HIV-1 and hepatitis C virus (HCV) circulate among men who have sex with men (MSM). We conducted a study to investigate the overlap of these epidemics among MSM in the Netherlands using a phylogenetic approach.
Data were derived from the observational ATHENA and MOSAIC cohort studies. We included 5,038 MSM who were diagnosed with a HIV subtype B infection between 1981 and 2014. HIV subtype was based on the availability of a pol sequence. Of them, 562 (11.2%) were (ever) coinfected with HCV (until October 2014). Time from HIV diagnosis to HCV infection was calculated using the Kaplan-Meier method. HCV NS5B sequences were available for 126/562 (26.7%) coinfected MSM, allowing phylogenetic analysis of both HIV and HCV. HIV phylogenetic clusters were defined as having ≥10 sequences with a bootstrap value >90 and a median pairwise distance within the clade smaller than the 5th percentile threshold of the pairwise distances in the whole tree. We investigated the presence of HIV clusters that had an increased risk for HCV infection.
In total, 118 HIV phylogenetic clusters were identified. These clusters included 3,084/5,038 (61.2%) MSM infected with HIV subtype B, and 97/118 (82.2%) clusters contained ≥1 HCV infection. Median HIV-1 cluster size of those with past or present HCV infection was comparable to those with no history of HCV. Median time between HIV diagnosis and HCV diagnosis was 3.3 years (IQR: 1.0-7.3), but decreased over time. HCV NS5B sequences were obtained from 150 HCV infections among 126 MSM; 21 MSM had ≥1 reinfection. Among 51 HIV clusters with ≥2 HCV sequences, 14 clusters contained HCV strains of concordant genotypes, but only 8/14 HIV clusters with ≥2 HCV sequences contained two HCV strains of the exact same HCV lineage. Ultimately, 19/150 (12.7%) coinfected MSM clustered on both HCV and HIV phylogeny.
In this study, HCV infection was not confined to specific HIV clusters, indicating there are no specific HIV clusters with elevated risk of HCV infection. When multiple HCV infections were present within an HIV cluster, concordance of HCV phylogeny was relatively uncommon, even among those with concordant HCV genotype. One explanation may be that HCV spreads in MSM networks that differ from the HIV transmission networks. The median duration from HIV diagnosis to HCV infection of 3.3 years suggests that these HCV networks are established some time after HIV infection.