Related Experiment Video
Updated: Sep 20, 2026
Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
A wild-type porcine encephalomyocarditis virus containing a short poly(C) tract is pathogenic to mice, pigs, and
Rebecca LaRue1, Suzanne Myers, Laurie Brewer
1Department of Veterinary Pathobiology, University of Minnesota, St. Paul, Minnesota 55108, USA.
Abstract:
Previous studies using wild-type Encephalomyocarditis virus (EMCV) and Mengo virus, which have long poly(C) tracts (61 to 146 C's) at the 5' nontranslated region of the genome, and variants of these viruses genetically engineered to truncate or substitute the poly(C) tracts have produced conflicting data on the role of the poly(C) tract in the virulence of these viruses. Analysis of the nucleotide sequence of an EMCV strain isolated from an aborted swine fetus (EMCV 30/87) revealed that the virus had a poly(C) tract that was 7- to 10-fold shorter than the poly(C) tracts of other EMCV strains and 4-fold shorter than that of Mengo virus. Subsequently, we investigated the virulence and pathogenesis of this naturally occurring short-poly(C)-tract-containing virus in rodents, pigs, and nonhuman primates. Infection of C57BL/6 mice, pigs, and cynomolgus macaques resulted in similar EMCV 30/87 pathogenesis, with the heart and brain as the primary sites of infections in all three animals, but with different disease phenotypes. Sixteen percent of EMCV 30/87-infected pigs developed acute fatal cardiac failure, whereas the rest of the pigs were overtly asymptomatic for as long as 90 days postinfection (p.i.), despite extensive myocardial and central nervous system (CNS) pathological changes. In contrast, mice infected with >/==" BORDER="0">4 PFU of EMCV 30/87 developed acute encephalitis that resulted in the death of all animals (n = 25) between days 2 and 7 p.i. EMCV 30/87-infected macaques remained overtly asymptomatic for 45 days, despite extensive myocardial and CNS pathological changes and viral persistence in more than 50% of the animals. The short poly(C) tract in EMCV 30/87 (CUC(5)UC(8)) was comparable to that of strain 2887A/91 (C(10)UCUC(3)UC(10)), another recent porcine isolate.
Insights
This study examines Encephalomyocarditis virus (EMCV) with a short poly(C) tract. The virus caused varied disease severity in mice, pigs, and primates, highlighting the poly(C) tract's role in EMCV virulence.
Area of Science:
- Virology
- Pathogenesis
- Molecular Biology
Background:
- Conflicting data exists on the role of the 5' nontranslated region poly(C) tract in Encephalomyocarditis virus (EMCV) and Mengo virus virulence.
- Previous studies used wild-type viruses with long poly(C) tracts or genetically engineered variants, yielding inconsistent results.
- A naturally occurring EMCV strain (30/87) with a significantly shorter poly(C) tract was identified in an aborted swine fetus.
Purpose of the Study:
- To investigate the virulence and pathogenesis of the short-poly(C)-tract EMCV strain (30/87) in animal models.
- To compare the disease outcomes and pathological changes in rodents, pigs, and nonhuman primates.
- To elucidate the impact of a naturally truncated poly(C) tract on EMCV pathogenicity.
Main Methods:
- Nucleotide sequence analysis of EMCV strain 30/87 to determine poly(C) tract length.
- Infection studies involving C57BL/6 mice, pigs, and cynomolgus macaques with EMCV 30/87.
- Clinical observation, pathological examination of heart and brain tissues, and viral persistence assessment post-infection.
Main Results:
- EMCV 30/87 infection led to primary pathogenesis in the heart and brain across all species, but with distinct disease phenotypes.
- Mice experienced acute fatal encephalitis, with all animals dying between days 2-7 post-infection.
- Pigs showed varied responses, with 16% developing fatal cardiac failure and the rest remaining asymptomatic despite myocardial and CNS pathology; macaques were asymptomatic for 45 days despite significant pathology and viral persistence.
Conclusions:
- The naturally short poly(C) tract in EMCV 30/87 influences viral pathogenesis and virulence.
- Despite conserved primary target organs (heart, brain), the short poly(C) tract results in differential disease outcomes across species.
- The findings contribute to understanding the structure-function relationship of viral RNA elements in determining disease severity.
