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. 2005 Sep;79(18):11981–11989. doi: 10.1128/JVI.79.18.11981-11989.2005

TABLE 2.

Drug resistance-associated mutations

Patient and sample Pro mutation(s)a RT mutation(s)
A
    A96pop M36L M41L, D67DN, K70KR, L210LW, T215Y
    A00pop L101, L33F, M41L, E44D, D67N, V118X, M184V,
M36L, G48V G190AG, L210W, T215HY, K219N,
154A, V82A F227FL
B
    B90pop M36L
    B96 M36L M41L, E44DE, V118IV, L2190W, T215Y
C
    C94pop M36L
    C99pop M36L
    C02pop M36L
D
    D99pop M36L
    D01pop M36L
    D02pop M36L
E
    E01pop M36L V75IV
F
    F02pop K20M, M36L
G
    G02pop K20M, M36L
H
    H98pop M36L M184V
I
    I99pop320 M36L V118X, M184V, T215Y
    I99pop506 M36L M184V, T215Y
a

Drug resistance-associated mutations in protease (Pro) and RT were identified according to the criteria of the International AIDS Society—USA (14). Protease mutations in bold represent major mutations. The ubiquitous M36L mutation has been shown to confer cross-resistance to atazanavir in combination with other known protease inhibitor resistance mutations, although it has not been selected for by atazanavir either in vitro or in vivo (3). However, no patient in this transmission chain has been treated with this drug. Also the K20M mutation is only important in combination with other protease inhibitor resistance mutations and should here be considered as natural polymorphism.