Skip to main content
. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Virology. 2014 Mar 13;0:215–226. doi: 10.1016/j.virol.2014.02.022

Figure 6. Absence of murine APOBEC3 does not alter MHV68 pathogenesis.

Figure 6

A. Schematic depicting the disruption of murine APOBEC3 (mA3) by the insertion of a β-geo cassette to generate mA3 knockout mice (mA3−/−). B. Genotype PCR analysis of DNA harvested from the splenocytes of infected WT C57BL/6 or mA3−/− mice. The locations of primers for either the WT or mutant mA3 gene are shown in panel A. C. Immunoblot demonstrating expression of mA3 in WT but not mA3−/− mice. D. Acute replication in the lungs of WT or mA3−/− lungs 4 and 7 days post intranasal infection with 1000 PFU of WT MHV68. E. Spleen weights from naïve WT, infected mA3−/− mice or infected WT mice 16 dpi. F. Latency is determined as the frequency of viral genome positive splenocytes determined by limiting dilution PCR. G. Frequency of reactivation from intact splenocytes determined by a limiting dilution explant reactivation assay 16 dpi. Open symbols represent preformed infectious virus from mechanically disrupted cells plated in parallel. The data shown represent three independent experiments with splenocytes pooled from three to five mice per experimental group.