TABLE 2.

Effects of inactivating vif on endogenous reverse transcription^a

Producer cellb	Permeabilizing agent	Effect(s) of vif inactivation on DNA synthesis	Reference
SupT1	1 mM β-octylglucoside	No effect	76
Jurkat	None; analysis of cDNA in purified virions	No effect	49
CEM	None; analysis of cDNA in purified virions	No effect	234
CEM	1 mM β-octylglucoside	>5-fold decrease in levels of early as well as full length products	76
Different chronically infected H9 clones with different levels of restrictionc	0.01 to 0.5% Nonidet P-40	Strong global defect correlated with the defect in intracellular reverse transcription	163
H9	None	No or little effect	55
H9	Melittin	Slight defect	55
H9	0.01% Triton X-100	Strong defect; no long double-stranded DNA products	55
H9	0.02% Triton X-100	8-fold decrease of nucleotide incorporation	49
H9	None; analysis of cDNA in purified virions	∼8-fold decrease in reverse transcription (similar effect on products of different lengths)	49
H9 or HUT78	Melittin	∼1.8-fold reduction	173
H9 or HUT78	0.01-0.04% Triton X-100 or Nonidet P-40	∼1.8-fold reduction	173
HUT78	Melittin	∼1.5-fold reduction	68

^aVirions produced by permissive and nonpermissive cells were purified, and the efficiencies of reverse transcription inside HIV-1 vif⁺ and Δvif virions were compared. Virions were either untreated or treated with different permeabilizing agents to facilitate the penetration of the dNTPs.

^bPermissive and nonpermissive cells are indicated in boldface type and with underlining, respectively.

^cThose authors compared levels of DNA synthesis by isogenic HIV-1 Vif⁻ mutants produced by different chronically infected H9 clones, which exhibit different degrees of impairment in their replicative capacity (163).