To determine the distribution of major blood lymphocyte subsets we evaluated blood lymphocytes by flow cytometry in adenovirus‐infected infants aged 30–730 d. In addition, interleukin‐1‐receptor antagonist, interleukin‐10 and transforming growth factor‐β1 were measured in serum by enzyme‐linked immunosorbent assay. According to clinical parameters, mechanical ventilation and outcome, infections were classified as moderate (n= 15), severe (n= 11) and fatal (n= 12). Controls were 13 healthy children. In severe and fatal infection, T cells (CD5+/CD19‐), NK effectors (CD16+), CD4+ T subset and B1 subset of B lymphocytes (CD5+/CD19+) were all significantly decreased. CD8+ cells were decreased in severe but not fatal cases. There was no difference in serum values of interleukin‐10; however, fatal cases had high interleukin 1‐receptor antagonist values. Interestingly, patients with moderate infection showed significantly increased values of transforming growth factor‐β1. These results demonstrate that life‐threatening adenoviral infection is associated with marked abnormalities in blood lymphocyte and cytokine profile.
Epidemiological and clinical findings from 1162 serologically confirmed measles cases occurring in Buenos Aires, Argentina in 1997 and 1998 were retrospectively reviewed. From 90 hospitalized children, measles virus was detected by direct RT-PCR from nasopharyngeal secretions. Patients were grouped as follows: (i) not vaccinated: infants < 12 months; (ii) regularly vaccinated: children 1-4 years not covered by the last catch-up; (iii) catch-up vaccinated: patients 5-19 years immunized during the 1993 campaign. Most cases were recorded in non-vaccinated infants (54%), and the lowest in catch-up vaccinated children (16%). Mean age of the 90 hospitalized children was 11.3 months. Pneumonia was the major hospitalization cause followed by pneumonitis. Two children required intensive care and one died. The 1993 catch-up campaign seemed to reduce the number of cases in the 5- to 19-year-old group. Lack of timely follow-up probably led to the accumulation of susceptible individuals allowing measles re-emergence. Direct viral detection by RT-PCR proved to be a sensitive tool for molecular epidemiology surveillance.
To determine the distribution of major blood lymphocyte subsets we evaluated blood lymphocytes by flow cytometry in adenovirus-infected infants aged 30-730 d. In addition, interleukin-1-receptor antagonist, interleukin-10 and transforming growth factor-beta1 were measured in serum by enzyme-linked immunosorbent assay. According to clinical parameters, mechanical ventilation and outcome, infections were classified as moderate (n = 15), severe (n = 11) and fatal (n = 12). Controls were 13 healthy children. In severe and fatal infection, T cells (CD5+/CD19-), NK effectors (CD16+), CD4+ T subset and B1 subset of B lymphocytes (CD5+/CD19+) were all significantly decreased. CD8+ cells were decreased in severe but not fatal cases. There was no difference in serum values of interleukin-10; however, fatal cases had high interleukin 1-receptor antagonist values. Interestingly, patients with moderate infection showed significantly increased values of transforming growth factor-beta1. These results demonstrate that life-threatening adenoviral infection is associated with marked abnormalities in blood lymphocyte and cytokine profile.
Subacute sclerosing panencephalitis (SSPE) is a neurodegenerative disorder due to persistent measles virus infection, with high level of measles-specific antibodies in cerebrospinal fluid (CSF). To analyze whether such response arises from a TH2-biased response, the authors determined TH1 (interferon [IFN]-gamma) and TH2 (interleukin [IL]-4 and IL-10) cytokines in CSF, taken at diagnosis, of eight SSPE patients (median age, 57.5 month, range 42 to 76 months). All patients presented IL-10 (median 29.3 pg/ml, range 4.3 to 162 pg/ml), but not IL-4 (<10 pg/ml); only one case showed IFN-gamma (162 pg/ml). These results are consistent with a TH2 bias or with a local, anti-inflammatory or neuroprotective mechanism involving IL-10.
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