Joost W Vanhommerig1, Daniela Bezemer, Richard Molenkamp, Ard I Van Sighem, Colette Smit, Joop E Arends, Fanny N Lauw, Kees Brinkman, Bart J Rijnders, Astrid M Newsum, Sylvia M Bruisten, Maria Prins, Jan T Van Der Meer, Thijs J Van De Laar, Janke Schinkel. 1. aLaboratory of Clinical Virology, Department of Medical Microbiology, Academic Medical Center, Amsterdam bDepartment of Infectious Diseases, Research and Prevention, Public Health Service of Amsterdam cStichting HIV Monitoring, Amsterdam dDepartment of Internal Medicine and Infectious Diseases, University Medical Center Utrecht, Utrecht eMC Slotervaart fDepartment of Internal Medicine, Onze Lieve Vrouwe Gasthuis, Amsterdam gDepartment of Internal Medicine and Infectious Diseases, Erasmus University Medical Center, Rotterdam hDepartment of Internal Medicine, Center of Infection and Immunity Amsterdam (CINIMA), Academic Medical Center iDepartment of Blood-Borne Infections, Sanquin Research, Amsterdam, the Netherlands. *Thijs J. Van De Laar and Janke Schinkel contributed equally to the article.
Abstract
OBJECTIVE: MSM are at increased risk for infection with HIV-1 and hepatitis C virus (HCV). Is HIV/HCV coinfection confined to specific HIV transmission networks? DESIGN AND METHODS: A HIV phylogenetic tree was constructed for 5038 HIV-1 subtype B polymerase (pol) sequences obtained from MSM in the AIDS therapy evaluation in the Netherlands cohort. We investigated the existence of HIV clusters with increased HCV prevalence, the HIV phylogenetic density (i.e. the number of potential HIV transmission partners) of HIV/HCV-coinfected MSM compared with HIV-infected MSM without HCV, and the overlap in HIV and HCV phylogenies using HCV nonstructural protein 5B sequences from 183 HIV-infected MSM with acute HCV infection. RESULTS: Five hundred and sixty-three of 5038 (11.2%) HIV-infected MSM tested HCV positive. Phylogenetic analysis revealed 93 large HIV clusters (≥10 MSM), 370 small HIV clusters (2-9 MSM), and 867 singletons with a median HCV prevalence of 11.5, 11.6, and 9.3%, respectively. We identified six large HIV clusters with elevated HCV prevalence (range 23.5-46.2%). Median HIV phylogenetic densities for MSM with HCV (3, interquartile range 1-7) and without HCV (3, interquartile range 1-8) were similar. HCV phylogeny showed 12 MSM-specific HCV clusters (clustersize: 2-39 HCV sequences); 12.7% of HCV infections were part of the same HIV and HCV cluster. CONCLUSION: We observed few HIV clusters with elevated HCV prevalence, no increase in the HIV phylogenetic density of HIV/HCV-coinfected MSM compared to HIV-infected MSM without HCV, and limited overlap between HIV and HCV phylogenies among HIV/HCV-coinfected MSM. Our data do not support the existence of MSM-specific sexual networks that fuel both the HIV and HCV epidemic.
OBJECTIVE: MSM are at increased risk for infection with HIV-1 and hepatitis C virus (HCV). Is HIV/HCV coinfection confined to specific HIV transmission networks? DESIGN AND METHODS: A HIV phylogenetic tree was constructed for 5038 HIV-1 subtype B polymerase (pol) sequences obtained from MSM in the AIDS therapy evaluation in the Netherlands cohort. We investigated the existence of HIV clusters with increased HCV prevalence, the HIV phylogenetic density (i.e. the number of potential HIV transmission partners) of HIV/HCV-coinfected MSM compared with HIV-infected MSM without HCV, and the overlap in HIV and HCV phylogenies using HCV nonstructural protein 5B sequences from 183 HIV-infected MSM with acute HCV infection. RESULTS: Five hundred and sixty-three of 5038 (11.2%) HIV-infected MSM tested HCV positive. Phylogenetic analysis revealed 93 large HIV clusters (≥10 MSM), 370 small HIV clusters (2-9 MSM), and 867 singletons with a median HCV prevalence of 11.5, 11.6, and 9.3%, respectively. We identified six large HIV clusters with elevated HCV prevalence (range 23.5-46.2%). Median HIV phylogenetic densities for MSM with HCV (3, interquartile range 1-7) and without HCV (3, interquartile range 1-8) were similar. HCV phylogeny showed 12 MSM-specific HCV clusters (clustersize: 2-39 HCV sequences); 12.7% of HCV infections were part of the same HIV and HCV cluster. CONCLUSION: We observed few HIV clusters with elevated HCV prevalence, no increase in the HIV phylogenetic density of HIV/HCV-coinfected MSM compared to HIV-infected MSM without HCV, and limited overlap between HIV and HCV phylogenies among HIV/HCV-coinfected MSM. Our data do not support the existence of MSM-specific sexual networks that fuel both the HIV and HCV epidemic.
Authors: Steven J Clipman; Priya Duggal; Aylur K Srikrishnan; Shanmugam Saravanan; Pachamuthu Balakrishnan; Canjeevaran K Vasudevan; David D Celentano; David L Thomas; Shruti H Mehta; Sunil S Solomon Journal: J Infect Dis Date: 2020-05-11 Impact factor: 5.226
Authors: Sofia R Bartlett; Andrey Verich; Joanne Carson; Samira Hosseini-Hooshyar; Phillip Read; David Baker; Jeffrey J Post; Robert Finlayson; Mark Bloch; Joseph S Doyle; David Shaw; Margaret Hellard; Maria Martinez; Philippa Marks; Gregory J Dore; Gail V Matthews; Tanya Applegate; Marianne Martinello Journal: Health Sci Rep Date: 2022-08-18
Authors: Tamara Sonia Boender; Colette Smit; Ard van Sighem; Daniela Bezemer; Catriona J Ester; Sima Zaheri; Ferdinand W N M Wit; Peter Reiss Journal: BMJ Open Date: 2018-09-24 Impact factor: 2.692