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. 2017 Sep 27;12(9):e0184929. doi: 10.1371/journal.pone.0184929

Table 1. Regression model for "time to rebound”.

Coeff P-value 95%CI-lower 95%CI-upper
Vaccine /placebo arm 1,228 0,103 -0,265 2,721
Disulfiram/ no disulfiram administration -0,075 0,919 -1,579 1,429
HLA protective / non- protective -0,429 0,551 -1,888 1,031
Viral Load pre cART 0,000 0,725 0,000 0,000
CD4 w0-STI -0,001 0,360 -0,003 0,001
Magnitude w0-STI
(SFC/106 PMBC)
0,000 0,762 0,000 0,000
Magnitude w12-STI
(SFC/106 PMBC)
0,000 0,572 0,000 0,000
Proviral DNA before vaccination
(HIV DNA copies/106 CD4 cells)
-0,003 0,029 -0,005 0,000
Residual Viremia baseline 0,094 0,650 -0,338 0,526
Number of gag HLA-associated escape mutations -0,926 0,751 -6,887 5,036

Regression model for the dependent variable "time to rebound” (weeks until detectable plasma viremia) was performed on all the individuals undergoing STI (n = 28) and including the following covariates: harboring protective HLA alleles (B*27, B*57 and B*51 (n = 14)), MVA-B vaccination (n = 19), magnitude of HIV-1 specific T cell responses at STI-start (n = 26) and after 12 weeks into STI (n = 24), disulfiram administration (n = 12), CTL virus adaptation (number of total Gag polymorphism and number of HLA-associated escape mutations in Gag) (n = 26), pre-HAART pVL (n = 25), CD4 cell counts (n = 28), residual viremia (n = 18) and levels of proviral HIV-1 DNA at the beginning of the study (n = 18). Coefficients and p-values are shown.