Abstract
Bovine viral diarrhea infections are seen in all ages and breeds of cattle worldwide and have significant economic impact due to the productive and reproductive losses. The infectious agents that cause this disease, Bovine viral diarrhea viruses (BVDVs) may occur as two biotypes, of which one is non-cytopathic (ncp) and the other cytopathic (cp), classified according to whether or not they produce visible changes in cell culture. Cytopathic biotypes of BVDV can be created through internal deletion or recombination of RNA of ncp biotypes. The mechanisms of this change are not sufficiently understood. In this review, we discuss the work that has been done to date in our laboratory using methods of proteomics, cellular and molecular biology, and immunology. We found that both biotypes cause numerous changes in the expression levels of the proteins in monocytes, including proteins related to professional antigen presentation, enzymes and receptors, and changes in the infected cell functions related to antigen uptake. However, the alterations caused by the cp and not by the ncp biotypes are consistent with the hypothesis that the virus cytotoxicity involves the mitochondrial dysfunction. Overall, our data show that, the three important signals, antigen-specific, co-stimulatory and cytokine, required to promote the effector activation of naive T cells to be delivered by professional antigen presenting cells (APCs) are impaired by both types of BVDV. In addition, cp and ncp BVDVs differentially target mitochondrial proteins and antioxidant enzymes that control the fate of infected cells and determine whether BVDVs produce cytopathic effects or replicate noncytopathically to establish persistent infection. This research is aimed to discover foundational knowledge related to host-pathogen interactions and facilitate the development of innovative disease preventatives for pathogens causing significant animal losses.
Highlights
Our finding indicates that ncp Bovine viral diarrhea viruses (BVDVs) unlike the cp counterpart, inhibited the level of communication of the ECM and cell differentiation promoting the establishment of persistent infection (PI)
We suggest that by altering expression levels in multiple proteins related to immune responses such as cell adhesion, apoptosis, antigen uptake, processing and presentation, and other acute phase response proteins cp BVDV could significantly compromise immune defense mechanisms
Our data suggest that cp BVDV infection induces monocytes to differentiate into macrophages, or, alternatively, that monocytes that have already embarked on the differentiation into macrophages are more susceptible to cp BVDV infection
Summary
Bovine viral diarrhea virus (BVDV) is a representative of the family Flaviviridae, which is thought to have emerged and dispersed during the early Ice Age [8], causes a very prevalent disease in cattle [9] The viruses have both cp and ncp biotypes. Within the recent 15 years, the work of our group focused on the attempts to understand molecular mechanisms of cytopathic and noncytopathic BVDV infection and how the cp biotype of the BVDV emerges from the ncp one. To this end, we analyzed differences between the two biotypes, using methods of cellular immunology, molecular biology biochemistry, and proteomics.
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