Occurrence Of Human Immunodeficiency Virus Type I (HIV-I)-Specific Cytolytic T Cell Activity In Apparently Uninfected Children Born To HIV-1-Infected Mothers

Maria, Andrea De; Cirillo, C.; Moretta, Lorenzo

doi:10.1093/infdis/170.5.1296

Cited by 134 publications

(64 citation statements)

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“…Previous studies by our group and others in perinatal HIV-exposed infants have reported evidence of HIV-specific immune response (4,(18)(19)(20)(21)(22)(23)(24)(25). HIV-specific immune response has also been observed in exposed noninfected adults (26)(27)(28)(29).…”

Section: Discussionsupporting

confidence: 53%

Imbalance of naive and memory T lymphocytes with sustained high cellular activation during the first year of life from uninfected children born to HIV-1-infected mothers on HAART

Ono

Santos

Succi

et al. 2008

Braz J Med Biol Res

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The immune consequences of in utero HIV exposure to uninfected children whose mothers were submitted to highly active antiretroviral therapy (HAART) during gestation are not well defined. We evaluated 45 HIV-exposed uninfected (ENI) neonates and 45 healthy unexposed control (CT) neonates. All HIV-infected mothers received HAART during pregnancy, and the viral load at delivery was <50 copies/mL for 56.8%. Twenty-three ENI neonates were further evaluated after 12 months and compared to 23 unexposed healthy age-matched infants. Immunophenotyping was performed by flow cytometry in cord and peripheral blood. Cord blood lymphocyte numbers did not differ between groups. However, ENI neonates had a lower percentage of naive T cells than CT neonates (CD4+, 76.6 vs 83.1%, P < 0.001; CD8+, 70.9 vs 79.6%, P = 0.003) and higher percentages of central memory T cells than CT neonates (CD4+, 13.9 vs 8.7%, P < 0.001; CD8+, 8.6 vs 4.8%, P = 0.001). CD38 mean fluorescence intensity of T cells was higher in ENI neonates (CD4+, 62.2 vs 52.1, P = 0.007; CD8+, 47.7 vs 35.3, P < 0.001). At 12 months, ENI infants still had higher mean fluorescence intensity of CD38 on T cells (CD4+, 34.2 vs 23.3, P < 0.001; CD8+, 26.8 vs 19.4, P = 0.035). Despite effective maternal virologic control at delivery, HIV-exposed uninfected children were born with lower levels of naive T cells. Immune activation was present at birth and remained until at least 12 months of age, suggesting that in utero exposure to HIV causes subtle immune abnormalities.

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Section: Discussionsupporting

confidence: 53%

Imbalance of naive and memory T lymphocytes with sustained high cellular activation during the first year of life from uninfected children born to HIV-1-infected mothers on HAART

Ono

Santos

Succi

et al. 2008

Braz J Med Biol Res

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“…Those studies suggest that ␤-chemokines are synthesized by normal CD8 ϩ T cells that have a CTL effector phenotype. Thus, it is possible that ␤-chemokines contribute to the correlations between CTL and the reduction of viral loads (14)(15)(16)(17)(18) or protection against infection with HIV-1 (19)(20)(21)(22).…”

mentioning

confidence: 99%

Perforin-low memory CD8⁺cells are the predominant T cells in normal humans that synthesize the β-chemokine macrophage inflammatory protein-1β

Kamin-Lewis

Abdelwahab

Trang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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The synthesis of antiviral ␤-chemokines has joined cytolysis as a potential mechanism for the control of HIV-1 infection by CD8 ؉ T cells. Recent evidence suggests that these two effector functions can diverge in some individuals infected with HIV-1; however, little is known about the CD8 ؉ T cell subsets in normal individuals that synthesize antiviral ␤-chemokines. In this report, we have used mutliparameter flow cytometry to characterize the T cell subsets that secrete the antiviral ␤-chemokine macrophage inflammatory protein (

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“…There are also some individuals who remain seronegative despite high risk and/or multiple exposures to HIV-1. These exposed seronegatives (ES) include infants born to HIV-1 infected mothers [5][6][7], commercial sex workers in epidemic areas [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25], hemophiliacs who received HIV contaminated factor VIII preparations [26,27], and sexual partners of known HIV-1 infected persons [28][29][30][31][32][33]. Understanding the mechanisms that account for slower disease progression in LTNP and the protection against HIV-1 infection observed with ES is important for the development of more potent therapeutic regimens and a vaccine.…”

Section: Introductionmentioning

confidence: 99%

Global human genetics of HIV-1 infection and China

et al. 2005

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Occurrence Of Human Immunodeficiency Virus Type I (HIV-I)-Specific Cytolytic T Cell Activity In Apparently Uninfected Children Born To HIV-1-Infected Mothers

Cited by 134 publications

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Imbalance of naive and memory T lymphocytes with sustained high cellular activation during the first year of life from uninfected children born to HIV-1-infected mothers on HAART

Imbalance of naive and memory T lymphocytes with sustained high cellular activation during the first year of life from uninfected children born to HIV-1-infected mothers on HAART

Perforin-low memory CD8⁺cells are the predominant T cells in normal humans that synthesize the β-chemokine macrophage inflammatory protein-1β

Global human genetics of HIV-1 infection and China

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Occurrence Of Human Immunodeficiency Virus Type I (HIV-I)-Specific Cytolytic T Cell Activity In Apparently Uninfected Children Born To HIV-1-Infected Mothers

Cited by 134 publications

References 0 publications

Imbalance of naive and memory T lymphocytes with sustained high cellular activation during the first year of life from uninfected children born to HIV-1-infected mothers on HAART

Imbalance of naive and memory T lymphocytes with sustained high cellular activation during the first year of life from uninfected children born to HIV-1-infected mothers on HAART

Perforin-low memory CD8+cells are the predominant T cells in normal humans that synthesize the β-chemokine macrophage inflammatory protein-1β

Global human genetics of HIV-1 infection and China

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Perforin-low memory CD8⁺cells are the predominant T cells in normal humans that synthesize the β-chemokine macrophage inflammatory protein-1β