot for evidence of antibodies to SPV. SPV capsid protein was expressed in insect cells, and SPV was cultured in human and macaque bone marrow mononuclear cells., Results: Fifty-one percent of exposed handlers (n=65) were found to be SPV seropositive, compared with 35% of nonexposed individuals (n=124). In 17% of exposed handlers, compared with 6% of nonexposed individuals, antibodies were directed to SPV but not to B19. SPV capsid proteins, like those of B19, self-assembled to form parvovirus-like particles, and these capsids, like B19 capsids, bound to globoside, suggesting that globoside is also the receptor for SPV. We demonstrated that SPV could replicate in vitro in both human and macaque bone marrow mononuclear cells and that it was cytotoxic to erythroid progenitor cells., Conclusions: Our data suggest that SPV may infect human bone marrow mononuclear cells in vitro and in vivo and should be considered a potential zoonosis.

The presence of human erythrovirus DNA in 2,440 blood donations from the United Kingdom and sub-Saharan Africa (Ghana, Malawi, and South Africa) was screened. Sensitive qualitative and real-time quantitative PCR assays revealed a higher prevalence of persistent infection with the simultaneous presence of immunoglobulin G (IgG) and viral DNA (0.55 to 1.3%) than previously reported. This condition was characterized by a low viral load (median, 558 IU/ml; range, 42 to 135,000 IU/ml), antibody-complexed virus, free specific IgG, and potentially infectious free virus. Human erythrovirus genotype 1 (formerly parvovirus B19) was prevalent in the United Kingdom, Malawi, and South Africa. In contrast, only human erythrovirus genotype 3 (erythrovirus variant V9) was prevalent in Ghana. Genotype 3 had considerable genetic diversity, clustering in two probable subtypes. Genotype 1-based antibody assays failed to detect 38.5% of Ghanaian samples containing antibodies to genotype 3 virus but did not fail to detect cases of persistent infection. This study indicates a potential African origin of genotype 3 human erythrovirus and considerable shortcomings in the tools currently used to diagnose erythrovirus infection.

Objectives: To examine the potential association of human B19 or V9 erythrovirus infection and onset of ANCA-positive vasculitides., Methods: We tested the sera of 13 adults with newly diagnosed ANCA-positive vasculitides. Each was age- and sex-matched to three sera obtained from healthy controls. All samples were tested for B19- and V9-specific immunoglobulin (Ig) G and IgM antibodies (Ab) (third-generation ELISA), and B19 or V9 DNA was sought with the polymerase chain reaction. Statistical analysis was performed by conditional logistic regression., Results: Patient diagnoses comprised six cases of Wegener's granulomatosis, six of microscopic polyangiitis and one of Churg-Strauss syndrome. IgG Ab to B19 were detected equally in patient and control sera (77 and 79% respectively) (odds ratio=0.84, P=0.84). All 13 cases and 39 controls were negative for IgM Ab and viral DNA., Conclusion: These results suggest that neither acute nor chronic B19 or V9 infection is an aetiological factor in ANCA-associated vasculitides.

Erythrovirus (formerly parvovirus) B19 causes a wide range of diseases in humans, including anemia due to aplastic crisis. Diagnosis of B19 infection relies on serology and the detection of viral DNA by PCR. These techniques are usually thought to detect all erythrovirus field isolates, since the B19 genome is known to undergo few genetic variations. We have detected an erythrovirus (V9) markedly different from B19 in the serum and bone marrow of a child with transient aplastic anemia. The B19 PCR assay yielded a product that hybridized only very weakly to the B19-specific probe and whose sequence diverged more from those of 24 B19 viruses (11 to 14%) than the divergence found within the B19 group (