Table 1. Details of the W12 clones studied.
Clone | Integration site | Ploidy |
HPV16 gene copy number |
HPV16 E6/E7 expression per template | Expression per template category | ||||
---|---|---|---|---|---|---|---|---|---|
E6 | E7 | Mean E6/E7 | E2-5′ | E2-3′ | |||||
F | 4q13.3 | 2N | 1 | 1 | 1 | 1 | 1 | 248.6 (±31.8) | HIGH |
A5 | 8p11.21 | 2N | 1 | 1 | 1 | 1 | 1 | 215.6 (±14.9) | |
D2 | 18q21.2 | 2N | 3 | 4 | 4 | 0 | 3 | 118.5 (±12.0) | MEDIUM |
H | 4q21.23 | 2N | 1 | 1 | 1 | 0 | 1 | 100.1 (±12.4) | |
G2 | 21q22.1 | 2N | 3 | 3 | 3 | 3 | 0 | 37.5 (±4.2) | LOW |
All virus gene copy numbers were adjusted for cell ploidy and rounded to the nearest whole number. Levels of HPV16 E6 and E7 transcripts per template were referenced individually to low passage episome-containing W12 cells (W12 Series6 p11) and mean values (±s.e.m.) were determined from three biological replicates. Clone G2 showed three different virus–host junction transcripts by RNA-sequencing and clone D2 showed four different virus–host junction transcripts (data not shown). All clones tested (F, A5, D2 and G2) reformed an LSIL in organotypic tissue culture.