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United States Department of Agriculture

Agricultural Research Service

Title: A Wild-Type Porcine Encephalomyocarditis Virus Containing a Short Poly(c) Tract Is Pathogenic to Mice, Pigs, and Cynomolgus Macaques

Authors
item Larue, Rebecca - UNIV OF MN-ST PAUL, MN
item Myers, Suzanne - PA STATE UNIV - PA
item Brewer, Laurie - UNIV OF MN-ST PAUL, MN
item Shaw, Daniel - PA STATE UNIV - PA
item Brown, Corrie - UNIV OF GA-ATHENS, GA
item Seal, Bruce
item Njenga, Kariuki - UNIV OF MN-ST PAUL, MN

Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 4, 2003
Publication Date: August 25, 2003
Citation: Larue, R., Myers, S., Brewer, L., Shaw, D.P., Brown, C., Seal, B.S., Njenga, K.M. 2001. A Wild-Type Porcine Encephalomyocarditis Virus Containing A Short Poly(C) Tract Is Pathogenic To Mice, Pigs, And Cynomolgus Macaques. Journal of Virology, v.77, p. 9136-9146, 2003.

Interpretive Summary: Encephalomyocarditis virus (EMCV) may infect a variety of species including pigs very severely causing infections of the heart and brain. The beginning portion of the genome that does not code for proteins, designated the five prime untranslated region, have been correlated to how virulent these virus types are in animals. A naturally occurring EMCV isolate from an aborted pig fetus with a short untranslated region caused acute heart failure in sixteen percent of the pigs when infected with that virus. The remaining pigs not develop any outward clinical signs of illness even though the virus caused damage to heart muscle and could be detected in the brain of those animals. Mice infected with the EMCV isolate from pigs all developed an infection in the brain that resulted in death of the animals. This EMCV isolate examined is genetically similar to another recent virus from pigs.

Technical Abstract: Previous studies using wild-type Encephalomyocarditis virus (EMCV) and Mengo virus, which have long poly(C) tracts (61 to 146 Cs) at the 5 prime untranslated 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 EMCV. Nucleotide sequence nalyssi 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 and pigs. Infection of C57BL/6 mice and pigs resulted in similar EMCV 30/87 pathogenesis, with the heart and brain as the primary sites of infections, 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 EMCV 30/87 developed acute encephalitis that resulted in the death of all animals (n = 25) between days 2 and 7 p.i. The short poly(C) tract in EMCV 30/87 was comparable to that of strain 2887A/91, another recent porcine isolate.

Last Modified: 8/21/2014
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