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Leemann, C.

Publications and source records attributed to Leemann, C..

2 recordsLinked to original sources

Substantial Deceleration of Adaptation of HIV-1 Within 1,500 Generations in an Experimental Evolution: A Genomic Perspective

Numerous experimental evolution studies have suggested that adaptation rate of microbial populations evolving in stable environments decline over time. Despite the generality of this phenomenon across different domains of life, the timing and magnitude of decline in adaptation can vary greatly based on the idiosyncrasies of the biological system. To investigate the characteristics of adaptation deceleration in a fast-evolving virus, we propagated HIV-1 in two human T-cell lines (MT-2 and MT-4) for approximately 4.8 years and tracked its genome evolution through next-generation sequencing. The curated sequencing data covering the whole-genome can be accessed and explored via LTEEviz, an interactive web application. Time-resolved sequencing data uncovered that despite constant fixation rate of 0.085 (MT-2) and 0.042 (MT-4) mutations per generation, the fixation kinetics of adaptive mutations changed considerably over time. The rate of fixation of adaptive parallel mutations decreased by 44% per 300 generations, while their conferred fitness gain decreased by 27% (MT-2) and 18% (MT-4) per every added adaptive mutation in their genetic background. The early and substantial deceleration of adaptation in our HIV-1 populations can, at least in part, be explained by diminishing gains of adaptive mutations. Furthermore, we identified genomic patterns consistent with a hard selective sweep that occurred in one population later in the experiment. Together, our results confirm that HIV-1 genomic evolution is characterized by a swift and substantial deceleration of adaptation, while also revealing that episodes of positive selection can occur beyond the initial adaptive phase.

evolutionary biology↗

Anti-HIV-1 Effect of the Fluoroquinolone Enoxacin and Modulation of Pro-viral hsa-miR-132 Processing

BackgroundDespite tremendous advances in antiretroviral therapy (ART) against HIV-1 infections no cure or vaccination is available. Therefore, discovering novel therapeutic strategies remains an urgent need. In that sense, miRNAs and miRNA therapeutics have moved intensively into the focus of recent HIV-1 related investigations. A strong reciprocal interdependence has been demonstrated between HIV-1 infection and changes of the intrinsic cellular miRNA milieu. This interrelationship may direct potential alterations of the host cells environment beneficial for the virus or its suppression of replication. Whether this tightly balanced and controlled battle can be exploited therapeutically, remains to be further addressed. In this context, the fluoroquinolone antibiotic Enoxacin has been demonstrated as a potent modulator of miRNA processing. Here, we test the hypothesis that this applies also to selected HIV-1 related miRNAs. MethodsWe studied the effect of Enoxacin on HIV-1 replication coupled with miRNA qRT-PCR analysis of HIV-1 related miRNAs in CEM-SS and MT-4 T-cells. The effects of miRNA mimic transfections combined with Enoxacin treatment on HIV-1 replication were assessed. Finally, we employed an in vitro DICER1 cleavage assay to study the effects of Enoxacin on a pro-HIV-1 miRNA hsa-miR-132 processing. ResultsWe established that Enoxacin, but not the structurally similar compound nalidixic acid, exhibits strong anti-HIV-1 effects in the T-cell line CEM-SS, but not MT-4. We provide experimental data that this effect of Enoxacin is partly attributed to the specific downregulation of mature hsa-miR-132-3p, but not other pro- or anti-HIV-1 miRNAs, which is likely due to affecting DICER1 processing. ConclusionsOur findings show an anti-retroviral activity of Enoxacin at least in part by downregulation of hsa-miR-132-3p, which may be relevant for future antiviral therapeutic applications by modulation of the RNA interference pathway.

molecular biology↗