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. 2020 Jul 29;17:226. doi: 10.1186/s12974-020-01894-2

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — IFNAR1KO modifies the activity of functional, biological pathways affected by HIVgp120. Gene expression data obtained from RT² Profiler PCR Arrays were interrogated using Ingenuity Pathway Analysis (IPA) software to analyze neurotransmission-related biological pathways affected by HIVgp120 and IFNAR1 deficiency. Note that most pathways were predicted to be reduced in activity except for long-term potentiation in IFNAR1KO males. The dashed lines at 2 and − 2 on the axis for activation Z-score indicate the significance threshold for a predicted effect on the activity of the given pathway (*P < 0.05); n = 6 animals (3 males (a) and 3 females (b) per group/genotype (total n = 24 animals)