Increasing evidence has emerged for permucosal transmission of hepatitis C amongst HIV-infected MSM. A rising incidence of acute hepatitis C virus (HCV) in HIV-infected MSM has been observed since 2000 in Europe, Australia, USA and Asia. Transmission appears to occur through the permucosal rather than the more usual parenteral route. Although often multifactorial, permucosal risk factors can be classified as behavioural (sexual practices and mucosally administered drugs) and biological (HIV and sexually transmitted infections). This review will describe the epidemiology of HCV infection in this cohort. Current and future treatment strategies will also be outlined in the context of novel, orally bioavailable, directly acting antiviral therapies. An improved understanding of HCV epidemiology will allow implementation of more effective public health interventions to limit onward transmission of HCV.

Background. The frequency of protective antiviral memory B cells after hepatitis B virus (HBV) vaccination is unknown. Methods. A novel 2-step immunomagnetic protocol to assess the ex vivo frequency of protective HBV surface antigen (HBsAg)—specific memory B cells was used. Results. HBsAg-specific memory B cells were detected in vaccinated individuals, although at very low frequency (median, 0.2% of CD19⁺ cells [range, 0%–4% of CD19⁺ cells]). No correlation existed between the frequency of HBsAg-specific memory B cells and the corresponding serum antibody titer or B cell enzyme-linked immunosorbent spot findings. Conclusion. Our results indicate sustained B cell—mediated protection against HBV despite waning antibody titers, which is consistent with clinical observations.

Background. We aimed to characterize seminal hepatitis C virus (HCV) RNA dynamics in human immunodeficiency virus (HIV)–positive men with acute HCV infection given its potential role in sexual transmission of HCV.

Sustained viral response (SVR) rates for direct‐acting antiviral (DAA) therapy for hepatitis C virus (HCV) infection routinely exceed 95%. However, a small number of patients require retreatment. Sofosbuvir, velpatasvir and voxilaprevir (SOF/VEL/VOX) is a potent DAA combination primarily used for the retreatment of patients who failed by DAA therapies. Here we evaluate retreatment outcomes and the effects of resistance‐associated substitutions (RAS) in a real‐world cohort, including a large number of genotype (GT)3 infected patients. 144 patients from the UK were retreated with SOF/VEL/VOX following virologic failure with first‐line DAA treatment regimens. Full‐length HCV genome sequencing was performed prior to retreatment with SOF/VEL/VOX. HCV subtypes were assigned and RAS relevant to each genotype were identified. GT1a and GT3a each made up 38% (GT1a n = 55, GT3a n = 54) of the cohort. 40% (n = 58) of patients had liver cirrhosis of whom 7% (n = 4) were decompensated, 10% (n = 14) had hepatocellular carcinoma (HCC) and 8% (n = 12) had received a liver transplant prior to retreatment. The overall retreatment SVR12 rate was 90% (129/144). On univariate analysis, GT3 infection (50/62; SVR = 81%, p = .009), cirrhosis (47/58; SVR = 81%, p = .01) and prior treatment with SOF/VEL (12/17; SVR = 71%, p = .02) or SOF+DCV (14/19; SVR = 74%, p = .012) were significantly associated with retreatment failure, but existence of pre‐retreatment RAS was not when viral genotype was taken into account. Retreatment with SOF/VEL/VOX is very successful for non‐GT3‐infected patients. However, for GT3‐infected patients, particularly those with cirrhosis and failed by initial SOF/VEL treatment, SVR rates were significantly lower and alternative retreatment regimens should be considered.

Using deep sequencing technologies such as Illumina’s platform, it is possible to obtain reads from the viral RNA population revealing the viral genome diversity within a single host. A range of software tools and pipelines can transform raw deep sequencing reads into Sequence Alignment Mapping (SAM) files. We propose that interpretation tools should process these SAM files, directly translating individual reads to amino acids in order to extract statistics of interest such as the proportion of different amino acid residues at specific sites. This preserves per-read linkage between nucleotide variants at different positions within a codon location. The samReporter is a subsystem of the GLUE software toolkit which follows this direct read translation approach in its processing of SAM files. We test samReporter on a deep sequencing dataset obtained from a cohort of 241 UK HCV patients for whom prior treatment with direct-acting antivirals has failed; deep sequencing and resistance testing have been suggested to be of clinical use in this context. We compared the polymorphism interpretation results of the samReporter against an approach that does not preserve per-read linkage. We found that the samReporter was able to properly interpret the sequence data at resistance-associated locations in nine patients where the alternative approach was equivocal. In three cases, the samReporter confirmed that resistance or an atypical substitution was present at NS5A position 30. In three further cases, it confirmed that the sofosbuvir-resistant NS5B substitution S282T was absent. This suggests the direct read translation approach implemented is of value for interpreting viral deep sequencing data.

Objectives: The aim of the study was to evaluate the role of plasma Kaposi sarcoma herpesvirus (KSHV) as a diagnostic and prognostic biomarker in people living with HIV (PLWH) and diagnosed with KSHV‐associated diseases.Methods: Using quantitative nested polymerase chain reaction (PCR) targeting the open reading frame‐26 gene of KSHV, plasma levels of KSHV were measured in consecutive PLWH with KSHV‐associated diseases or as part of the investigation of lymphadenopathy.Results: Plasma KSHV assays were performed on samples from 684 PLWH and 20 HIV‐seronegative people with KSHV‐associated malignancies. In PLWH, plasma KSHV was detected in 39% of those with KS, 99% of those with multicentric Castleman disease (MCD), 9% of those with non‐Hodgkin lymphoma (NHL), 2% of those with non‐AIDS‐defining malignancies and 0% of those with nonmalignant lymphadenopathy. There was no significant difference in plasma KSHV viral load among those with KS, MCD and KSHV‐associated NHL. The 5‐year overall survival rate from KS diagnosis of 335 PLWH was 95.2% (95% confidence interval 92.6–97.8%). Plasma KSHV viraemia did not predict overall survival in those with KS (P = 0.73), nor when those with T0 stage KS (P = 0.52) or T1 stage KS (P = 0.62) were analysed separately.Conclusions: Measuring the plasma levels of KSHV as a biomarker in KSHV‐associated disease has a very limited value in either diagnosis or prognostication. The only potential role of clinical value is the suggestion that an undetectable plasma KSHV excludes a diagnosis of MCD in PLWH.