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. 2014 May 27;111(23):8595–8600. doi: 10.1073/pnas.1401215111

Fig. 4.

Fig. 4.

Characterization of MuLV isolates in vivo. (A) Approach used to determine if infectious MuLVs isolated from AML cells are responsible for AML induction. (B) Spleen weights of NSG mice from untreated controls (n = 12), infected with MuLV (Vp39) isolated from AML cells (n = 5), or transplanted (Tx) with either group I (G1; n = 11) or group II (G2; n = 14) patient samples. Mean and the SEM are shown. The P value for the observed difference between spleen weights was calculated by using a two-tailed unpaired t-test. (C) Quantitative assay to determine E-MuLV and P-MuLV transcript levels in infected NSG mice. Mice were analyzed up to 340 d after infection. Quantitative RT-PCR was performed on RNA isolated from livers or, as positive controls, from SC1 cells producing E-MuLV or 293T cells producing P-MuLV. (D) Representative histology sections demonstrating splenic hypocellularity in NSG controls or infected NSG mice. In contrast, the spleen of PMF-Tx mouse is hypercellular and large foci of myeloid cells are frequently detected (H&E staining, objective 20×).