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. 2019 Dec 13;71(11):2858–2868. doi: 10.1093/cid/ciz1186

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© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Resistance gene richness (α-diversity) is significantly higher in cotrimoxazole-treated human immunodeficiency virus–exposed, uninfected (HEU) infants (CTX-T) compared to HEU infants not treated with cotrimoxazole (CTX-N). Points represent individual patient samples colored by treatment group (red for CTX-T infants and blue for CTX-N infants), and lines represent predictions of simple linear regression models for the 2 groups. The x-axis for each plot is the day of life for each infant calculated from their day of birth, and the y-axis is richness. Models were made for microbial taxa (A), functional pathways (B), resistance genes (C), and trimethoprim- and sulfonamide-resistance (dfr/sul) genes (D). Formulas for each linear mixed-effects model are reported above the plots, and these models were compared using likelihood-ratio tests to null models made without the cotrimoxazole treatment variable (CTX) included. The P values for these comparisons of linear mixed-effects models are reported at top left of each graph.