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.

An outbreak of the atypical form of myxomatosis struck a rabbit farm in Hungary. The animals had previously been vaccinated with a vaccine containing Shope rabbit fibroma virus strain. The disease appeared in winter when the presence of mosquitoes and fleas is not common. The virus was isolated from an eyelid specimen of a naturally infected rabbit. The surviving animals were observed for four weeks, blood samples were collected and, after euthanasia, organ specimens were also examined by morphological methods including pathology and electron microscopy. Serum samples were examined by virus neutralisation for antibodies. Genetic analysis of the isolated virus was carried out by polymerase chain reaction (PCR) and direct sequencing. The primers were designed on the basis of the major envelope gene (Env) of the Lausanne reference strain in the GenBank. The viral proteins were examined by SDS-PAGE. The isolated virus (ref. no.: BP04/2001) was able to infect the susceptible animals directly, by contact. The disease was characterised by respiratory symptoms of the upper tracheal tract, conjunctivitis and high mortality by the 11th-14th day. Aerogenic infection with strain BP04/2001 resulted in 100% morbidity among the susceptible animals. Sequencing of the amplified 400-bp-long DNA revealed 97% homology with the Env gene of the Lausanne strain, which proves that strain BP04/2001 is a variant of the Lausanne strain having been enzootic throughout Europe. The live vaccine strain used in Hungary against myxomatosis, which is also a Lausanne-derived strain, protected the animals. According to the protein analysis a protein of 200 kDa in size is not expressed in strain BP04/2001. This is the first report on atypical myxomatosis in Central Europe. The virus spreads by airborne transmission and may cause severe losses in the rabbit population.

Animals persistently infected with BVDV are important in the epizootiology of the Bovine Viral Diarrhea (BVD) because they are a permanent source of contamination within a herd. These animals produce large quantities of virus and have, therefore, been proposed as responsible for generating antigenic variability. However, limited studies have failed to detect antigenic or genetic changes in viruses isolated at different time from persistently infected animals. One hypothesis to account for this stability is that the immunotolerance is accompanied by a selection against antigenic change. The presence of an immunotolerant persistently infected (IPI) animal in a herd would in turn lead to herd specific strains. To verify this hypothesis, we compared 17 BVDV strains isolated from IPI animals from 3 herds of Eastern Belgium. The comparison was based on the sequence of a 389 bp fragment of E2--a gene encoding for a highly variable glycoprotein. Sequences were strongly conserved within herds but were quite different between herds, indicating that BVDV herd-specific strains do exist and are associated with the presence of IPI animals.

Patients suffering from periodontitis or periodontosis were selected for the study. Further subdivision of these groups was based on the presence or absence of herpes and/or adenoviruses in their oral lymphocytes and epithelial cells. The phagocytic and bactericidal activities of oral leukocytes isolated from the same individuals were compared with virus carriage. In the periodontitis group, 60.5%, and in the periodontosis group 61.5% of patients carried viruses, while this was established only in 21.1% of control cases. On the other hand, emigration and sulcular gathering of the less viable polymorphonuclear leukocytes was elevated but their phagocytotic activity was decreased among periodontitis patients. Bactericidal capacity was significantly lowered among those subjects who carried viruses in their cells, as compared with virus-free persons, especially in the periodontitis group. The functions of the polymorphonuclear leukocytes accumulated in the sulcus gingivalis may be modified by mediators released from the virus-carrying cells. These mediators could achieve a greater concentration locally, and the damaged leukocytes would not be able to eliminate the microbes continuously so that the accumulation of bacterial products, among them endotoxins, could lead to periodontal inflammation.

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