Pathogenesis of intrauterine infections with bovine viral diarrhea virus.

BVDV shares with other Pestiviruses the ability to cross the placenta of pregnant host animals. The effects of fetal infections are complex and depend on a number of factors, e.g., age of the zygote/embryo stage, no infection seems to occur. During the last one third of gestation the infection is terminated by the ontogeny of the fetal immune system. This leaves a window of susceptibility during early stages of fetal development allowing establishment of viral persistence and/or the development of a number of fetopathologic effects. Additionally, fertility problems and abortions are observed. Calves that are born immunotolerant to BVDV and persistently viremic display a wide variety of abnormalities. However, there is an unknown proportion of calves born without any clinical signs indicative of persistent infection. The time of fetal infection during the first stages of pregnancy seems to play a crucial role with respect to the lesions induced. Generally, early infections seem to induce less damage compared with late infections, suggesting an indirect, possibly immune-mediated pathogenesis. Additionally, direct virus-cell interactions may play a role. Few data exist about the influence of differences in viral virulence on fetal pathology. Likewise the role of the viral target cell range is not clear.