Immunologic Targets of HIV Infection: T Cells

Autor: K Shah, P. Boyer, Ic Hanson, S Heaton, M Mchugh, Philip LaRussa, R Settlage, Sa Raphael, L Gragg, Steven D. Colan, We Berdon, G Johnson, S. Kaplan, O. Williams, R Doroshow, J Pitt, R Hirschhorn, Er Cooper, Jp Johnson, Douglas S. Moodie, R Elashoff, St Treves, S Fikrig, D Sanders, Welton M. Gersony, Jg Rigaperez, B Fyfe, E Singleton, Ki Li, C Lapin, R Sterba, Ss Bakshi, A Nahmias, A Mehta, Ram Yogev, R Dische, D Kearney, Kenneth McIntosh, L Taber, Ellen R. Cooper, Hw Lischner, Hw Berendes, C Acantilado, Lm Quittell, Yvonne J. Bryson, Johanna Goldfarb, Larry K. Pickering, Ryan Martin, Marilyn Doyle, R Miller, James M. Boyett, E J Orav, Y Alkhatib, B Baetzgreenwalt, F Bierman, Gerald J. Beck, Meyer Kattan, C Kozinetz, J Rosen, Antonio R. Perez-Atayde, Hh Peavy, Tn Denny, Bernard Gonik, Ruth Tuomala, S Steinbach, Ellen G. Chadwick, A Petru, W.T. Shearer, K Rich, P Edelson, J Bethel, C Marboe, C Diaz, Lm Mofenson, Mc Wu, H Keyserling, Steven E. Lipshultz, H Houser, A Hohn, Bp Wood, C Baker, A Kalica, Robert H. Schwartz, W Cranley, Stephen I. Pelton, Ac Koumbourlis, P Alderson, E Garciatrias, T Rakusan, Andrew A. Colin, D Chen, Claude Kasten-Sportes, S Nesheim, Meb Wohl, A Ludomirsky, Robert H. Cleveland, Tn Hansen, R Hawkins, M Bamji, J Chow, A Garson, A Rubinstein, Hal B. Jenson, Ic Guerrahanson, John Moye, G Demmler, Ej Abrams, W Moore, Cv Sumaya, Schluchter, Anne Willoughby, K Hoots, D Valacer, H Hammill, Robert P. Nugent, R Jacobson, Jlc Santini, [No Value] Boechat, S. Durako, Hm Rosenblatt, S Pahwa, M Garg, M Dyson, W Fleishman, K Krasinski, M Woo, N Ayers, Mw Kline, C Jordan, Moulay Meziane, W Henley, C Langston, T Bricker, Robert B. Mellins, Thomas J. Starc, L Bernstein, E Jimenez, A Platzker, C Weinstein, Rhoda S. Sperling, L Frenkel, Kirk Easley, P Hiatt, [No Value] Bonagura, C Vriem
Rok vydání: 1993
Předmět:
Zdroj: Annals of the New York Academy of Sciences. 693:35-51
ISSN: 1749-6632
0077-8923
DOI: 10.1111/j.1749-6632.1993.tb26255.x
Popis: One of the principal targets of HIV infection is the human peripheral blood CD4+ T cell, resulting in progressive CD4+ lymphocyte loss. Hypothesized mechanisms for this loss include apoptosis, cytolytic reactions, V-beta gene deletion of the T-cell receptor (TCR) by superantigens, CD4+ lymphocyte syncytium formation, and autoimmune reactions. In adults with HIV infection, the critical decline in CD4+ lymphocyte number that heralds the onset of AIDS-defining conditions is well characterized, whereas in infants and children the critical level of CD4+ cells predisposing to the development of AIDS-defining conditions or mortality is not fully characterized, due to an incomplete knowledge of CD4+ lymphocyte number and changes with age in normal and HIV-infected children. In a prospective study of 317 infants born to HIV-infected women, early results show that the monthly change in absolute CD4+ lymphocyte number over a 3- to 9-month period in HIV-infected infants was -109 cells/mm3 per month, at least double the rate of decline measured in HIV-noninfected infants in the study or that calculated from normal infants' values reported in the literature. In other clinical studies in HIV-infected infants and children, it was possible to study the effect of low CD4+ cell counts on clinical status and mortality. In HIV-infected pediatric patients younger than 1 year, it was possible to correlate low CD4+ cell number with advanced disease status (CDC pediatric class P-2). It was also possible to correlate extremely low CD4+ cell counts (< 200 cells/mm3) in HIV-infected children with a significant risk of mortality within the next 3 months of life. Sequential CD4+ cell analysis of HIV-high-risk infants will delineate the rate of HIV-related decline in CD4+ cells, thus facilitating the diagnosis of HIV infection and aiding in identification of HIV-infected children at high risk of disease progression or death.
Databáze: OpenAIRE
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