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  • Author contribution br Funding This work was supported by

    2022-01-13

    Author contribution
    Funding This work was supported by funding from St Vincent’s AMR. Hologic provided Panther equipment and Aptima HCV Quant Dx Viral Load assays. The sponsors had no rule in the analysis and interpretation of the study results, the manufacturer of reagents used in this study did not influence the study design, analysis of data or reporting of results. The Kirby Institute is funded by the Australian Government Department of Health and Ageing. NSW State Reference Laboratory for HIV, St Vincent’s Centre for Applied Medical Research and The Kirby Institute each receive funding from the Australian Government Department of Health and Ageing and the New South Wales Ministry of Health. The views expressed in this publication do not necessarily represent the position of the Australian Government. BC is supported by an Australian Postgraduate Award from UNSW Sydney and an Australian Government Research Training Program Scholarship provided by the Commonwealth Government. JG is supported by a National Health and Medical Research Council Career Development Fellowship (APP1112352). PL is a former employee of Hologic Australia. TA has received research grants from Abbott Diagnostics and travel grant from Cepheid. JG is a consultant/advisor and has received research grants from AbbVie, Bristol-Myers Squibb, Cepheid, Gilead Sciences and Merck/MSD.
    Acknowledgments
    Introduction Chronic hepatitis C virus (HCV) infection has emerged in the past two decades as a major cause of morbidity and mortality among persons living with the proteasome inhibitor (PLWH) in high-income countries [1]. HIV and HCV have overlapping modes of transmission, and in 2015 it has been estimated that 6.2% of the 36.9 million people living with HIV worldwide (i.e. approximately 2.3 million people) were coinfected with HCV [2]. Prevalence of HCV infection among persons with HIV varies in different population groups, being highest among in men who have sex with men (6.4%), and in injecting drug users (82.4%) [2]. Recently, it has been shown that treatment regimens including new direct acting antivirals (DAAs) can achieve high rates of sustained viral response also in HCV-HIV coinfected persons [3]. Modeling studies and preliminary observational data show that a widespread use of DAAs may determine a reduction in HCV prevalence and prevent onwards transmission among PLWH [4], [5]. Nonetheless, high rates of HCV detection and treatment will be needed to achieve these goals [5], [6]. It is generally estimated that a high proportion of persons living with HCV is undiagnosed [7], although little information is available on undiagnosed HIV-HCV coinfection. We aimed to estimate temporal trends of prevalence and determinants of undiagnosed HCV infection among persons proteasome inhibitor newly diagnosed with HIV.
    Material and methods We analyzed data on persons newly diagnosed with HIV at “Lazzaro Spallanzani” Institute for Infectious Diseases in Rome, Italy, during 2004–2015, enrolled in a prospective observational study (SENDIH) [8]. For person enrolled in this study, demographic, epidemiological, laboratory and clinical data and information on previously diagnosed infections, including HCV, are prospectively collected through a standardized interview. HCV serology is routinely offered to all HIV-positive individuals, and if anti-HCV positive, HCV RNA is performed. The study was approved by the Institute’s Ethic committee, and enrolled individuals provide written informed consent. We included in the analysis persons for whom HCV serology was available within 3 months HIV diagnosis and those for whom anamnestic anti-HCV positivity was available. We defined HCV-unaware, anti-HCV positive individuals who did not report a diagnosis of hepatitis C or a positive HCV test before HIV diagnosis. Staging of liver disease among anti-HCV positive individuals was obtained by the Fibrosis 4 (FIB-4) score, calculated as: age (years)×AST (U/L)/platelets (109/L)×ALT (U/L)1/2. A FIB-4 score higher than or equal to 3.25 was used to define advanced liver disease [9]. Late HIV diagnosis was defined as a CD4 count <350 cells/mmc or an AIDS-defining event within 3 months of HIV diagnosis [10].