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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Ruminant Diseases and Immunology Research » Research » Publications at this Location » Publication #311355

Title: Innate and adaptive immune responses to in utero infection with bovine viral diarrhea virus

item HANSEN, THOMAS - Colorado State University
item SMIRNOVA, NATALIA - Colorado State University
item WEBB, BRETT - Colorado State University
item BIELEFELDT-OHMANN, HELLE - Colorado State University
item Sacco, Randy
item VAN CAMPEN, HANA - Colorado State University

Submitted to: Animal Health Research Reviews
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/19/2015
Publication Date: 6/1/2015
Publication URL:
Citation: Hansen, T.R., Smirnova, N.P., Webb, B.T., Bielefeldt-Ohmann, H., Sacco, R.E., Van Campen, H. 2015. Innate and adaptive immune responses to in utero infection with bovine viral diarrhea virus. Animal Health Research Reviews. 16(1):15-26. DOI: 10.1017/S1466252315000122.

Interpretive Summary: Bovine viral diarrhea virus (BVDV) infects cattle worldwide resulting in disease in both dairy and beef production units. Frequently BVDV is introduced into a production unit by an animal persistently infected (PI) with BVDV. PI animals are the result of the infection of a fetus before the maturation of the immune system. This infection results in an animal that produces virus and sheds it to its pen mates throughout its lifetime. In the present paper, researchers from Colorado State University, School of Veterinary Science in Queensland, Australia, and the National Animal Disease Center have reviewed information available on immune responses following fetal infection with BVDV. Scientists trying to investigate methods to prevent development of PI animals would be beneficiaries of this current research, with the ultimate goal of providing intervention strategies to cattle producers.

Technical Abstract: Infection of pregnant cows with noncytopathic (ncp) BVDV induces rapid innate and adaptive immune responses resulting in clearance of the virus in less than 3 weeks. Seven to 14 days after inoculation of the cow, ncpBVDV crosses the placenta and induces a fetal viremia. Establishment of persistent infection (PI) with ncpBVDV in the fetus has been attributed to the inability to mount an immune response before 125 days of gestational age. The result is “immune tolerance”, persistent viral replication and shedding of ncpBVDV. In contrast, we describe the chronic upregulation of fetal type I IFN pathway genes and the induction of IFN-' pathways in fetuses of cows infected on day 75 of gestation. PI fetal IFN-' concentrations also increased at day 97 at the peak of fetal viremia and IFN-' mRNA was significantly elevated in fetal thymus, liver and spleen 14-22 days post maternal inoculation. PI fetuses respond to ncpBVDV infection through induction of type I IFN and IFN-' activated genes leading to a reduction in ncpBVDV titer. We hypothesize that fetal infection with BVDV persists because of impaired induction of IFN-' in the face of activated type I IFN responses. Clarification of the mechanisms involved in the IFN associated pathways during BVDV fetal infection may lead to better detection methods, antiviral compounds and selection of genetically resistant breeding animals.