Fig. 9: Distinct evolutionary trajectories of M66I-carrying variants yield differential infection outcomes in nondividing cells. | Nature Communications

Fig. 9: Distinct evolutionary trajectories of M66I-carrying variants yield differential infection outcomes in nondividing cells.

From: Recurrent and novel evolutionary pathways drive in vitro HIV-1 lenacapavir resistance with diverse phenotypic consequences

Fig. 9: Distinct evolutionary trajectories of M66I-carrying variants yield differential infection outcomes in nondividing cells.The alternative text for this image may have been generated using AI.

a, c Representative flow cytometry plots showing GFP expression in TZM-bl cells infected with HIV-1 variants carrying the indicated capsid mutations, in the absence (top row, −Aph) or presence (bottom row, +Aph) of aphidicolin. Percentages indicate the proportion of GFP-positive cells. b, d Quantification of infectivity in the presence or absence of aphidicolin. Infectivity was assessed by GFP expression and normalized to the untreated (−Aph) condition for each virus. Bars represent the mean ± SEM of biological replicates. Statistical analysis in (b) was performed using an unpaired two-tailed t-test; ****p < 0.0001. WT (n = 8), Q67N (n = 6), M66I + Q67N (n = 4), and M66I + Q67N + E187K (n = 4). In (d) (n = 4), statistical significance was assessed by one-way ANOVA followed by Dunnett’s multiple comparisons test comparing M66I to the other mutants. ****p < 0.0001; **p < 0.01; *p < 0.05. Source data are provided as a Source data file.

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