literature

HIV mutation literature information.

Significantly improved HIV inhibitor efficacy prediction employing proteochemometric models generated from antivirogram data.

PMID: 23436985 2013 PLoS computational biology

Result: Some mutations are slightly underestimated, these include V90I and V106I.

Figure: In particular the specific profiles of V106I, Y181C and G190A are reproduced well.

Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.

PMID: 23469241 2013 PloS one

Table: V106I

Description of HIV-1 group M molecular epidemiology and drug resistance prevalence in Equatorial Guinea from migrants in Spain.

PMID: 23717585 2013 PloS one

Table: V106I

HIV-1 drug-resistance surveillance among treatment-experienced and -naive patients after the implementation of antiretroviral therapy in Ghana.

PMID: 23977189 2013 PloS one

Result: However, polymorphisms at NNRTI-resistance mutation loci, V90I, E138A, and V106I, were found in 6 cases (10.2% in Table 4).

Table: V106I

HIV type 1 virological response and prevalence of HIV type 1 drug resistance among patients receiving antiretroviral therapy, Shandong, China.

PMID: 22563717 2012 AIDS research and human retroviruses

Abstract: The most common mutations were thymidine-analog mutations (22.5%) and M184V (10%) to nucleoside reverse transcriptase inhibitors (NRTIs), and V106I/A /M (17.5%), Y181C (15%), and H221Y (12.5%) to non-NRTIs (NNRTIs); 13 patients had mutations to both NRTIs and NNRTIs.

Minority variants associated with resistance to HIV-1 nonnucleoside reverse transcriptase inhibitors during primary infection.

PMID: 22818969 2012 Journal of clinical virology

Abstract: The 11 RAMs not detected by bulk sequencing were A98G (n=2), L100I (n=3), K101E (n=2), V106I (n=3) and E138G (n=1).

Comparison of predicted susceptibility between genotype and virtual phenotype HIV drug resistance interpretation systems among treatment-naive HIV-infected patients in Asia: TASER-M cohort analysis.

PMID: 23095645 2012 BMC research notes

Discussion: A combination of V106I and V179D has been shown to confer significant resistance to efavirenz .

Discussion: Among TASER-M patients, only 1 had a combination of V106I and V179D.

Virological failure rates and HIV-1 drug resistance patterns in patients on first-line antiretroviral treatment in semirural and rural Gabon.

PMID: 23199801 2012 Journal of the International AIDS Society

Result: Major NNRTIs DRMs were also obtained at positions P225H (n=12), K101E (n=11), Y181C (n=10), G190A (n=7), Y188L (n=6), V90I (n=5), E138A/G (n=5), M230L (n=4), A98G (n=3), H221Y (n=3), L100I (n=3), V179D (n=2), and V106I (n=1).

Baseline-transmitted V106V/I/M non-nucleoside reverse transcriptase inhibitor resistance in HIV-1 subtype B infection.

PMID: 23230246 2012 BMJ case reports

Abstract: The V106V/I/M mutation represents a mixture of virus strains conferring resistance to the non-nucleoside reverse transcriptase inhibitor antiretrovirals efavirenz and nevirapine.

Abstract: We report a case in which an antiretroviral therapy (ART)-naive patient diagnosed with HIV-1 subtype B presented with baseline genotype and phenotype resistance tests, confirming a V106V/I/M nucleoside resistance mutation.

Impact of HIV type 1 subtype on drug resistance mutations in Nigerian patients failing first-line therapy.

PMID: 20964479 2011 AIDS research and human retroviruses

Abstract: Among NNRTI mutations, subtype G patients had an increased risk for A98G (AOR = 2.40, p = 0.036) and V106I (AOR = 6.15, p = 0.010), whereas subtype CRF02_AG patients had an increased risk for V90I (AOR = 3.16; p = 0.003) and a decreased risk for A98G (AOR = 0.48, p = 0.019).

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