Additional file 4 of Estimation of delay to diagnosis and incidence in HIV using indirect evidence of infection dates

Comma-separated value file containing posterior covariance matrix for parameters of model fitted to the calibration dataset (without accounting for inter-lab variation in nucleotide ambiguity proportions). (CSV 52 kb

Additional file 1 of Estimation of delay to diagnosis and incidence in HIV using indirect evidence of infection dates

Supplementary Appendices. Contains further details of model specifications, computational notes, parameter summaries in the calibration dataset and examples of predictions in individual patients. (PDF 206 kb

Additional file 3 of Estimation of delay to diagnosis and incidence in HIV using indirect evidence of infection dates

Comma-separated value file containing posterior mean values for parameters of model fitted to the calibration dataset (without accounting for inter-lab variation in nucleotide ambiguity proportions). (CSV 4 kb

Additional file 5 of Estimation of delay to diagnosis and incidence in HIV using indirect evidence of infection dates

Stan model template file (which is annotated and can be viewed as plain text) to fit the ‘incidence and delay-to-diagnosis’ model with change in incidence prior to and during observation window. (STAN 17 kb

Change in viral load over time due to selection.

<p>The estimated log₁₀ change in viral load per year due to selection and environmental effects (see also <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004112#ppat.1004112.s002" target="_blank">Fig. S2</a>).</p

Estimates of viral genetic influence on set-point viral load in HIV subtype B in the UK.

<p>Estimates of viral genetic influence on set-point viral load in HIV subtype B in the UK.</p

The estimated node effect plotted onto the phylogeny.

<p>The estimated phylogenetic effect of each node on log₁₀ viral load plotted back onto the phylogeny from the 652-sample BEAST analysis. The axis shows the time in years from the most recent sequence, which was taken in 2009. Branches have been colored by the scale of the effect. Clusters of branches have been collapsed to improve readability, and are colored by the average tip effect within each cluster. As the number of bifurcations in the tree reduces at around 17.5 years before 2009, this used as the threshold for collapsing. Nodes that have a similar effect on viral load cluster together, as expected if some of the variation in viral load is heritable.</p

EBNA-1 sequence variation identified with next-generation sequencing technology, and impact on HLA-DRB1*15 binding affinity within known epitopes.

<p>The two most frequent variants for the A) AEG epitope and B) MVF epitope are printed in bold, the most frequent variant is underlined. All epitopes are predicted to be weak binders (affinity 50nM-500nM).</p

EBNA-1 quasispecies detected with FLX sequencing.

<p>Minority EBV sequence variants at a level of ≥10% were detected in two samples only. Sequence mixtures present at a ≥5% threshold revealed minority variants in 3.6% of investigated nucleotide positions (27/749 nucleotides sequenced,), increasing to 5.0% at a ≥2% cut-off (37/749 nucleotides,) and 8.3% at a ≥1% cut-off (62/749 nucleotides,). Samples 7, 8 and 13 did not have minority species present at ≥1%.</p

Extended axoglial brain protein dataset with HLA-DRB1*1501 predicted brain epitopes overlapping with predicted EBV binders.

<p>Extended axoglial brain protein dataset with HLA-DRB1*1501 predicted brain epitopes overlapping with predicted EBV binders.</p