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INTRODUCTION: B19 virus (B19V) and bocavirus 1 (HBoV1) are human pathogenic parvoviruses that are prevalent worldwide and are responsible for a diverse and not yet fully established spectrum of clinical manifestations. OBJECTIVE: To screen B19V and HBoV1 in patients with clinical manifestations associated with acquisition of the infection during gestation. METHODS: A retrospective, observational study was performed that included serum samples from patients without a previous known aetiology. B19V and HBoV1 were determined by end-point PCR. Positive samples were genotyped. RESULTS: A total of 106 serum samples were analysed, 61 from pregnant women and 45 from neonates and paediatric patients. None were positive for HBoV1, while B19V was detected in 37/106 [34.9â%, 95â% confidence interval (CI): 26.5-44.4] of the samples studied. In the group of pregnant women, 28/61 (45.9â%, 95â% CI: 34.0-58.3) were B19V-positive, and 2 of them had foetal anaemia followed by hydrops and foetal death, 3 were associated with a history of recurrent pregnancy loss and there was 1 case of spontaneous abortion. B19V was also detected in cases of maternal febrile exanthema, polyhydramnios, oligohydramnios and foetal ascites. In the group of children, 9/45 (20.0â%, 95â% CI: 10.9-33.8) neonatal patients were B19V-positive, and this was associated with foetal hydrops, TORCH syndrome and cardiac alterations. The nucleotide sequences analysed confirmed the identity of B19V genotype 1. CONCLUSIONS: We found no evidence to indicate the presence of HBoV1 in maternal blood or in the newborns/paediatric patients (hence providing no support for the supposed vertical transmission). On the other hand, the high frequency of B19V in the pathologies studied indicates the importance of molecular diagnosis in both the mother and the child. Future efforts should contribute to early detection and characterization of infections.
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PURPOSE: Human parvovirus B19 (B19V) can cause anemia in immunocompromised patients. We aimed to investigate the presence of B19V in HIV+ adults with different CD4+ T cell counts, to recognise the frequency of B19V in these different conditions and its possible association with anemia. METHODOLOGY: We studied B19V specific IgM, IgG and DNA in 98 HIV+ patients and in 52 healthy individuals. HIV load, CD4+ counts and haemoglobin level were also determined in the patients. RESULTS: No individual in the control group had detectable IgM, 41/52 (78.8â%) had IgG and 5/52 (9.6â%) had B19V DNA. Among HIV+ patients, we found 5/98 (5.1â%) IgM+, 66/98 (67.3â%) IgG+ and 15/98 (15.3â%) had B19V DNA (no significant differences between the two groups compared). Considering the CD4+ cell range in HIV patients, 37 had <200 CD4+ cells ml-1, 31 had 200-500, and 30 had >500. Anti-B19V IgG prevalence in patients with >500 CD4+ cells ml-1 was significantly higher than in the rest (P=0.004) and compared to the control (P=0.046). B19V DNA concentration was always <103 IU ml-1, including 5 healthy individuals and 15 HIV+ patients. There was no significant association between B19V IgM or DNA and anemia nor between B19V DNA and HIV load. CONCLUSIONS: The results indicate that B19V is not a high-risk factor for anemia in adult HIV+ patients under HAART treatment. Further studies will contribute to elucidate the mechanisms and significance of B19V DNA prevalence/persistence in adults, independently of the CD4+ cell status.