作者: John Zaunders , Wayne B. Dyer , Melissa Churchill , C Mee Ling Munier , Philip H. Cunningham
DOI: 10.1016/S2055-6640(20)30056-X
关键词: Long terminal repeat 、 Antibody 、 Biology 、 CD8 、 Peripheral blood mononuclear cell 、 Genotype 、 T cell 、 Virology 、 Viral load 、 Epitope
摘要: Abstract Background Subject C135 is one of the members Sydney Blood Bank Cohort, infected in 1981 through transfusion with attenuated nef/3′ long terminal repeat (LTR)-deleted HIV-1, and has maintained undetectable plasma viral load steady CD4 cell count, absence therapy. Uniquely, combines five factors separately associated control viraemia: nef/LTR-deleted HLA-B57, HLA-DR13, heterozygous CCR5 Δ32 genotype vigorous p24-stimulated peripheral blood mononuclear (PBMC) proliferation. Therefore, we studied detail burden immunological responses this individual. Methods PBMC gut lymph node biopsy samples were analysed for proviral HIV-1 DNA by real-time nested PCRs, nef/LTR alleles PCR. HIV-specific antibodies Western blotting, CD4+ CD8+ T lymphocyte measured proliferation cytokine production vitro. Results from 1996, but not since, showed amplification nef gross deletions. Infectious was never recovered. Proviral detected recent or samples. a consistently weak antibody response substantial proliferative to previously described HLA-DR13-restricted epitope p24 vitro, which augmented an immunodominant HLA-B57-restricted p24, while his cells show reduced levels CCR5. Conclusions C135's early PCR results are consistent limited infection poorly replicating strain HIV-1. With gag-specific CD8 helper responses, appears have cleared 37 years after transfusion.