Author
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Ridpath, Julia |
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Bayles, Darrell |
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Neill, John |
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Falkenberg, Shollie |
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BAUERMANN, FERNANDO - Universidade Federal De Santa Maria |
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HOLLER, LARRY - South Dakota State University |
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BRAUN, LLOYD - South Dakota State University |
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YOUNG, D - South Dakota State University |
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KANE, SUE - South Dakota State University |
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CHASE, C - South Dakota State University |
Submitted to: Virology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/30/2015 Publication Date: 8/28/2015 Publication URL: http://handle.nal.usda.gov/10113/61907 Citation: Ridpath, J.F., Bayles, D.O., Neill, J.D., Falkenberg, S.M., Bauermann, F.F., Holler, L., Braun, L.J., Young, D.B., Kane, S.E., Chase, C.C. 2015. Comparison of the breadth and complexity of bovine viral diarrhea (BVDV) populations circulating in 34 persistently infected cattle generated in one outbreak. Virology. 485:297-304. doi. 10.1016/j.virol.2015.07.022. Interpretive Summary: Bovine viral diarrhea viruses (BVDV) infect cattle worldwide. These viruses cause two types of infections, acute and persistent. Acute infections happen when animals are infected after they are born. Typically acute infections last from two to three weeks. Persistent infections happen when an animal is infected while still in the womb. Persistent infections last for the life span of the animal. There are a number of different outcomes of persistent infection. Some persistently infection animals (PI) have multiple defects while some appear completely normal. It is not know why there is so much variation in the outcome of persistent infections. In this study 34 PI from the same BVDV outbreak were studied. It was found that there was a lot of variation in the viral populations that were circulating in each PI animal even though they arose in the same outbreak. This finding suggests that host factors affect the outcome of persistent infection. That is, some animals may be genetically predispositioned to respond to persistently infection in one way and other animals may be genetically predispositioned to respond in a different way. In addition to showing that an individuals genetic make up determines how they respond to persistent infection these studies resulted in the development a tool (also known as a metric) that can be used to compare differences in response. Using this tool could contribute to the development of means that will help animals develop better defenses or that will help producers to identify animals with better defense systems. Technical Abstract: Exposure to bovine viral diarrhea viruses (BVDV) may result in acute and persistent infections. Persistent infections are the consequence of in utero exposure during the first trimester of gestation. The resulting persistently infected (PI) animals are immunotolerant to the virus. Clinical presentation in PI animals runs the gamut from clinically normal and thriving to ill thrift with multiple congenital defects. Further, PI animals vary in the amount of virus associated with circulating white blood cells and in their ability to transmit virus to naïve co-horts. It is not known whether these variations are due to differences in viral strains or host factors or a combination of the two. Similar to other viruses with single stranded RNA genomes, BVDV isolates exist as quasispecies, or a swarm of individual viruses, each with variable numbers of nucleotide variations. Studies were conducted that compared viral populations among 34 PI animals generated during one BVDV2 outbreak. In addition, a small scale study was conducted that compared viral populations between PI animals generated under controlled conditions. It was found that PI animals generated in the same outbreak or generated under controlled conditions, using the same inoculum and at the same gestational stage, can carry circulating viral populations that differ widely in size and diversity. The size and diversity of the circulating viral populations within PI animals is a quantifiable phenotype. Studies can now be designed that compare this phenotype to other PI phenotypes such as growth rate, congenital defects, viral shed and cytokine expression. Such studies may help to unravel the tangled array of host processes that are involved in the maintenance of immunotolerance and suppression of immune responses. |