Submitted to: Abstracts World Buiatrics Congress
Publication Type: Abstract only
Publication Acceptance Date: 2/5/2004
Publication Date: 7/12/2004
Citation: Elmowalid, G., Braun, L., Ridpath, J.F., Chase, C. 2004. Rethinking bovine viral diarrhea virus pathogenesis: understanding the importance of BVDV strain on the innate immune system [abstract]. 23rd World Buiatrics Congress. Paper No. 028(1548). Interpretive Summary:
Technical Abstract: Bovine viral diarrhea virus (BVDV) continues to be the bane of the US beef and dairy industry. BVDV infections cause symptoms that vary from peracute death to inapparent infection. Even these inapparent BVDV infections can result in persistent infection (PI) of susceptible fetuses. The macrophage expresses cell surface markers that are important for phagocytosis and bacteria killing and also for stimulation of T helper cells and for immune surveillance and killing by cytotoxic T cells (CTL). In this study, our objective was to measure the effect of BVDV on the macrophage function (phagocytosis and pathogen killing) and surface marker expression (CD14, MHCI and MHCII). Bovine macrophages were developed from bovine monocytes and then infected with eight different strains of BVDV, 6 noncytopathic (NCP) and 2 cytopathic (CP). There were 3 type 1 and 5 type 2 viruses. The six noncytopathic strains were two highly virulent strains that cause severe acute (SA) disease, one strain that causes moderate disease and three strains that cause inapparent disease with high persistence (IDHP) in susceptible fetuses. Each of the strains was used to infect the macrophages and the phagocytic ability, microbicidal activity (fungal and bacteria) and NO production (microbicidal killing product) were measured. Surface marker expression for CD14 (receptor for gram negative bacteria) was measured using flow cytometry. Infection of macrophages with the highly virulent SA resulted in 50-60% decrease in phagocytosis by 24 hrs. These viruses had a similar effect on the microbicidal activity against bacteria and fungi and also decreased NO production. On the other hand the IDHP strains had no effect on phagocytosis or any of the other functions. Analysis of surface markers indicated that in macrophages infected with SA strains had a 40-60% decrease in CD14 expression while the IDHP strains had no effect on CD14 expression. The most interesting aspect of this research is that the clinical symptoms seen with the NCP viruses correlate directly to their effect on macrophages. This research indicates that virulence is not related to genotype and that different NCP BVDV isolates cause a wide spectrum clinical disease that correlates to effect on macrophages.