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Grande-Perez, A.

Publications and source records attributed to Grande-Perez, A..

2 recordsLinked to original sources

QuasiFlow: a bioinformatic tool for genetic variability analysis from next generation sequencing data

Populations of RNA and ssDNA viruses within their hosts contain a heterogeneous collection of variant genomes known as quasispecies. Large variability in mitochondrial DNA has also been found within the same organism, drawing an interesting parallel between the two situations. The advent of next-generation sequencing technologies facilitated studying genetic variation, but many open-source bioinformatic tools have to be combined in a non-trivial approach. Here it is presented QuasiFlow, a workflow based on well-stablished software that extracts reliable mutations and recombinations, even at low frequencies (~10-4), provided that at least 250 million nucleotides are analysed. Accurate prediction of mutations and recombinations has been demonstrated with synthetic reads and with in vitro rolling-circle amplification of a plant geminivirus. An in-depth analysis of viral quasispecies was performed and QuasiFlow revealed the coexistence in the plant of three virus genomes and distinct recombinations between some of them. Human mitochondrial variants were also investigated and high level of heteroplasmy (75%) was confirmed, and the relation between low-frequency heteroplasmy (0.1- 0.2%) and some human diseases, regardless of sex, was established. Hence, we propose that QuasiFlow may find use with known and emerging viruses to reveal evolutionary jumps and co-infections, with mitochondrial DNA to detect relevant heteroplasmy would otherwise be elusive, or even in other population studies such as those considering single cell sequencing.

bioinformatics↗

Guanosine inhibits hepatitis C virus replication and increases indel frequencies, associated with altered intracellular nucleotide pools

In the course of experiments aimed at deciphering the inhibition mechanism of mycophenolic acid and ribavirin in hepatitis C virus (HCV) infection, we observed an inhibitory effect of the nucleoside guanosine (Gua). Here, we report that Gua and not the other standard nucleosides inhibits HCV replication in human hepatoma cells. Gua did not directly inhibit the in vitro polymerase activity of NS5B, but it modified the intracellular levels of nucleoside di- and tri-phosphate (NDPs and NTPs), leading to deficient HCV RNA replication and reduction of infectious progeny virus production. Changes in the concentrations of NTP or NDP modified NS5B RNA polymerase activity in vitro, in particular de novo RNA synthesis and template switching. Furthermore, the Gua-mediated changes were associated with a significant increase in the number of indels in viral RNA, which may account for the reduction of the specific infectivity of the viral progeny, suggesting the presence of defective genomes. Thus, a proper NTP:NDP balance appears to be critical to ensure HCV polymerase fidelity and minimal production of defective genomes. Author summaryRibonucleoside metabolism is essential for replication of RNA viruses. In this article we describe the antiviral activity of the natural ribonucleoside guanosine (Gua). We demonstrate that hepatitis C virus (HCV) replication is inhibited in the presence of increasing concentrations of this ribonucleoside and that this inhibition does not occur as a consequence of a direct inhibition of HCV polymerase. Cells exposed to increasing concentrations of Gua show imbalances in the intracellular concentrations of nucleoside-diphosphates and triphosphates and as the virus is passaged in these cells, it accumulates mutations that reduce its infectivity and decimate its normal spreading capacity.

microbiology↗