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Snoeck J

HIV-1 protease mutation 82M contributes to phenotypic resistance to protease inhibitors in subtype G.

OBJECTIVES:
The purpose of this study was the qualitative and quantitative assessment of the in vitro effect of HIV-1 protease (PR) mutation 82M on replication capacity and susceptibility to the eight clinically available PR inhibitors (PIs).
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RegaDB: Community-driven data management and analysis for infectious diseases

RegaDB is a free and open source data management and analysis environment for infectious diseases. RegaDB allows clinicians to store, manage and analyse patient data, including viral genetic sequences. Moreover, RegaDB provides researchers with a mechanism to collect data in a uniform format and offers them a canvas to make newly developed bioinformatics tools available to clinicians and virologists through a user friendly interface.
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ALISPORIVIR – A HOST-TARGETING ANTIVIRAL, PROVIDES LOW VIRAL BREAKTHROUGH RATE AND HIGH BARRIER TO RESISTANCE IN HCV GENOTYPE 1 TREATMENT-NAiVE PATIENTS IN THE PHASE IIB ESSENTIAL STUDY.

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HIV-1 subtype is an independent predictor of reverse transcriptase mutation k65r in HIV-1 patients treated with combination antiretroviral therapy including tenofovir

Subtype-dependent selection of HIV-1 reverse transcriptase resistance mutation K65R was previously observed in cell culture and small clinical investigations. We compared K65R prevalence across subtypes A, B, C, F, G, and CRF02_AG separately in a cohort of 3,076 patients on combination therapy including tenofovir. K65R selection was significantly higher in HIV-1 subtype C. This could not be explained by clinical and demographic factors in multivariate analysis, suggesting subtype sequence-specific K65R pathways.
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Decreasing population selection rates of resistance mutation K65R over time in HIV-1 patients receiving com- bination therapy including tenofovir

The use of tenofovir is highly associated with the emergence of mutation K65R, which confers broad resistance to nucleoside/nucleotide analogue reverse transcriptase inhibitors (NRTIs), especially when tenofovir is combined with other NRTIs also selecting for K65R. Although recent HIV-1 treatment guidelines discouraging these combinations resulted in reduced K65R selection with tenofovir, updated information on the impact of currently recommended regimens on the population selection rate of K65R is presently lacking.
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DEB025 (Alisporivir) inhibits hepatitis C virus replication by preventing a cyclophilin A induced cis-trans isomerisation in domain II of NS5A

DEB025/Debio 025 (Alisporivir) is a cyclophilin (Cyp)-binding molecule with potent anti-hepatitis C virus (HCV) activity both in vitro and in vivo. It is currently being evaluated in phase II clinical trials. DEB025 binds to CypA, a peptidyl-prolyl cis-trans isomerase which is a crucial cofactor for HCV replication.
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A near-full length genotypic assay for HCV1b

A near-full genome genotypic assay for HCV1b was developed, which may prove useful to investigate antiviral drug resistance, given new combination therapies for HCV1 infection. The assay consists of three partially overlapping PCRs followed by Sanger population or Illumina next-generation sequencing.
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