BVD infection results in a wide variety of clinical signs, due to its immunosuppressive effects, as well as having a direct effect on respiratory disease and fertility.

Following viral entry and contact with the mucosal lining of the mouth or nose, replication occurs in epithelial cells. BVDV replication has a predilection for the palatine tonsils, lymphoid tissues and epithelium of the oropharynx.

Phagocytes take up BVDV or virus-infected cells and transport them to peripheral lymphoid tissues; the virus can also spread systemically through the bloodstream. Viraemia occurs 2–4 days after exposure and virus isolation from serum or leukocytes is generally possible between 3–10 days post infection

During systemic spread the virus is able to gain entry into most tissues with a preference for lymphoid tissues. Neutralising antibodies can be detected from 10–14 days post infection with titres continuing to increase slowly for 8–10 weeks. After 2–3 weeks, antibodies effectively neutralise viral particles, promote clearance of virus and prevent seeding of target organs