KSHV targets multiple leukocyte lineages during long-term productive infection in NOD/SCID mice
J. Clin. Invest. Christopher H. Parsons, et al. 116:1963 doi:10.1172/JCI27249 [Go to this article.]

Figure 1
Sequential increases in KSHV genomic DNA, latent (ORF73) and lytic (ORF50 and ORF65) transcripts within the spleens of KSHV-injected NOD/SCID mice. Mice were administered 3 weekly doses of KSHV (squares, solid lines) or UV-KSHV (triangles, dashed lines) intravenously and euthanized 1 day (DNA only) and 1, 2, and 4 months following the third injection. (A) Genomic KSHV DNA values were determined using qPCR to calculate the ΔC_t, representing KSHV C_t normalized to mouse GAPDH C_t (mean of triplicate determinations for each) for each sample. (B–D) Total splenic RNA was subjected to qRT-PCR using primers specific for ORFs 73 (B), 50 (C), and 65 (D) as well as mouse GAPDH. ΔδC_t = (ΔC_t(G)) – (ΔC_t(K)), where ΔC_t(K) and ΔC_t(G) are the differences between the C_t of each sample (mean of duplicate determinations) without and with reverse transcriptase (RT) for KSHV (K) and GAPDH (G), respectively. Each symbol represents the mean and SE of ΔC_t (A) or ΔδC_t (B–D). Numbers of mice are indicated in parentheses. Graph-wide dotted lines mark the lower limit of sensitivity of each assay. Of note, UV-KSHV did not establish infection within either primary dermal microvascular endothelial cells (pDMVECs) or HeLa cells in vitro (not shown).