{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T16:03:53Z","timestamp":1768320233580,"version":"3.49.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2017,2,3]],"date-time":"2017-02-03T00:00:00Z","timestamp":1486080000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1"},{"start":{"date-parts":[[2017,2,3]],"date-time":"2017-02-03T00:00:00Z","timestamp":1486080000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:p>Hepatic steatosis (HS) is common in individuals with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections, but the independent contributions of HCV and HIV to HS are unclear. Magnetic resonance imaging and spectroscopy were used to measure visceral adipose tissue (VAT) and liver fat fraction (LFF) (total lipids\/[total lipids\u2009+\u2009water]) in 356 adults: 57 with HCV monoinfection, 70 with HIV\/HCV coinfection, 122 with HIV monoinfection, and 107 with neither infection. Participants who were infected with HCV genotype 3 were excluded because of the genotype's reported steatogenic effects. For prevalence estimates, HS was defined as LFF\u2009\u2265\u20090.05. We estimated the association of HIV and HCV status with LFF using multivariable linear regression, adjusting for demographics, lifestyle, and metabolic factors including the homeostasis model assessment estimate of insulin resistance (HOMA\u2010IR) and liver fibrosis defined using the aspartate aminotransferase\u2010to\u2010platelet ratio index (APRI). The prevalence of HS was highest in the uninfected (33%) and HIV\u2010monoinfected (28%), followed by the HCV\u2010monoinfected (19%) and HIV\/HCV\u2010coinfected (11%) (<jats:italic toggle=\"yes\">P<\/jats:italic>\u2009=\u20090.003 across groups). Compared with uninfected participants\u2014and after adjusting for demographics, lifestyle, and metabolic factors\u2014HIV monoinfection, HCV monoinfection, and HIV\/HCV coinfection were associated with 19% (95% confidence interval [CI], \u221239% to 6%), 38% (95% CI, \u221255% to \u221212%), and 42% (95% CI, \u221259% to \u221218%) lower LFF, respectively. HCV monoinfection and HIV\/HCV coinfection remained strongly associated with lower LFF after further adjusting for APRI, and results were unchanged after excluding subjects with suspected cirrhosis. Among the entire cohort, Hispanic ethnicity, male sex, VAT, and HOMA\u2010IR were independently associated with greater LFF.<jats:italic toggle=\"yes\">Conclusion<\/jats:italic>: Contrary to expectations, HIV\/HCV\u2010coinfected and HCV\u2010monoinfected adults had significantly less liver fat than uninfected adults, even after adjusting for demographics, lifestyle, metabolic factors, and hepatic fibrosis. Our findings suggest that non\u2013genotype 3 HCV infection may be protective against HS. The mechanisms by which this occurs and the impact of HCV treatment on HS requires further investigation. (H<jats:sc>epatology<\/jats:sc>2017;65:853\u2010863)<\/jats:p>","DOI":"10.1002\/hep.28968","type":"journal-article","created":{"date-parts":[[2016,12,17]],"date-time":"2016-12-17T14:09:10Z","timestamp":1481983750000},"page":"853-863","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":26,"title":["Human immunodeficiency virus\u2013infected and uninfected adults with non\u2013genotype 3 hepatitis C virus have less hepatic steatosis than adults with neither infection"],"prefix":"10.1097","volume":"65","author":[{"given":"Jennifer C.","family":"Price","sequence":"first","affiliation":[{"name":"Department of Medicine,University of California,San Francisco,countryCode=\"US\" CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yifei","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Medicine,University of California,San Francisco,countryCode=\"US\" CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rebecca","family":"Scherzer","sequence":"additional","affiliation":[{"name":"Department of Medicine,University of California,San Francisco,countryCode=\"US\" CA"},{"name":"Medical Service, Department of Veteran Affairs Medical Center,San Francisco,CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Natalie","family":"Korn","sequence":"additional","affiliation":[{"name":"Department of Radiology and Biomedical Imaging,University of California,San Francisco,CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kyle","family":"Tillinghast","sequence":"additional","affiliation":[{"name":"Department of Radiology and Biomedical Imaging,University of California,San Francisco,CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marion G.","family":"Peters","sequence":"additional","affiliation":[{"name":"Department of Medicine,University of California,San Francisco,countryCode=\"US\" CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan M.","family":"Noworolski","sequence":"additional","affiliation":[{"name":"Department of Radiology and Biomedical Imaging,University of California,San Francisco,CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Phyllis C.","family":"Tien","sequence":"additional","affiliation":[{"name":"Department of Medicine,University of California,San Francisco,countryCode=\"US\" CA"},{"name":"Medical Service, Department of Veteran Affairs Medical Center,San Francisco,CA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","published-online":{"date-parts":[[2017,2,3]]},"reference":[{"key":"hep28968-bib-0001-20241017","doi-asserted-by":"crossref","first-page":"729","DOI":"10.1053\/jhep.2002.35064","article-title":"Steatosis in chronic hepatitis C: relative contributions of obesity, diabetes mellitus, and 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