[Role of cytokines and chemokines in the non-progression of HIV infection in vertically infected children].
BACKGROUND
To study the cytokine production in vertically HIV-1-infected children with more of 7 years of HIV infection and different pattern of progression.


METHODS
We study 32 HIV-1-infected children: 8 NA children (age > 7 years, asymptomatic or with light symptoms, without antiretroviral treatment and TCD4+ > 25%); 10 NE1 children (> 6 years, symptomatic, with antiretroviral treatment and TCD4+ > 25%); 14 NE2-3 children (> 6 years, symptomatic, with antiretroviral treatment and TCD4+ < 25%) and 16 (C) controls, children non-VIH+. The peripheral mononuclear cells of HIV-infected children (PBLs) were cultivated and cytokine production was quantified in the supernatant.


RESULTS
The non-stimulated PBMC from HIV-infected children produced more TNF-alpha and less IL-2 that C-group. The production of IFN-gamma was lower in the groups NE1 and NE2-3 than in C-group. The production of IFN-gamma was higher in group NA than in NE2-3. In the phytohaemagglutinin (PHA) stimulated PBLs, the production of TNF-alpha was higher in NA and NE1 than in controls. The production of IL-2 was similar in NA and NE1 than in controls. The production of IL-2 was similar in NA and NE1 than in control group, but the groups NE2-3 produced less IL-2 than control and NE1 groups. The production of IFN-gamma and RANTES were significantly higher in NA than in controls. The groups NE1 and NE2-3 produced lower levels of IL-5 than control and NA groups. The groups NE2-3 produced lower levels of IL-10 than control group. The ratio IFN-gamma/IL-5 and IFN-gamma/IL-10 were higher in group NA than in control and NE1.


CONCLUSIONS
In non-progressors HIV-infected children the immune response is conserved and we have observed an increased Th1 response, while in progressors HIV-infected children receiving antiretroviral treatment we could observe a diminished Th2 response. Moreover, our data clearly indicate that the decrease of IL-2 is an early marker of HIV-infection.
Resino
S
S
División de Inmunología, Hospital General Universitario Gregorio Marañón, Madrid.
Bellón
J M
JM
Jiménez
J L
JL
Gurbindo
M D
MD
Muñoz-Fernández
M A
MA
D000293:Adolescent; D002455:Cell Division; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000097:blood; D002648:Child; D018450:Disease Progression; D015658:HIV Infections / Q000097:blood / Q000276:immunology* / Q000635:transmission*; D006801:Humans; D018445:Infectious Disease Transmission, Vertical; D020382:Interleukin-18 / Q000097:blood; D007378:Interleukins / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D018946:Chemokine CCL5; D020382:Interleukin-18; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha