Subject population clinical and virological characteristics.

a<p>CSF white blood cell counts.</p>b<p>AIDS dementia complex staging <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002286#ppat.1002286-Price1" target="_blank">[1]</a> conformed to the American Academy of Neurology criteria used at the time of diagnosis, and would also conform to current criteria for HAD diagnosis based on the degree of functional impairment in both cognitive and motor spheres. 0, neurologically asymptomatic; 1, mild neurological impairment; 2–3, moderate to severe HAD; U, uncertain ADC stage determination related to confounding conditions, see text for further discussion.</p>c<p>Mean change from baseline (score of 0.0) of a four-item quantitative neurological performance battery score.</p>d<p>Compartmentalized HIV-1 population phenotype. M-tropic, macrophage-tropic; T-tropic, R5 T cell-tropic; N/A, not applicable.</p>e<p>Half-life in days of total viral RNA decay in the CSF after the initiation of antiretroviral therapy. The decay rate is listed next to the sample date that was closest to the date when therapy was initiated. Data summarized from ref. <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002286#ppat.1002286-Schnell1" target="_blank">[20]</a>. Subject antiretroviral drug regimens and CNS penetration effectiveness rank calculations for drug regimens, and CSF-compartmentalized variant decay calculations are described in detail in ref. <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002286#ppat.1002286-Schnell1" target="_blank">[20]</a>.</p>

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