Result: In addition to the five accessory mutations in Table 2 (K43E, E44D, V118I, H208Y, and D218E), other NRTI mutations that consistently followed TAMs included the known treatment-selected mutations T69D and T69N.
Result: Positively associated mutation pairs consisted primarily of Type I or II thymidine analog mutations (TAMs; as defined in Methods); accessory NRTI mutations that occurred in combination with Type I or II TAMs (K43E, E44D, V118I, H208Y, D218E); and Q151M<
The use of beta-D-2,6-diaminopurine dioxolane with or without mycophenolate mofetil in drug-resistant HIV infection.
Abstract: VR was more frequent with < or = 5 baseline NRTI mutations (P = 0.12) or < 4 thymidine-associated mutations (TAMs) without E44D or V118I (P = 0.08).
Improved interpretation of genotypic changes in the HIV-1 reverse transcriptase coding region that determine the virological response to didanosine.
PMID: 18008248
2007
The Journal of infectious diseases
Abstract: The best correlation with response was found with the derived score (M41L x 2) + E44D/A/G + T69D/S/N/A + (L210W x 2) + T215Y or revertants + L228H/R - D123E/N/G/S, by use of which viruses were categorized as being susceptible (score < or =0), as having intermediate resistance (1-3), and as being resistant (> or =4) to didanosine.
Evidence of differential selection of HIV-1 variants carrying drug-resistant mutations in seroconverters.
Abstract: Among the mutations not detected in viruses from SCs, the RT E44D, V1081, Q151M and Y188C/H/L, and the protease D30N, G48V and V82A/F/S/T substitutions appeared to be negatively selected.
Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.
PMID: 19825125
2005
Journal of the International AIDS Society
Table: E44A/D
Table: E44D
Treatment response and drug resistance in patients infected with HIV type 1 group O viruses.
PMID: 16060830
2005
AIDS research and human retroviruses
Abstract: One selected changes M41L, E44D, D67N, V75M, M184V, and T215Y at the RT, and G48M, F53L, I54V, V82A, and L90M at the protease.
Antiretroviral resistance and genetic diversity of human immunodeficiency virus type 1 isolates from the Federal District, Central Brazil.
PMID: 15761606
2004
Memorias do Instituto Oswaldo Cruz
Abstract: Many mutations associated with reduced susceptibility to nucleoside or non-nucleoside reverse transcriptase inhibitors were detected: M41L (11%), E44D (4%), D67N (11%), T69D (2%), K70R (11%), L74V (2%), L100I (4%), K103N (18%), V118I (9%), Y181C (11%), M184V (18%), G190A (4%), T215Y (4%), and K219E (4%).
Genotypic determinants of the virological response to tenofovir disoproxil fumarate in nucleoside reverse transcriptase inhibitor-experienced patients.
Abstract: RESULTS: The strongest association with decrease in viral load was observed with a set of seven mutations (TDF mutation score) that consisted of M41L, E44D, D67N, T69D/N/S, L74V, L210W and T215Y/F RT mutations.
Primary drug-resistance in HIV-positive patients on initiation of first-line antiretroviral therapy in Germany.
PMID: 15257882
2004
European journal of medical research
Mutations E44D and V118I in the reverse transcriptase of HIV-1 play distinct mechanistic roles in dual resistance to AZT and 3TC.
PMID: 12819190
2003
The Journal of biological chemistry
Abstract: Both mechanisms show a certain degree of incompatibility; however, previous clinical data revealed that mutations E44D and V118I, when present in a background of classical AZT mutations (M41L,
Abstract: These biochemical data make clear that mutations E44D and V118I play distinct mechanistic roles in dual resistance to AZT and 3TC.
Abstract: We found that enzymes containing E44D in a background of these latter mutations increase the efficiency of excision of 3TC-MP.
Abstract: We have purified RT enzymes that contain E44D and V118I either alone or in a background of different combinations of AZT mutations to study the underlying biochemical mechanisms.
HIV mutation literature information.
PMID: 
2007
PLoS computational biology
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