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,
D67N,
L210W, and
T215Y), confer dual resistance to AZT and 3TC.
Abstract: The additional presence of mutations
M41L,
D67N,
L210W, and
T215Y can partially neutralize this deficit, which helps to explain the concurrent presence of these changes in resistant isolates.