Figures and data
Characteristics of study participants
Plasma viral load and total HIV DNA in acute treated and chronic treated individuals.
A) peak viral load and total HIV DNA measured at peak viral load in untreated (pre-therapy) and acute treated individuals B) longitudinal viral load and total HIV DNA in untreated acute infection and after 6 and 12 months of treatment C) longitudinal viral load and total HIV DNA in acute treated individuals D) viral load and total HIV DNA after 1 year of treatment in chronic and acute treated individuals.
Multivariate analysis of factors that predict total HIV-1 proviral DNA load after 1 year of treatment.
Genotypic characterisation of HIV-DNA sequences.
A) PBMC sequencing timepoints in untreated (red), chronic treated (green) and early treated (blue) study participants where each dot represents a sampling time point. Time of treatment initiation is shown by the vertical grey bar. B) Approximately-maximum-likelihood phylogenetic tree of intact HIV-1 DNA genomes constructed using FastTree2. This method was chosen to resolve full-viral-genome sequences with extreme homology; branch lengths were likely inflated. Viral genomes derived from acute treated participants are marked with (*). C) Comparison of intraparticipant mean pairwise distances between early and late treated participants. D) Spectrum of HIV genome sequences detected during untreated acute infection, late treated chronic infection, and acute treated infection.
Evolution of the proviral genetic landscape.
Relative proportions of intact and defective viral genomes measured longitudinally in A) untreated acute infection for 2 years B) late (chronic) treated infection for 1 year and C) early (acute) treated infection for 1 year. The number of genomes sampled at each time point is indicated above each vertical bar.
Decay kinetics of intact and defective proviruses.
Absolute frequencies of intact and defective HIV-1 DNA sequences per million PBMCs during the 1st year of infection following treatment during A) acute infection and B) chronic infection. Longitudinal analysis of the change in (C) intact and (D) defective provirus copies in the 6 months after ART initiation, comparing the acute treated (blue) and chronic treated (green) groups. Dots represent a measurement from a given participant; solid lines are slopes estimated from linear mixed effect model. (E) Comparison of the monthly rate of decay of intact and defective proviruses in acute and chronic treated infection.
Comparison of CTL epitope diversity in late compared to early treated participants.
Proportion of participants with wildtype, variant and CTL escape at baseline (within 1 month of infection) and up to 1 year of infection in Gag (A, D, G, J), Pol (B, E, H, K) and Nef (C, F, I, L) epitopes in participants with protective HLA genotypes (A, B, C, G, H, I) and without protective HLA genotypes ( D, E, F, J, K, L).
In this cohort of HIV-1 subtype C, genome deletions were most frequently observed between integrase and envelope relative to Gag (p<0.0001–0.001).
Clonal expansion of infected cells was detected in both defective (orange) and intact (blue) genomes in late and early treated study participants. This analysis was performed with all sequences available for each participant at all time points.
