Nuclear aggregates induced by HSV1-XFPVP26 impair nuclear capsid egress.

<p>Vero cells were infected (inf.) with 10 PFU/cell of HSV1(17⁺)blueLox (A, wild type), HSV1(17⁺)blueLox-mRFPVP26_{Δaa<b>1</b>–7} (B), or HSV1(17⁺)blueLox-GFPVP26_{Δaa<b>1</b>–7}(C), and fixed at 9 h with PFA. Alternatively, cells were transfected (transf.) with pHSV1(17⁺)blueLox-GFPVP26_{Δaa<b>5</b>–7} (D) or pHSV1(17⁺)blueLox-GFPVP26_{Δaa<b>1</b>–7} (E), and fixed at 24 h. In addition to the intrinsic fluorescence of the XFPVP26 constructs (mRFPVP26 or GFPVP26), the subcellular localization of VP26 (α-VP26) and VP5 (MAb 5C10) were analyzed after permeabilization with TX-100 and immunolabeling by confocal fluorescence microscopy. The nuclei were stained with TO-PRO-3 (A, E). Arrows highlight cytoplasmic capsids (A–D) or incoming capsids at the nuclear rim of a neighboring cell (Ei). Scale bar: 10 µm.