Effects of acyclovir on HIV replication and identification of resistant
variants. A, inhibition of HIV infectivity by acyclovir. HIV
pseudoviruses derived from the wild-type (WT) clone, NL4-3, and the
isogenic clones varying only at positions T69N, V75I, or M184V were used to
infect primary CD4+ cells in the presence of varying amounts of acyclovir.
GFP-expressing cells were analyzed 72 h after infection. The results are
expressed as a percentage of maximal infection, which is determined from (the
number of GFP-expressing cells in the presence of acyclovir divided by the
GFP-expressing cells in the absence of a drug effect) × 100. The
horizontal dotted line represents 50% inhibition. The IC50
values were ∼5 μm for wild-type virus, ∼50
μm for the T69N or M184V point mutants, and >300
μm for the V75I point mutant. When shown, error bars
represent the standard deviation from three or more replicates from two or
more normal blood donors. B, acyclovir prevents the appearance of
reverse transcription products. Primary CD4+ T cells were infected with
wild-type NL4-3 pseudovirus in the absence or presence of acyclovir. The
amounts of early, intermediate, and late reverse transcripts were quantified
by real-time PCR from DNA isolated at defined times and a standard curve
generated from known concentrations of pNL4-3-ΔE-eGFP with appropriate
primer pairs. The negative control (–Cont) infection was
performed at 4 °C, and signal represents residual plasmid from the viral
production step. Shown are representative data from one of three experiments
with similar results. C, acyclovir selects for mutations in HIV RT.
Replication-competent HIV was cultured in the presence of increasing
concentrations of acyclovir. The graph presents quantification of proviral
variants generated under the selective pressure of acyclovir. The percentage
of variants was determined from a minimum of 25 independent sequences at the
indicated days in culture. The solid black line denotes the
percentage of V75I variant appearing as a function of time.