We undertook a study of the dynamics of HIV-1 CTL-escape mutations by analyzing through statistical approaches and phylogenetic methods the viral gene gag sequenced in plasma samples collected between the years 1987 and 2006 from 302 drug-naïve HIV-positive patients.
However, these studies were primarily designed to identify biallelic gene mutations by analyzing the residual non-deleted 5q31.2 allele using MDS samples, AML samples, or cell lines containing a cytogenetically visible 5q31.2 deletion, and they only examined 20 of the 28 5q31.2 genes [6], [7], [8], [9], [10].
The detection of somatic mutations by analyzing sequence data involves a number of steps to filter out technical errors.
Because the average coverage depth is so high (82.72×), we opted for a lenient criteria for consensus identification in an effort to reduce false negative mutation calls by analyzing as many sites for putative mutations as possible.
We further corroborated our qMSP and somatic mutation results by analyzing The Cancer Genome Atlas (TCGA) publicly available data from 279 HNSCC patients (https://tcga-data.nci.nih.gov).
In addition, we extend the timescale over which this putative mutation rate variation holds by analyzing the frequency of coincident single nucleotide substitutions (cSNSs) between human chimpanzee and orangutan rhesus genomes.
Transformants were selected at 30°C on phleomycin (Pm) containing plates (the phleomycin gene - pmr - is located just upstream of dnaE) and the presence of the dna(Ts) mutation was checked by analyzing cell growth and filamentation at restrictive temperature by plating and optical microscopy analysis.
The stability of the H275Y mutation was demonstrated by analyzing pyrosequencing data of the viruses shed by the infected ferrets.
GeneSV evaluates the probability of selected mutation(s) first by analyzing its (their) frequency (frequencies) as observed in the genomic sequence databases.
DOI: http://dx.doi.org/10.7554/eLife.06322.011 For 27 samples with no confirmed point mutation in MVK, PMVK, MVD, and FDPS genes, large deletion or duplication mutations were interrogated by analyzing the copy number of promoters and all exons in these genes.
