literature

HIV mutation literature information.

Human immunodeficiency virus type 1 (HIV-1) genotyping in Rio de Janeiro, Brazil: assessing subtype and drug-resistance associated mutations in HIV-1 infected individuals failing highly active antiretroviral therapy.

PMID: 15867968 2005 Memorias do Instituto Oswaldo Cruz

Abstract: The K103N mutation was the most prevalent to the non-nucleoside RT inhibitor and the resistance associated to protease inhibitor showed the minor mutations L63P, L10F/R, and A71V as the more prevalent.

[Primary resistance to antiretroviral therapy in patients with HIV/AIDS in Chile].

PMID: 15880183 2005 Revista medica de Chile

Abstract: Ten mutations were identified: V179D, L10I/V, M361, L63P, A71T/V, Y115F, V118I and K20R.

Induction of T-cell immunity to antiretroviral drug-resistant human immunodeficiency virus type 1.

PMID: 15919925 2005 Journal of virology

Abstract: Novel CD8 T-cell responses were detected against the common L63P and L10I protease inhibitor fitness mutations.

Subtype analysis and mutations to antiviral drugs in HIV-1-infected patients from Mozambique before initiation of antiretroviral therapy: results from the DREAM programme.

PMID: 15977236 2005 Journal of medical virology

Abstract: The pattern of covariation observed for K20R and D60E (but not L63P and M36I) was different between C and B subtype isolates from PR-inhibitor-treated patients.

[Genotypic antiretroviral resistance testing and phylogenetic analysis of protease and reverse transcriptase in antiretroviral drug-naive AIDS patients in Henan province].

PMID: 16053762 2005 Zhonghua liu xing bing xue za zhi

Abstract: Minor mutation rate of resistance was 100%, including types of L63PS (36/36), I93L (35/36), V77IL (34/36), A71IVT (10/36) and D60E (2/36).

Effect of polymorphisms on the replicative capacity of protease inhibitor-resistant HIV-1 variants under drug pressure.

PMID: 14759236 2004 Clinical microbiology and infection

Abstract: Importantly, the polymorphic change L63P, although not conferring inhibitor resistance by itself, provided a significant replication benefit to both mutant viruses, particularly under drug pressure, and may reveal a far-reaching compensating power of polymorphic changes.

Abstract: The role of drug pressure on the replicative capacity of protease inhibitor-resistant HIV-1 variants and the contribution of a common amino-acid polymorphism in the protease gene (L63P) to this process were investigated.

Protease mutations in HIV-1 non-B strains infecting drug-naive villagers in Cameroon.

PMID: 15008125 2004 AIDS research and human retroviruses

Abstract: Secondary PI resistance-associated mutations were identified at five sites: L10I/V (16%), K20R (8%), M36I (98%), L63P (13%), and V77I (6%).

Comparison of drug resistance mutations and their interpretation in patients infected with non-B HIV-1 variants and matched patients infected with HIV-1 subtype B.

PMID: 15097148 2004 Journal of acquired immune deficiency syndromes (1999)

Abstract: In the protease gene, differences between patients infected with B or non-B strains were mainly observed for mutations playing a minor role in drug resistance and known to occur mainly as a natural polymorphism in non-B strains: K20R/M/I, M36I, L63P, A71V/T, and V77I.

Mutation D30N is not preferentially selected by human immunodeficiency virus type 1 subtype C in the development of resistance to nelfinavir.

PMID: 15155216 2004 Antimicrobial agents and chemotherapy

Abstract: Significant differences were found in the rates of M36I (98 and 36%), L63P (35 and 59%), A71V (3 and 32%), V77I (0 and 36%), and I93L (91 and 32%) (0.0001 < P < 0.05) in C and B, respectively.

Persistence of mutations during replication of an HIV library containing combinations of selected protease mutations.

PMID: 15168798 2004 Antiviral research

Abstract: Other amino acid substitutions, i.e., L10I, I54V, L63P, A71V and V82A, were well retained (t(1/2) > 36 days).

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