In some infants infected perinatally with HIV, a pattern of lymphocyte depletion develops that resembles the pattern in congenital thymic deficiency. Since HIV disease progresses rapidly in such infants, they may be candidates for early antiviral therapy and attempts at immune reconstitution.

The effect of human immunodeficiency virus (HIV)-induced thymic dysfunction (TD) on mortality was studied in 265 infected infants in the CDC Perinatal AIDS Collaborative Transmission Study. TD was defined as both CD4 and CD8 T cell counts below the 5th percentile of joint distribution for uninfected infants within 6 months of life. The 40 HIV-infected infants with TD (15%) had a significantly greater mortality than did the 225 children without TD (44% vs. 9% within 2 years). Infants with TD infected in utero had higher mortality than did those infected intrapartum (70% vs. 37% within 2 years), while no significant difference was noted between infants without TD with either mode of transmission. The TD profile was independent of plasma virus load. Virus-induced TD by particular HIV strains and the time of transmission are likely to explain the variation in pathogenesis and patterns of disease progression and suggest the need for early aggressive therapies for HIV-infected infants with TD.

These results suggest that higher immune activation in children contributes to higher viral loads, and that the level of pre-existent immune activation may have a role in determining which infants have detectable virus in peripheral blood at birth.

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The authors evaluated the lymphocyte subsets in eight children with the DiGeorge anomaly, compared with 48 age-matched control infants. Of particular interest was the finding that the percentage and number of CD5 þ B lymphocytes were decreased in seven of the eight cases. This observation may provide insight into thymic function and the interaction of the B and T cell systems in some forms of congenital and acquired immunodeficiencies.Dr A.J. Nahmias, Division of Pediatric Infectious Diseases, Epidemiology and Immunology, 69 Butler Street, SE, Atlanta, GA, 30303, USA INTRODUCTIONThe DiGeorge anomaly (DGA) results from a developmental field defect of the third and fourth pharyngeal pouches and includes thymic and parathyroid aplasia or hypoplasia, conotruncal heart defects and facial abnormalities [1][2][3][4]. There is considerable overlap in clinical features with other syndromes such as the velocardiofacial syndrome and conotruncal anomaly face [2]. Microdeletions of the chromosome 22q11 have been found in a significant proportion of these patients, although other genetic defects have also been associated with DGA [2,4]. The degree of thymic involvement in DGA varies greatly, with the more severe cases demonstrating marked decreases in CD4 þ and CD8 þ T lymphocyte counts and poor responses to mitogen and antigen in lymphocyte proliferation assays [1][2][3].We describe here the marked decrease noted in the number of CD5 þ B lymphocytes found in the blood of children with DGA, suggesting significant interaction between CD5 þ B lymphocytes and the thymus or thymus-derived T cells. PATIENTS AND METHODSEight patients aged from 10 days to 24 months were diagnosed with severe DGA at our paediatric clinics from 1991 to 1997. The characteristics of the patients are similar to those described by others [1][2][3][4]. Briefly, all patients were lymphopenic, hypocalcaemic, and had congenital heart defects of the conotruncus; five of them had consistent facial dysmorphology, and in four the thymus was noted to be absent at surgery; in the other four this information is lacking. In the five patients in whom fluorescent in situ hybridization (FISH) studies were performed, a 22q11 deletion was found. None of the patients had received a blood product transfusion in the 2 months before their blood samples were obtained. Forty eight healthy children, followed at our paediatric clinics, served to provide age-adjusted normal values for the various lymphoid cell subsets (informed consent obtained).A whole-blood staining technique was used to determine peripheral blood mononuclear cell subpopulations by two-colour immunofluorescence, as described previously [5]. A single laser FACScan flow cytometer (Becton-Dickinson), which discriminates forward and right-angle light scatter, was used with appropriate software package (SimulSET Becton-Dickinson). Lymphocytes were gated using CD45, and approximately 10,000 events were counted. The lymphocyte subset counts were calculated based on their percentage and the total lymphocyte count. The ...