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Journal of Virology, September 2005, p. 12100-12105, Vol. 79, No. 18
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.18.12100-12105.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Unique Acquisition of Cytotoxic T-Lymphocyte Escape Mutants in Infant Human Immunodeficiency Virus Type 1 Infection{dagger}

Thillagavathie Pillay,1 Hua-Tang Zhang,1 Jan W. Drijfhout,2 Nicola Robinson,1 Helen Brown,1 Munira Khan,3 Jagadesa Moodley,3 Miriam Adhikari,4 Katja Pfafferott,1 Margaret E. Feeney,5 Anne St. John,6 Edward C. Holmes,7 Hoosen M. Coovadia,8 Paul Klenerman,1 Philip J. R. Goulder,1 and Rodney E. Phillips1*

The Peter Medawar Building for Pathogen Research and Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, United Kingdom,1 Department of Immunohaematology, Leiden University Medical Centre, Leiden, The Netherlands,2 Nelson R. Mandela Medical School, Department of Obstetrics and Gynaecology, University of Natal, Durban, South Africa,3 Nelson R. Mandela Medical School, Department of Paediatrics and Infant Health, University of Natal, Durban, South Africa,4 Partners AIDS Research Center and Infectious Disease Division, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts,5 Queen Elizabeth Hospital, Bridgetown, Barbados,6 Department of Evolutionary Biology, University of Oxford, Oxford, United Kingdom,7 Centre for HIV and AIDS Networking, University of Natal, Durban, South Africa8

Received 27 January 2005/ Accepted 24 May 2005

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.

* Corresponding author. Mailing address: University of Oxford, The Peter Medawar Building for Pathogen Research, OX1 3SY Oxford, United Kingdom. Phone: 44-1865-281880. Fax: 44-1865-281890. E-mail: rodney.phillips{at}ndm.ox.ac.uk.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, September 2005, p. 12100-12105, Vol. 79, No. 18
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.18.12100-12105.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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