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Some studies have suggested altered<jats:styled-content style=\"fixed-case\">SMX<\/jats:styled-content>biotransformation in<jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>infection, but hepatic biotransformation pathways have not been evaluated directly. Systemic lupus erythematosus (<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>) is another chronic inflammatory disease with a higher incidence of sulfonamide<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>, but it is unclear whether retroviral infection and<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>share risk factors for drug<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>. We hypothesized that retroviral infection would lead to dysregulation of hepatic pathways of<jats:styled-content style=\"fixed-case\">SMX<\/jats:styled-content>biotransformation, as well as pathway alterations in common with<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>that could contribute to drug<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>risk. We characterized hepatic expression profiles and enzymatic activities in an<jats:styled-content style=\"fixed-case\">SIV<\/jats:styled-content>\u2010infected macaque model of retroviral infection, and found no evidence for dysregulation of sulfonamide drug biotransformation pathways. Specifically,<jats:italic><jats:styled-content style=\"fixed-case\">NAT<\/jats:styled-content>1<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">NAT<\/jats:styled-content>2<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C8<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C9<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">CYB<\/jats:styled-content>5R3<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">MARC<\/jats:styled-content>1\/2<\/jats:italic>, and glutathione\u2010related genes (<jats:italic><jats:styled-content style=\"fixed-case\">GCLC<\/jats:styled-content><\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">GCLM<\/jats:styled-content><\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">GSS<\/jats:styled-content><\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">GSTM<\/jats:styled-content>1<\/jats:italic>, and<jats:italic><jats:styled-content style=\"fixed-case\">GSTP<\/jats:styled-content>1<\/jats:italic>) were not differentially expressed in drug na\u00efve<jats:styled-content style=\"fixed-case\">SIV<\/jats:styled-content>mac239\u2010infected male macaques compared to age\u2010matched controls, and activities for<jats:styled-content style=\"fixed-case\">SMX<\/jats:styled-content><jats:italic>N<\/jats:italic>\u2010acetylation and<jats:styled-content style=\"fixed-case\">SMX<\/jats:styled-content>hydroxylamine reduction were not different. However, multiple genes that are reportedly over\u2010expressed in<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>patients were also up\u2010regulated in retroviral infection, to include enhanced immunoproteasomal processing and presentation of antigens as well as up\u2010regulation of gene clusters that may be permissive to autoimmunity. These findings support the hypothesis that pathways downstream from drug biotransformation may be primarily important in drug<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>risk in<jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>infection.<\/jats:p>","DOI":"10.1002\/prp2.312","type":"journal-article","created":{"date-parts":[[2017,4,27]],"date-time":"2017-04-27T03:36:45Z","timestamp":1493264205000},"source":"Crossref","is-referenced-by-count":1,"title":["Hepatic expression profiles in retroviral infection: relevance to drug hypersensitivity risk"],"prefix":"10.1002","volume":"5","author":[{"given":"Yat Yee","family":"Wong","sequence":"first","affiliation":[{"name":"Department of Medical Sciences School of Veterinary Medicine Madison Wisconsin"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brian","family":"Johnson","sequence":"additional","affiliation":[{"name":"Molecular and Environmental Toxicology Center School of Medicine and 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