literature

HIV mutation literature information.

Evolution of genetic diversity and drug resistance mutations in HIV-1 among untreated patients from Mali between 2005 and 2006.

PMID: 18556706 2008 The Journal of antimicrobial chemotherapy

Abstract: Resistance mutations found in RT and PR genes are in agreement with the highly active antiretroviral therapy regimen available in Mali, except for V90I, V106I and A98G mutations which are associated with etravirine resistance, but polymorphic in non-B subtypes.

Profile of primary resistance in HIV-1-infected treatment-naive individuals from Western India.

PMID: 18593351 2008 AIDS research and human retroviruses

Abstract: The resistance mutation observed in the protease gene was V82A, whereas in the RT gene, M41L, D67N, M184V, and A98G were documented.

Evaluating the role of etravirine in the second-line antiretroviral therapy after failing an initial non-nucleoside reverse transcriptase inhibitor-based regimen in a resource-limited setting.

PMID: 18855659 2008 Current HIV research

Abstract: We focused on etravirine-RAMs previously described: V90I, A98G, L100I, K101E/P, V106I, V179D/F, Y181C/I/V, and G190A/S.

Etravirine: a second-generation NNRTI for treatment-experienced adults with resistant HIV-1 infection.

PMID: 19881888 2008 Future HIV therapy

Conclusion: Etravirine RAMs include V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S and M230L.

Introduction: A total of 13 mutations were initially identified as etravirine RAMs, including V90I, A98G, L100I, K101E/P, V106I, V179D/F, Y181C/I/V and G190A/S (Table 5).

Table: A98G

Sequential emergence and clinical implications of viral mutants with K70E and K65R mutation in reverse transcriptase during prolonged tenofovir monotherapy in rhesus macaques with chronic RT-SHIV infection.

PMID: 17417971 2007 Retrovirology

Table: A98G

HIV-1 subtype B protease and reverse transcriptase amino acid covariation.

PMID: 17500586 2007 PLoS computational biology

Method: NNRTI-selected mutations included A98G, L100I, K101E/P/N/H, K103N/S, V106A/M, V108I, V179D/E, Y181C/I/V, Y188L/C/H, G190A/S/E/Q, P225H, F227L, M230L, P236L, and K238T.

Drug-resistant HIV infection among drug-naive patients in Israel.

PMID: 15655750 2005 Clinical infectious diseases

Abstract: In addition, 1 subject with A subtypes, 2 with subtype B, and 10 with subtype C had secondary mutations (protease: M46I; reverse transcriptase: A98G, K101Q, and V108I).

Genetic variation at NNRTI resistance-associated positions in patients infected with HIV-1 subtype C.

PMID: 15060438 2004 AIDS (London, England)

Abstract: In NNRTI experienced patients, the number of A98G/S changes was significantly higher in subtype C patients treated with either efavirenz or nevirapine (P < 0.0001), and V106M was higher in efavirenz-treated subtype C-infected patients (P < 0.0001).

Genotypic variation of HIV-1 reverse transcriptase and protease: comparative analysis of clade C and clade B.

PMID: 11504976 2001 AIDS (London, England)

Abstract: RESULTS: There were 87 clade B (14 naive) and 78 clade C (20 naive) [corrected] with significant differences in the prevalence of known drug-resistance mutations between the clades: in naive patients in the protease region M36I 7% and 95% (P < 0.0001), K20R 0% and 27% (P = 0.063), A71V 18% and 0% (P = 0.063), M46I 0% and 13%, and V77I 18% and 0% (P = 0.063), respectively, and in the reverse transcriptase region A98G/S 0% and 20% (P = 0.12), respectively.

Abstract: There were also significant differences (P < 0.03 to < 0.0001) in treated patients in clades B and C: in the protease region L10I 40% and 12%, M3

The biological effects of structural variation at the meta position of the aromatic rings and at the end of the alkenyl chain in the alkenyldiarylmethane series of non-nucleoside reverse transcriptase inhibitors.

PMID: 11708913 2001 Journal of medicinal chemistry

Abstract: Additionally, ADAMs 19 (44-fold) and 21 (29-fold) were more effective against the A98G mutation (found in association with nevirapine resistance in vitro), and ADAM 21 was 5-fold and 2-fold more potent against the Y181C inactivation mutation than the previously reported ADAMs 15 and 17, respectively.

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