Research
Mechanisms of HIV non-progression; robust and sustained CD4+ T-cell proliferative responses to p24 antigen correlate with control of viraemia and lack of disease progression after long-term transfusion-acquired HIV-1 infection
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* Corresponding author: Wayne B Dyer wdyer@arcbs.redcross.org.au
1 Australian Red Cross Blood Service, 153 Clarence Street, Sydney, NSW 2000, Australia
2 Transfusion Medicine and Immunogenetics Research Unit, Central Clinical School, Faculty of Medicine, University of Sydney, Sydney, NSW, Australia
3 Centre for Immunology, St. Vincent's Hospital and University of NSW, Sydney, NSW, Australia
4 Retroviral Genetics Division, Centre for Virus Research, Westmead Millennium Institute, University of Sydney, Sydney, NSW, Australia
5 National Serology Reference Laboratory, St Vincent's Institute, Melbourne, VIC, Australia
6 Department of Microbiology and Immunology, University of Melbourne, Parkville, VIC, Australia
7 Centre for Virology, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, VIC, Australia
8 Department of Medicine, Monash University, Melbourne, VIC, Australia
Retrovirology 2008, 5:112 doi:10.1186/1742-4690-5-112
Published: 11 December 2008Additional files
Additional File 1:
Clinical status of the study subjects. ¶LTNP cohort identified in 1994, consisting of the SBBC and "cohort 2" non-progressors. ‡SBBC members. * Data current at 1/1/2008, or at time of death. §Antiretroviral therapy (date commenced). ΔGenotypes associated with slow disease progression are indicated in bold font, increased disease progression by bold italic font. TLR polymorphisms: TLR2 753 Arg/Gly; TLR4 299 Asp/Gly; TLR4 399 Thr/Ile. wt (wild type, or default genotype).
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Additional File 2:
Sequential T cell reactivity (indicated by X) detected by INF-γ ELISPOT against HIV-1 Gag T cell epitopes (identified by responses at intersecting peptide pools). Sequential T cell reactivity (indicated by X) detected by INF-γ ELISPOT against HIV-1 Gag T cell epitopes (identified by responses at intersecting peptide pools) throughout the study period in living non-progressors (A) C49, (B) C64, (C) C13, (D) C53, (E) in a deceased SBBC non-progressor with low viraemia (C18), and (F) in a deceased Cohort 2 non-progressor who lost viral control (C122). Individual peptides were tested on PBMC from at least one time point per recipient, and the magnitude of responses reported as spot forming cells/106 PBMC, with limit of detection at 50 (<).
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