Following the traditional assumption that individuals, while being infected with one strain, are temporarily not susceptible to the other [ 52, 53, 62, 67], most of all these models consider only subsequent infection (i.e., individuals that recovered from primary infection with one strain were further infected by others).
This giant virus is in turn, targeted by an infectious virophage (Sputnik 2), which is then further infected by transpovirons (bits of parasitic DNA) [124].
More importantly, when BMI-1 knockdown cells were further infected with the lentivirus encoding a BMI-1 wobble mutant, cell migration was substantially rescued (P<0.05).
MCF10A-NHERF1-Neo cells were further infected with PTEN-siRNA retrovirus to knockdown PTEN expression, which was determined by PTEN immunoblotting.
At this stage, MCF7 cells were further infected with either Ad5hTRAIL or AdCMVLacZ vector at increasing doses.
For the co-infected group, after a 12 h incubation at 37°C in 5% CO2 with virus, cells were further infected with S. suis (10 CFU/well, MOI 10).
The subcloned line was then further infected with pE retroviral vectors encoding murine ICAM-1, CD48 and ICOS-L [ 9], followed by selection with G418, hygromycin and zeocin, respectively.
Some clones were further infected with a retrovirus containing either H-RasV12 (pBabe-puro H-RasV12) (Yu et al, 2001) or wild-type ErbB-2 (pBabe-puro ErbB-2) (Yu et al, 2001) and selected in 5 μg/ml puromycin for another 5 days.
Primary myoblasts isolated from C57BL/6 mice, already transduced to express the β-galactosidase marker gene (lacZ), were further infected at high efficiency (Springer & Blau, 1997) with retroviruses carrying the cDNA of murine VEGF164 linked through an Internal Ribosome Entry Sequence (IRES) to a truncated murine CD8a as a FACS-sortable marker (Misteli et al, 2010).
