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Given that highly active antiretroviral therapy (HAART) has been demonstrated useful to restore immune competence in type-1 human immunodeficiency virus (HIV-1)-infected subjects, we evaluated the specific antibody response to influenza vaccine in a cohort of HIV-1-infected children on HAART so as to analyze the quality of this immune response in patients under antiretroviral therapy. Sixteen HIV-1-infected children and 10 HIV-1 seronegative controls were immunized with a commercially available trivalent inactivated influenza vaccine containing the strains A/H1N1, A/H3N2, and B. Serum hemagglutinin inhibition (HI) antibody titers were determined for the three viral strains at the time of vaccination and 1 month later. Immunization induced a significantly increased humoral response against the three influenza virus strains in controls, and only against A/H3N2 in HIV-1-infected children. The comparison of post-vaccination HI titers between HIV-1+ patients and HIV-1 negative controls showed significantly higher HI titers against the three strains in controls. In addition, post vaccination protective HI titers (defined as equal to or higher than 1:40) against the strains A/H3N2 and B were observed in a lower proportion of HIV-1+ children than in controls, while a similar proportion of individuals from each group achieved protective HI titers against the A/H1N1 strain. The CD4+ T cell count, CD4/CD8 T cells ratio, and serum viral load were not affected by influenza virus vaccination when pre- vs post-vaccination values were compared. These findings suggest that despite the fact that HAART is efficient in controlling HIV-1 replication and in increasing CD4+ T cell count in HIV-1-infected children, restoration of immune competence and response to cognate antigens remain incomplete, indicating that additional therapeutic strategies are required to achieve a full reconstitution of immune functions. COL0008639 COL0058784 COL0012444

A 5-month-old girl presented with symptoms of malnutrition and severe urinary tract infection, with signs of sepsis and acute renal failure: serum creatinine, 1.4 mg/dl. Both blood and urine cultures were positive for Escherichia coli, and antibiotic therapy was started. Severe, almost symmetrical, bilateral nephromegaly was evident on computed tomography (Figure 1). Voiding cystourethrography showed no urinary tract abnormalities. Bilateral renal biopsies were performed and bilateral malakoplakia was diagnosed. Malakoplakia is the result of a defect in macrophage function, causing impairment of bactericidal activity. The large macrophages that are present at sites of infection (von Hansemann cells) exhibit numerous secondary lysosomes containing partially digested organisms. Calcification of these lysosomes results in the formation of intracytoplasmic bodies called Michaelis–Gutmann bodies (Figure 2), considered pathognomonic of the disease. Renal parenchymal involvement may produce varying degrees of renal enlargement. Other relatively frequent described causes of massive bilateral non-cystic nephromegaly include renal infiltration by hematolymphoid diseases, nephroblastomatosis, megalocystic interstitial nephritis, xanthogranulomatous pyelonephritis, and other infections. At 6 months after diagnosis, the patient is well, but nephromegaly continues and her serum creatinine level is 0.7 mg/dl (creatinine clearance 33 ml/min). Prognosis of renal malakoplakia in children is variable: some patients recover completely, others develop end-stage renal disease, and others may die.