Human parvovirus B19 (B19V) causes glomerulopathy or microangiopathy, but not tubulopathy. We experienced an 11-year-old girl with spherocytosis who developed acute kidney injury on a primary infection of B19V. She presented with anuria, encephalopathy, thrombocytopenia, and coagulopathy, along with no apparent aplastic crisis.

Continuous hemodiafiltration, immunoglobulin, and intensive therapies led to a cure.

A kidney biopsy resulted in a histopathological diagnosis of tubulointerstitial nephritis without immune deposits. The virus capsid protein was limitedly expressed in the tubular epithelial cells with infiltrating CD8-positive cells.

Viral and histopathological analyses first demonstrated B19-infected tubulointerstitial nephritis due to the aberrant viremia with hereditary spherocytosis.

Parvovirus B19 (B19V) and human bocavirus 1 (HBoV1), members of the large Parvoviridae family, are human pathogens responsible for a variety of diseases. For B19V in particular, host features determine disease manifestations. These viruses are prevalent worldwide and are culturable in vitro, and serological and molecular assays are available but require careful interpretation of results. Additional human parvoviruses, including HBoV2 to -4, human parvovirus 4 (PARV4), and human bufavirus (BuV) are also reviewed. The full spectrum of parvovirus disease in humans has yet to be established. Candidate recombinant B19V vaccines have been developed but may not be commercially feasible. We review relevant features of the molecular and cellular biology of these viruses, and the human immune response that they elicit, which have allowed a deep understanding of pathophysiology.

Reports of neurologic manifestations of human parvovirus B19 (B19) infection have been on the rise. Acute encephalitis and encephalopathy is the most common, accounting for 38.8% of total B19-associated neurological manifestations. To date, 34 children with B19 encephalitis and encephalopathy have been reported, which includes 21 encephalitis and 13 encephalopathy cases. Ten (29%) were immunocompromised and 17 (39%) had underlying diseases. Fever at the onset of disease and rash presented in 44.1% and 20.6% of patients, respectively. Neurological manifestations include alteration of consciousness occurred in all patients, seizures in 15 (44.1%) patients, and focal neurologic signs in 12 (35.3%) patients. Anemia and pleocytosis in cerebrospinal fluid (CSF) occurred in 56.3% and 48.1% of patients, respectively. Serum Anti-B19 IgM (82.6%) and CSF B19 DNA (90%) were positive in the majority of cases. Some patients were treated with intravenous immunoglobulins and/or steroids, although an accurate evaluation of the efficacy of these treatment modalities cannot be determined. Nineteen (57.6%) patients recovered completely, 11 (33.3%) patients had some neurological sequelae and 3 (8.8%) patients died. Although the precise pathogenesis underlying the development of B19 encephalitis and encephalopathy is unclear, direct B19 infection or NS1protein of B19 toxicity in the brain, and immune-mediated brain injuries have been proposed.

We investigated the incidence of human parvovirus B19 (HPV B19) infection after renal transplantation as well as the risk of anemia and renal allograft damage among infected transplant recipients in China.

We selected 114 patients at 1-18 months after renal transplantation for detection of HPV B19 DNA copies compared with a control population. Renal function and hematopoiesis were compared between infected and noninfected groups.

Twenty-seven patients diagnosed with HPV B19 infection during follow-up (18.75%),which was a significantly higher number than among the general population over the same period. Infected versus nonaffected patients exhibited a significantly higher incidence of anemia and urinary abnormalities in addition to significantly lower values of hemoglobin, higher serum creatinine concentrations, and lower glomerular filtration rates. The 2 groups did not differ in the types or doses of calcineurin inhibitor (CNI) immunosuppressants. Two cases of pure red cell aplasia (PRCA) as confirmed using bone marrow biopsy, were observed in the infected group. They displayed HPV B19 DNA copy numbers >10(7)/mL and segmental mesangial cell proliferation on renal biopsy. The PRCA cases were cured with immunomodulatory therapy.

The HPV B19 infection rate was significantly higher among renal transplant recipients than normal controls. Infections correlated with damage to the renal allograft, which may in turn cause PRCA. Immunomodulation therapy was effective to treat this complication of HPV B19 infection.