TABLE 1.
Virus | Total no. of integrations | Cell type | % Integration into RefSeq genesb
|
|
---|---|---|---|---|
N02 | J03 | |||
ASV | 226 | HeLa | 39.8e | 42.0e |
HIV-1c | 524 | SupT1 | 61.0 | (71.7) |
HIV-1d | 379 | H9/HeLa | 57.8f | (67.9) |
HIV-1d | 135 | HeLa | 50.0 | (58.8) |
MLVd | 903 | HeLa | 34.2g | (40.2) |
Randomd | 10,000 | Simulated | 22.4 | (26.3) |
Results from the present study are shown in boldface.
N02, November 2002 assembly of RefSeq genes (18,214 genes); J03, July 2003 assembly of RefSeq genes (21,404 genes). Values in parentheses indicate extrapolated proportional increase in RefSeq targets by using the July 2003 assembly versus the November 2002 assembly used by Wu et al. (43).
Raw data are from the work of Schröder et al. (34) and were reevaluated by Wu et al. (43) using RefSeq genes. Values were compared with ASV by using the 2 × 2 chi-square test with the Yates correction (P ≤ 1.3 × 10−7).
From the work of Wu et al. (43).
Values are significantly different from random integration (P ≤ 2.13 × 10−7) with the 2 × 2 chi-square test with the Yates correction.
Value was reported to be significantly different from random integration (43).
Value was reported to be significantly different from random integration and HIV-1 value of 57.8 (43). Value is indistinguishable from ASV value (39.8) (P = 0.134), by the 2 × 2 chi-square test with the Yates correction.