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. 2001 Jan;39(1):146-53.
doi: 10.1128/JCM.39.1.146-153.2001.

Pathogenesis of primary respiratory disease induced by isolates from a new genetic cluster of bovine viral diarrhea virus type I

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Pathogenesis of primary respiratory disease induced by isolates from a new genetic cluster of bovine viral diarrhea virus type I

C Baule et al. J Clin Microbiol. 2001 Jan.

Abstract

The pathogenesis of infection induced by cytopathogenic isolates from the newly identified genetic cluster Id of bovine viral diarrhea virus (BVDV) type I was studied in two experimental infections of previously seronegative, immunocompetent calves. Experiment 1 focused on the evaluation of clinical patterns, viremia, and serological responses. All infected calves in this experiment developed respiratory symptoms and seroconverted to BVDV positivity. Contact calves also contracted a respiratory tract infection following exposure to infected animals. Viremia was demonstrated between postinfection days 2 and 17, and the virus was detected in organ specimens of all but one each of the infected and contact calves. In experiment 2, the distribution of BVDV in various tissues of calves euthanized at defined days postinfection was studied. In two of these calves recurrent shedding of BVDV in nasal secretions was shown. BVDV was detected in various tissues of all infected calves throughout the experiment and also following seroconversion and the clearance of BVDV from the circulatory system. Despite the widespread distribution of the virus in various organs, significant tissue damage was found mainly in respiratory tract and lymphoid tissues. These experiments revealed that viruses from cluster Id of BVDV are able to induce primary respiratory disease in previously seronegative, immunocompetent calves. Contact transmission and virus recurrence, contrary to observations from acute experimental infections with noncytopathogenic BVDV, are likely to reflect differences in biological features of these cytopathogenic isolates. Virus shedding and its presence in tissues following peripheral clearance and in the presence of antibodies may have implications in the diagnosis, pathogenesis, and epidemiology of BVDV-induced syndromes in cattle.

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Figures

FIG. 1
FIG. 1
Pattern of clinical symptoms, viremia, and serology. Data for representative animals from experiment 1 (A) and experiment 2 (B) are shown. (A) Seronegative, immunocompetent calves were experimentally infected with cp isolates of BVDV Mo1 (group 1, calf no. 31) and Mo2 (group II, calf no. 36) in experiment 1. Calves no. 32 and 39 were contact controls in the respective groups. (B) In experiment 2, seronegative, immunocompetent calves were experimentally infected with cp isolate BVDV Mo1 and euthanized at different days postinfection. Solid bars, duration of clinical symptoms; V, detection of virus; +, virus positive; −, virus negative (for details, see Table 1); S, seroconversion; †, time point after initial infection when the calf was euthanized. For both panels A and B, the top row of each table indicates day(s) postinfection and the left column of each table indicates type of diagnosis or event (see key in panel B).
FIG. 2
FIG. 2
Distribution of BVDV in tissues in experiment 2. Specimens from 26 tissues were collected from each calf at different days following experimental infection with cp isolate BVDV Mo1. The specimens were analyzed by virus isolation (VI) and reverse transcription-PCR (PCR).

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