Unique acquisition of cytotoxic T-lymphocyte escape mutants in infant human immunodeficiency virus type 1 infection

被引:37
|
作者
Pillay, T
Zhang, HT
Drijfhout, JW
Robinson, N
Brown, H
Khan, M
Moodley, J
Adhikari, M
Pfafferott, K
Feeney, ME
John, AS
Holmes, EC
Coovadia, HM
Klenerman, P
Goulder, PJR
Phillips, RE [11 ]
机构
[1] John Radcliffe Hosp, Nuffield Dept Med, Oxford, England
[2] Leiden Univ, Med Ctr, Dept Immunohaematol, Leiden, Netherlands
[3] Univ KwaZulu Natal, Dept Obstet & Gynaecol, Nelson R Mandela Med Sch, Durban, South Africa
[4] Univ KwaZulu Natal, Dept Paediat & Infant Hlth, Nelson R Mandela Med Sch, Durban, South Africa
[5] Massachusetts Gen Hosp, Partners AIDS Res Ctr, Boston, MA USA
[6] Massachusetts Gen Hosp, Ctr Infect Dis, Boston, MA USA
[7] Harvard Univ, Sch Med, Boston, MA USA
[8] Queen Elizabeth Hosp, Bridgetown, Barbados
[9] Univ Oxford, Dept Evolut Biol, Oxford, England
[10] Univ KwaZulu Natal, Ctr HIV & AIDS Networking, Durban, South Africa
[11] Univ Oxford, Peter Medawar Bldg Pathogen Res, Oxford OX1 9SY, England
关键词
D O I
10.1128/JVI.79.18.12100-12105.2005
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The role of cytotoxic T-lymphocyte (CTL) escape in rapidly progressive infant human immunodeficiency virus type 1 (HIV-1) infection is undefined. The data presented here demonstrate that infant HIV-1-specific CTL can select for viral escape variants very early in life. These variants, furthermore, may be selected specifically in the infant, despite the same CTL specificity being present in the mother. Additionally, pediatric CTL activity may be compromised both by the transmission of maternal escape variants and by mother-to-child transmission of escape variants that originally arose in the father. The unique acquisition of these CTL escape forms may help to explain the severe nature of some pediatric HIV infections.
引用
收藏
页码:12100 / 12105
页数:6
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