Fig. 10. Impact of MOI on the sensitivity of HIV-1 to ARVs.

(A) The SupT1 T cell line was exposed to a range of VSV-G–pseudotyped eGFP reporter virus inputs in the absence of drugs. eGFP MFI was markedly increased when SupT1 T cells were exposed to high input of VSV-G–pseudotyped viruses. Data representative of three independent experiments are shown. (B) DTG sensitivity of VSV-G–pseudotyped eGFP reporter virus harboring WT-IN or the catalytically inactive IN-D116N mutant. The SupT1 T cell line was infected with a 30-fold range of viral inputs in the presence of the indicated concentrations of DTG. The number of infected cells was enumerated by flow cytometry. Sensitivity of VSV-G–pseudotyped eGFP reporter viruses to (C) INSTIs RAL and CAB, (D) NNRTIs RPV and EFV, (E) NRTI FTC, and (F) NRTTI EFdA and (G) PI DRV. (H) Experimental design of abrogation experiments. The SupT1 T cell line was exposed to VSV-G–pseudotyped HIV-1 (dark virus) over a range of viral inputs together with a fixed amount of VSV-G–pseudotyped eGFP reporter virus. The amount of dark virus was 0.3, 1, 3, or 10 times the amount of eGFP reporter virus. Viral inputs were normalized by RT activity, except for the catalytically inactive RT-D186N mutant, in which case viral inputs were normalized by Gag Western blots. (I) DTG sensitivity of VSV-G–pseudotyped eGFP reporter virus in the presence of dark virus harboring WT-Pol, IN-D116N, or RT-D186N. (J) RPV sensitivity of VSV-G–pseudotyped eGFP reporter virus in the presence of WT dark virus. Data from at least three independent experiments are shown as means ± SEM. *P < 0.05, unpaired t test.