Except for viral strain virulence, the authors report that the factors which affect the pathogenesis of BVD infection are poorly defined. These factors include host animal’s age and immunological status, the latter affected by stress and co-infection by other pathogens. Researchers have stated that early immunosuppression and subsequent persistence of BVDV in lymphoid tissues contribute to the initial low levels of neutralising antibodies at 10-14 days and the slow titre increase for the subsequent 8 - 10 weeks. The aim of this study was to research the effects of viral dose and immunological parameters on BVDV-1 replication and clinical disease.
Materials and Methods – 3 - 4 month old calves were randomly allocated to groups which were inoculated intra-nasally with either low or medium doses of BVDV-1. One group also received five doses of dexamethasone to induce immunosuppression, alongside BVD infection. A number of calves were introduced to the groups, after inoculation, to act as sentinels, and post mortem examination was performed at various days post infection (dpi). A later trial inoculated a group of seven week old and five month old calves with a high dose of BVDV-1 to assess the maturation of the immune system.
Findings - The authors found that viral dose has an effect on the range of symptoms and the severity of disease. In addition, more clinical effects were detected in younger animals, this was considered to demonstrate the effect of immunological maturity on progression of clinical disease.
The immunosuppressed group displayed more severe clinical signs; WBC concentrations were significantly decreased and thrombocytopaenia was more pronounced, compared to the group which received the same inoculation dose but was not immunosuppressed. In this same group, the period of viral shedding was prolonged and the transmission of virus to sentinels increased. This suggests that immunosuppression delays the immune response and enhances the ability of BVDV to establish a productive infection. The authors hypothesised that severe episodes of BVD, seen occasionally in the field, may be a result of immunosuppression caused by other agents.
Finally, BVDV-1 was found to be actively replicating, beyond acute infection and seroconversion, for between 80 and 85 dpi, depending on the initial inoculating dose. At this time virus isolation was negative and clinical signs absent, suggesting an impaired cellular immunity with incomplete removal of infected cells. The authors propose the possibility of a persistent, but restricted, infection.