Deletion, insertion and stop codon mutations in vif genes of HIV-1 infecting slow progressor patients

Rangel, Héctor R.; Garzaro, Domingo; Rodríguez, Anny Karely; Ramírez, Alvaro; Ameli, Gladys; Gutiérrez, Cristina Del Rosario; Pujol, Flor H.

doi:10.3855/jidc.471

Cited by 21 publications

(17 citation statements)

References 42 publications

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“…No primary resistance mutation was detected and no differences were observed in the frequency of secondary mutation associated with drug resistance between pol sequences obtained from HIV-1-positive patients co-infected or not with GBV-C. In vif, the amino acid substitution R132K has been associated with lower viral load in patients harboring viruses with this polymorphism compared to patients carrying viruses with wild type vif [12,18]. Although this substitution was observed in 18/47 (38.3%) of the sequenced viruses, no statistically significant difference was observed in the frequency of this polymorphism between HIV-1 + GBV-C + and HIV-1 + GBV-C -( Table 2).…”

Section: Resultsmentioning

confidence: 93%

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HIV-1 and GBV-C co-infection in Venezuela

Rodríguez

Garzaro

Loureiro

et al. 2014

J Infect Dev Ctries

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Introduction: Co-infection with GB virus C (GBV-C) in patients infected with human immunodeficiency virus 1 (HIV-1) has been associated with prolonged survival. The aim of this study was to evaluate the prevalence of GBV-C infection among HIV-1-infected patients in Venezuela, and to determine the effects of the co-infection on the levels of relevant cytokines. Methodology: Plasma samples were collected from 270 HIV-1-seronegative and 255 HIV-1-seropositive individuals. GBV-C infection was determined by RT-PCR of the NS5 region and genotyped by sequence analysis of the 5´UTR region. HIV-1 strains were characterized by sequence analysis of pol, vif, env, and nef genes. Selected cytokines were evaluated by ELISA. Results: Ninety-seven of 525 (18.5%) plasma samples tested positive for GBV-C RNA. A significantly higher prevalence of GBV-C was found among HIV-1 patients compared to HIV-1-seronegative individuals (67/255, 26% versus 30/270, 11%; p < 0.001). Statistical difference was observed in the viral load between HIV-1+GBV-C+ and HIV-1+GBV-C-(p = 0.014), although no differences in CD4 + cell counts were found between both groups. TNFα concentration was higher in HIV-1

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Section: Resultsmentioning

confidence: 93%

“…Partial or complete coding regions of HIV-1 pol, vif, env, and nef genes were amplified and sequenced as previously described [12,16]. For the pol gene, only antiretroviral-naïve patients were selected for sequence analysis.…”

Section: Hiv-1 Molecular Characterizationmentioning

confidence: 99%

HIV-1 and GBV-C co-infection in Venezuela

Rodríguez

Garzaro

Loureiro

et al. 2014

J Infect Dev Ctries

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“…Regarding gross deletions, to date, only two patients have demonstrated gross deletions in the vif gene [17, 18] and only one patient has demonstrated the insertion of two amino acids, and these patients were part of a nonprogressing mother-child pair [28]. However, in our present study, of the 10 LTSP patients who were assessed, four patients demonstrated gross deletion in the vif gene during KRG intake prior to receiving HAART (1.5%).…”

Section: Discussionmentioning

confidence: 99%

Effects of Korean Red Ginseng and HAART onvifGene in 10 Long-Term Slow Progressors over 20 Years: High Frequency of Deletions and G-to-A Hypermutation

Cho

Kim

Chang

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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To investigate if Korean red ginseng (KRG) affects vif gene, we determined vif gene over 20 years in 10 long-term slowly progressing patients (LTSP) who were treated with KRG alone and then KRG plus HAART. We also compared these data with those of 21 control patients who did not receive KRG. Control patient group harbored only one premature stop codon (PSC) (0.9%), whereas the 10 LTSP revealed 78 defective genes (18.1%) (P < 0.001). The frequency of small in-frame deletions was found to be significantly higher in patients who received KRG alone (10.5%) than 0% in the pre-KRG or control patients (P < 0.01). Regarding HAART, vif genes containing PSCs were more frequently detected in patients receiving KRG plus HAART than patients receiving KRG alone or control patients (P < 0.01). In conclusion, our current data suggest that the high frequency of deletions and PSC in the vif gene is associated with KRG intake and HAART, respectively.

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“…Mutations at positions 72 and 77 in Vpr, disrupting the viral protein function, were frequently detected in non-progressors [58, 59]. Finally, single or large insertions in Vpu [60] and amino acid substitutions in Vif [61, 62] have also been associated with non-progression in HIV-1 disease.…”

Section: Introductionmentioning

confidence: 99%

Impaired human immunodeficiency virus type 1 replicative fitness in atypical viremic non-progressor individuals

et al. 2017

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BackgroundProgression rates from initial HIV-1 infection to advanced AIDS vary significantly among infected individuals. A distinct subgroup of HIV-1-infected individuals—termed viremic non-progressors (VNP) or controllers—do not seem to progress to AIDS, maintaining high CD4+ T cell counts despite high levels of viremia for many years. Several studies have evaluated multiple host factors, including immune activation, trying to elucidate the atypical HIV-1 disease progression in these patients; however, limited work has been done to characterize viral factors in viremic controllers.MethodsWe analyzed HIV-1 isolates from three VNP individuals and compared the replicative fitness, near full-length HIV-1 genomes and intra-patient HIV-1 genetic diversity with viruses from three typical (TP) and one rapid (RP) progressor individuals.ResultsViremic non-progressors and typical patients were infected for >10 years (range 10–17 years), with a mean CD4+ T-cell count of 472 cells/mm3 (442–529) and 400 cells/mm3 (126–789), respectively. VNP individuals had a less marked decline in CD4+ cells (mean −0.56, range −0.4 to −0.7 CD4+/month) than TP patients (mean −10.3, −8.2 to −13.1 CD4+/month). Interestingly, VNP individuals carried viruses with impaired replicative fitness, compared to HIV-1 isolates from the TP and RP patients (p < 0.05, 95% CI). Although analyses of the near full-length HIV-1 genomes showed no clear patterns of single-nucleotide polymorphisms (SNP) that could explain the decrease in replicative fitness, both the number of SNPs and HIV-1 population diversity correlated inversely with the replication capacity of the viruses (r = −0.956 and r = −0.878, p < 0.01, respectively).ConclusionIt is likely that complex multifactorial parameters govern HIV-1 disease progression in each individual, starting with the infecting virus (phenotype, load, and quasispecies diversity) and the intrinsic ability of the host to respond to the infection. Here we analyzed a subset of viremic controller patients and demonstrated that similar to the phenomenon observed in patients with a discordant response to antiretroviral therapy (i.e., high CD4+ cell counts with detectable plasma HIV-1 RNA load), reduced viral replicative fitness seems to be linked to slow disease progression in these antiretroviral-naïve individuals.Electronic supplementary materialThe online version of this article (doi:10.1186/s12981-017-0144-0) contains supplementary material, which is available to authorized users.

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Deletion, insertion and stop codon mutations in vif genes of HIV-1 infecting slow progressor patients

Cited by 21 publications

References 42 publications

HIV-1 and GBV-C co-infection in Venezuela

HIV-1 and GBV-C co-infection in Venezuela

Effects of Korean Red Ginseng and HAART onvifGene in 10 Long-Term Slow Progressors over 20 Years: High Frequency of Deletions and G-to-A Hypermutation

Impaired human immunodeficiency virus type 1 replicative fitness in atypical viremic non-progressor individuals

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