Natural viral suppressors of HIV-1 have a unique capacity to maintain gammadelta T cells.
OBJECTIVE
To evaluate Vgamma2Vdelta2 T cells in a group of HIV-infected patients who suppress HIV replication without antiretroviral therapy (natural viral suppressors, NVSs).


METHODS
: It is a cross-sectional study.


METHODS
We compared Vgamma2Vdelta2 T-cell frequency, T-cell repertoire, and responses to isopentenyl pyrophosphate stimulation between NVSs (n = 21) and HIV-uninfected controls (n = 27) and between NVSs and HIV-infected patients taking HAART with suppressed viral replication (HIV-P; n = 25).


RESULTS
NVSs had a mean frequency of 1.06 +/- 0.82% CD3Vdelta2+ cells among total lymphocytes, which was significantly higher than both control groups (HIV-negative: 0.50 +/- 0.53%, P = 0.042; HIV-P: 0.34 +/- 0.37%, P = 0.002). The proportion of Vgamma2 chains correlating with the Vgamma2-Jgamma1.2 rearrangement was reduced among NVSs compared with HIV-negative controls (0.57 +/- 0.06 vs. 0.32 +/- 0.04; P = 0.016) but was increased compared with HIV-P patients (0.32 +/- 0.04 vs. 0.22 +/- 0.03; P = 0.03). NVSs had a similar baseline frequency of CD27/CD45RA effector cells (19.6 +/- 4.2%) compared with HIV-negative controls (20.8 +/- 12.9%; P = 0.35).


CONCLUSIONS
The altered gammadelta T-cell receptor repertoire among NVS was consistent with the known effect of HIV-1 on these cells. Uniquely among all HIV-infected groups, NVS reconstituted the gammadelta T-cell population, eventually reaching levels significantly above controls. This capacity to recover gammadelta T-cell numbers and function distinguishes individuals who control HIV-1 with and without HAART.
Riedel
David J
DJ
Division of Infectious Diseases, Institute of Human Virology, University of Maryland School of Medicine, 725 W.Lombard Street, Baltimore, MD 21201, USA.
Sajadi
Mohammad M
MM
Armstrong
Cheryl L
CL
Cummings
Jean-Saville
JS
Cairo
Cristiana
C
Redfield
Robert R
RR
Pauza
C David
CD
D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D019002:CD56 Antigen / Q000097:blood; D002478:Cells, Cultured; D003430:Cross-Sectional Studies; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy / Q000235:genetics / Q000276:immunology* / Q000821:virology*; D020276:HIV Long-Term Survivors; D015497:HIV-1 / Q000502:physiology*; D015235:HLA-B Antigens / Q000235:genetics; D045782:Hemiterpenes / Q000276:immunology; D006801:Humans; D017493:Leukocyte Common Antigens / Q000097:blood; D008213:Lymphocyte Activation / Q000276:immunology; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D009943:Organophosphorus Compounds / Q000276:immunology; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000032:analysis*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000097:blood; D014779:Virus Replication
D019002:CD56 Antigen; D015235:HLA-B Antigens; C103707:HLA-B57 antigen; D045782:Hemiterpenes; D009943:Organophosphorus Compounds; D016692:Receptors, Antigen, T-Cell, gamma-delta; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7; C004809:isopentenyl pyrophosphate; D017493:Leukocyte Common Antigens