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. 2014 Jan 9;10(1):e1003868. doi: 10.1371/journal.ppat.1003868

Figure 6. HIV-1 CTL escape variants invariably preserve CA-CPSF6 interactions in vivo during their evasion from the restrictive action of CPSF6.

Figure 6

(A) HeLa cells were infected with VSV-G-pseudotyped GFP reporter viruses in the presence or absence of aphidicolin (Aph). Only RKLM and SH8127 were significantly blocked in aphidicolin-treated cells (p<0.05). (B) HeLa cells were transfected with siRNA targeting CPSF6 or CypA and infected with VSV-G-pseudotyped GFP reporter viruses. All the “in vivo” viruses were less sensitive to CPSF6 or CypA depletion (p<0.02). However, among these “in vivo” viruses only SH8127 had significant increase relative to control upon CPSF6 or CypA depletion (p<0.05). (C) CEM cells were infected with replication-competent GFP reporter viruses for spreading infections. (D) VSV-G-pseudotyped GFP reporter viruses were used to infect HeLa cells stably transduced with the control vector LPCX or one overexpressing CPSF6-358. (E) VSV-G-pseudotyped GFP reporter viruses were used to infect control HeLa cells or those stably overexpressing TRIM19-CypA. (F) Control Jurkat cells and those lacking CypA were infected with VSV-G-pseudotyped GFP reporter viruses. Results are one representative experiment of at least two triplicate experiments. Standard deviations (except for F) or standard errors of the mean of a single experiment are indicated with the error bars.