human
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['To study the ability of HIV constructs containing the M184V substitution in reverse transcriptase (RT), which causes resistance to lamivudine, to evolve mutations that compensate for deletions within the HIV genome.', 'Viruses containing deletions in non-coding regions of the viral genome were examined in tissue culture to see whether the additional presence of M184V delays the reestablishment of wild-type replication kinetics. Potential compensatory mutations were identified by sequencing, and site-directed mutagenesis was carried out to confirm the biological relevance of such substitutions. The rate of initiation of reverse transcription was measured using either recombinant wild-type RT or RT containing M184V.', 'M184V-containing viruses were unable to undergo compensatory mutagenesis to reestablish wild-type replication kinetics, whereas viruses that did not contain M184V were able to mutate extensively. This ability was demonstrated most extensively in viruses deleted of an "A-rich loop", located upstream of the primer-binding site, which is involved in initiation of reverse transcription. The rate of such initiation was severely diminished in virus containing the RT enzyme carrying the M184V substitution. This inhibitory effect was significantly enhanced in a biochemical system that included both the M184V mutant enzyme and a viral DNA template that contained the deletion in the A-rich loop.'] Does the M184V mutation in HIV-1 reverse transcriptase reduce the restoration of wild-type replication by attenuated viruses?
OUTPUT:

agent
yes
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['To study the ability of HIV constructs containing the M184V substitution in reverse transcriptase (RT), which causes resistance to lamivudine, to evolve mutations that compensate for deletions within the HIV genome.', 'Viruses containing deletions in non-coding regions of the viral genome were examined in tissue culture to see whether the additional presence of M184V delays the reestablishment of wild-type replication kinetics. Potential compensatory mutations were identified by sequencing, and site-directed mutagenesis was carried out to confirm the biological relevance of such substitutions. The rate of initiation of reverse transcription was measured using either recombinant wild-type RT or RT containing M184V.', 'M184V-containing viruses were unable to undergo compensatory mutagenesis to reestablish wild-type replication kinetics, whereas viruses that did not contain M184V were able to mutate extensively. This ability was demonstrated most extensively in viruses deleted of an "A-rich loop", located upstream of the primer-binding site, which is involved in initiation of reverse transcription. The rate of such initiation was severely diminished in virus containing the RT enzyme carrying the M184V substitution. This inhibitory effect was significantly enhanced in a biochemical system that included both the M184V mutant enzyme and a viral DNA template that contained the deletion in the A-rich loop.'] Does the M184V mutation in HIV-1 reverse transcriptase reduce the restoration of wild-type replication by attenuated viruses?
OUTPUT:
