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. 2024 May 23;9:88. doi: 10.1038/s41541-024-00877-1

Fig. 3. CCHF VRP reduces clinical disease by controlling viral load and improving liver function.

Fig. 3

a Tissues including liver, spleen, ovary/testis (gonad), kidney, lung, heart, eye, brain, and whole blood were collected from mice in all vaccine cohorts at the time of euthanasia 3 or 6 days post infection (dpi). Viral RNA was quantified via RT-qPCR using primers/probe specific for the NP ORF of the CCHFV S gene segment. b Clinical chemistry analytes from each animal were assessed using whole blood collected peri-mortem (intracardiac bleed) in lithium heparin and analyzed via the General Chemistry 13 Panel on the Piccolo Xpress analyzer. GLU glucose, BUN blood urea nitrogen, ALB albumin, ALT alanine aminotransferase, AST aspartate aminotransferase, TP total protein, CRE creatinine. Viral load and clinical chemistry statistics for each vaccine group were calculated as significant change compared to unvaccinated control animals (No VRP, given DMEM alone) at equivalent timepoint (3 or 6 dpi) using multiple two-tailed I-tests (Mann-Whitney). Only statistically significant results are reported; *p < 0.5; **p < 0.01 (Supplementary Tables 1-2). Individual animals are represented. Bars and error bars indicate mean ± SEM.