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In Argentina, more than 3 million people suffer from asthma, with numbers rising. When asthma patients acquire viral infections which, in turn, trigger the asthmatic response, they may develop subsequent bacterial infections, mainly by Streptococcus (S.) pneumoniae. This encapsulated Gram+ bacterium has been considered historically a T cell-independent antigen. Nevertheless, several papers describe the role of T cells in the immune response to S. pneumoniae. We evaluated the response to S. pneumoniae and compared it to the response to Mycobacterium (M.) tuberculosis, a different type of bacterium that requires a T helper type 1 ( Th1) response, in cells from atopic asthmatic children, to compare parameters for the same individual under exacerbation and in a stable situation whenever possible. We studied asthma patients and a control group of age-matched children, evaluating cell populations, activation markers and cytokine production by flow cytometry, and cytokine concentration in serum and cell culture supernatants by enzyme-linked immunosorbent assay ( ELISA). No differences were observed in γδ T cells for the same patient in either situation, and a tendency to lower percentages of CD4+ CD25hi T cells was observed under stability. A significantly lower production of tumour necrosis factor ( TNF)-α and a significantly higher production of interleukin ( IL)-5 was observed in asthma patients compared to healthy individuals, but no differences could be observed for IL-4, IL-13 or IL-10. A greater early activation response against M. tuberculosis, compared to S. pneumoniae, was observed in the asthmatic patients' cells. This may contribute to explaining why these patients frequently acquire infections caused by the latter bacterium and not the former. [ABSTRACT FROM AUTHOR]

Background The aim of this study is to show that human T-cell lymphotropic virus type 2 (HTLV-2) infection produces symptoms resembling those described for HTLV-1-associated myeloneuropathy and to highlight the role of sexual transmission in the silent dissemination of HTLV-2. Methods Patient samples were tested by particle agglutination and indirect immunofluorescence assay. The HTLV type was defined by molecular techniques. Nucleotide sequence analysis of HTLV-2 long terminal repeat region, T cell CD3/CD4 and T cell CD3/CD8 counts and typing of human leucocyte antigen (HLA) alleles A, B, C and DRB1 were also performed. Results HTLV-2 subtype b infection was confirmed in two blood donors and their sexual partners. Two patients exhibited distinctive signs and symptoms of progressive neurological disease. Three infected patients carried HLA-C*04. Both patients with neurological disease also carried HLA-A*31 and HLA-DRB1*07 alleles. Conclusions Herein we describe for the first time sexual transmission of HTLV-2 in a non-endemic region of Argentina, highlighting the relevance of this transmission route in HTLV-2 silent dissemination out of the clusters of endemicity. We also provide evidence that HTLV-2 infection causes symptoms resembling those described for HTLV-1-associated myeloneuropathy. The evidence presented herein points to the critical need for public health strategies to reduce the spread of this neglected infection. [ABSTRACT FROM AUTHOR]