Differential gene expression of soluble CD8+ T-cell mediated suppression of HIV replication in three older children.
Suppression of human immunodeficiency virus (HIV) replication by CD8+ T-cells (CD8 suppression) contributes to survival in adults and children <1 year. Soluble CD8 suppression can also be seen in some older children with AIDS. The factor responsible, CD8-derived antiviral factor (CAF), acts at the level of HIV RNA transcription. Differential gene expression techniques have been used to define the gene(s) mediating this phenomenon in adults. Recently, CAF has been linked to exosomes secreted by CD8+ T-cells. To compare the gene expression profiles from pediatric patients with each other, with those reported in 2 previous studies in adults and in those reportedly related to exosomes, we used differential gene expression to study three older children with HIV infection, one who did demonstrate soluble CD-8 suppression and two who did not. Eighteen differentially expressed genes were also seen in one adult study (P = 0.002, χ(2) test), and 38 such genes (P < 0.0001, χ(2) test) in a second adult study. In addition, two exosome components and some RNA's related to exosomal proteins were also differentially expressed. In children with HIV infection, we found significant differentially expressed genes that correlated to those previously reported in two studies in adults. Our data also lends some support to the recent identification of CAF with exosomes secreted by CD8+ T-cells.
Department of Pediatrics, Northwestern University Feinberg School of Medicine and Children's Memorial Hospital, Chicago, Illinois 60614, USA. bkatz@northwestern.edu
Ben Z
BZ
Katz
Babak
B
Salimi
Samantha L
SL
Gadd
Chiang-Ching
CC
Huang
William J
WJ
Kabat
Donna
D
Kersey
Chris
C
McCabe
Taylor
T
Heald-Sargent
Elyssa D
ED
Katz
Ram
R
Yogev
D000293:Adolescent; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002648:Child; D055354:Exosomes / Q000201:enzymology / Q000276:immunology; D020869:Gene Expression Profiling; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D008297:Male; D014158:Transcription, Genetic; D014779:Virus Replication