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Figure 4 | Retrovirology

Figure 4

From: Modification of a loop sequence between α-helices 6 and 7 of virus capsid (CA) protein in a human immunodeficiency virus type 1 (HIV-1) derivative that has simian immunodeficiency virus (SIVmac239) vifand CA α-helices 4 and 5 loop improves replication in cynomolgus monkey cells

Figure 4

Saturation of intrinsic antiviral factors resulting from inoculation of high dose of virus particles. (A) Rhesus LLC-MK2 cells or hamster TK-ts13 cells were pre-treated with equal amounts of VSV-G pseudotyped particles with WT HIV-1 (white squares: Wt), with SIVmac L4/5 (white triangles: 4/5S), with SIVmac L6/7 (white circles: 6/7S), with SIVmac L4/5 and L6/7 (white diamonds: 4/5S6/7S), with SIVmac239 (pluses: SIVmac) or none (crosses) for 2 hours. The cells were then infected with the GFP expressing HIV-1 vector carrying SIVmac L4/5 (A: HIV-1-L4/5S-GFP) or GFP expressing HIV-1 vector with WT capsid (B: HIV-1-WT-GFP). Representative data of four independent experiments are shown. (C) Saturation activities were assessed in the presence or absence of functional TRIM5α. Before particle treatment, cells were infected with Sendai virus (SeV) expressing TRIM5 without the SPRY domain (black symbols), or an empty vector, parental Z strain of SeV (white symbols). Sixteen hours after SeV infection, cells were treated with particles for 2 hours and then infected with HIV-1-L4/5S-GFP. Representative data from six independent experiments are shown.

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