TABLE 2.
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 |
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.