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HIV infection and hepatitis C virus genotype 1a are associated with phylogenetic clustering among people with recently acquired hepatitis C virus infection
Affiliation:1. Kirby Institute, UNSW Australia, Sydney, Australia;2. Inflammation and Infection Research Centre (IIRC), UNSW Australia, Sydney, Australia;3. Burnet Institute, Melbourne, Australia;1. Department of Hygiene, Epidemiology and Medical Statistics, Medical School, National and Kapodistrian University of Athens, Athens, Greece;2. Medical School, University of Cyprus, Nicosia, Cyprus;3. First Department of Internal Medicine, Laiko General Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece;4. Hellenic Center for Disease Control and Prevention, Amarousio, Greece;5. Departments of Medicine and Public Health Sciences, and The Chicago Center for HIV Elimination, University of Chicago, Chicago, USA;6. Medical School, National and Kapodistrian University of Athens, Athens, Greece;7. National Development and Research Institutes (NDRI), New York, USA;8. The Baron Edmond de Rothschild Chemical Dependency Institute, Icahn School of Medicine at Mount Sinai, New York, USA;1. Biostatistics, Harvard School of Public Health, Boston, MA, USA
Abstract:The aim of this study was to identify factors associated with phylogenetic clustering among people with recently acquired hepatitis C virus (HCV) infection. Participants with available sample at time of HCV detection were selected from three studies; the Australian Trial in Acute Hepatitis C, the Hepatitis C Incidence and Transmission Study — Prison and Community. HCV RNA was extracted and Core to E2 region of HCV sequenced. Clusters were identified from maximum likelihood trees with 1000 bootstrap replicates using 90% bootstrap and 5% genetic distance threshold. Among 225 participants with available Core-E2 sequence (ATAHC, n = 113; HITS-p, n = 90; and HITS-c, n = 22), HCV genotype prevalence was: G1a: 38% (n = 86), G1b: 5% (n = 12), G2a: 1% (n = 2), G2b: 5% (n = 11), G3a: 48% (n = 109), G6a: 1% (n = 2) and G6l 1% (n = 3). Of participants included in phylogenetic trees, 22% of participants were in a pair/cluster (G1a-35%, 30/85, mean maximum genetic distance = 0.031; G3a-11%, 12/106, mean maximum genetic distance = 0.021; other genotypes-21%, 6/28, mean maximum genetic distance = 0.023). Among HCV/HIV co-infected participants, 50% (18/36) were in a pair/cluster, compared to 16% (30/183) with HCV mono-infection (P = < 0.001). Factors independently associated with phylogenetic clustering were HIV co-infection [vs. HCV mono-infection; adjusted odds ratio (AOR) 4.24; 95%CI 1.91, 9.39], and HCV G1a infection (vs. other HCV genotypes; AOR 3.33, 95%CI 0.14, 0.61).HCV treatment and prevention strategies, including enhanced antiviral therapy, should be optimised. The impact of targeting of HCV treatment as prevention to populations with higher phylogenetic clustering, such as those with HIV co-infection, could be explored through mathematical modelling.
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