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Virological and pathomorphological aspects in experimental infections with some triassociated pneumotropic viruses in the white mouse.

Experimental infections were induced in white mice by intranasal administration of parainfluenza virus type 3, 739-2D strain, to which influenza virus A/Beijing, 353/89 (H3N2) strain, and respiratory syncytial virus, Long strain, were associated. The model was organized so as to obtain a triassociated infection, parainfluenza virus type 3 being inoculated the first and the other two viruses, in the following stages-II and III-, alternately. The infections were revealed by the presence of positive immunofluorescence reactions in the pulmonary tissue, of histological, histochemical and histoenzymatic lesions at the level of the respiratory apparatus, as well as of pathomorphological changes in other organs. At the pulmonary parenchyma level the inflammatory lesion had a 100% frequency. The severest pathomorphological picture was the diffuse, lymphohistiocytic and macrophagic bronchopneumonia. The cytoinfiltrate was characterized by a proportionality between lymphocytes and histiocytes and the lower but not insignificant presence of macrophages. The prevalent lesion was the thickening of interparietoalveolar septa, as a consequence of stasis hyperemia, oedema and lymphohistiomacrophagocytic infiltrate, to which dystrophic lesions, especially of biocytes, are often added. Different lesions are present in other organs, such as: in the liver-inflammatory, dystrophico-inflammatory and dystrophic lesions; in the kidney, pancreas, cerebellum and thymus--vascular changes, stasis hyperemia; in the spleen--hyperplasia of megakaryocytes. Generally, the type and severity of lesions vary from one viral-association-induced infection to another.

Animals↗

Viral receptors on isolated murine and human ependymal cells.

Viruses that infect ependyma cause ependymitis in humans and hydrocephalus in experimental animals. We report that reovirus type 1 (which induces hydrocephalus in mice) binds to the surface of isolated human and murine ciliated ependymal cells. With the use of recombinant viral clones, the binding property was mapped to the type 1 viral hemagglutinin, which also determines in vivo the affinity of reovirus type 1 for ependyma. Mumps virus, measles virus, parainfluenza type 3, and herpes simplex virus type 1 bind to murine ependyma cells, whereas reovirus type 3, herpes simplex virus type 2, and poliovirus type 2 do not.

Animals↗

Reactivation of Bovid herpesvirus 1 and 2 and parainfluenza-3 virus in calves latently infected.

Two experiments were carried out to determine whether Bovid herpesvirus (BHV) 2 is able to induce a recurrent infection in experimentally infected calves. In the first experiment the stress induced by dexamethasone (DMS) treatment failed to reactivate the clinical condition or to induce shedding of BHV2. However, treatment with DMS reactivated a latent BHV1 infection in all calves previously inoculated with BHV2 and also in two noninoculated controls. Probably, because of the interference by BHV1 the study failed to resolve the question as to whether BHV2 could induce a recurrent infection. Consequently, a second experiment was performed using calves devoid of antibody to BHV1 and, therefore, probably, free of virus. By this study it was demonstrated that BHV2 can remain as a latent infection in cattle, which, when immunosuppressed as with DMS, can be reactivated. A finding of considerable interest in this experiment was that in 1 calf a concurrent piroplasma infection was also, unexpectedly, discovered. Recrudescence of latent BHV1 infection was induced by DMS treatment of calves possessing antibody to the virus. The infection once reactivated, was readily transmitted by contact to three other calves devoid of antibody to BHV1. In the same experiment Parainfluenza-3 (PI-3) virus was unexpectedly isolated from all calves. It was speculated that all calves were latently infected with PI-3 virus with concurrent infection by HBV1 acting as a stress inducing PI-3 reactivation. These studies seem to indicate that mixed infections could have an important role in the mechanism involved in the establishment of latent infections and viral reactivation.

Animals↗

Methods for the detection of viruses in bovine serum.

An evaluation of selected commonly used procedures for the recovery of endogenous viral contaminants in bovine serum was undertaken. Low speen centrifugation (25,000 x g) was found to be efficient for the recovery of bovine herpesvirus type 1 (BHV-1) and parainfluenza virus type 3(PI-3) in bovine serum. Decreased infectivity titers were obtained when parainfluenza virus type 3, and to a lesser extent bovine herpes virus type 1, were concentrated using high speed centrifugation (100,000 x g) for extended time periods. In neither case could infectious virus be recovered from serum containing sufficient titers of homologous neutralizing antibody, although electron microscopy examination revealed the presence of the viruses previously added. In the presence of homologous antibody, virus particles appeared to have a diffuse, poorly defined outer membrane. Neutralizing antibody titers to bovine herpesvirus type 1 and outer membrane. Neutralizing antibody titers to bovine herpesvirus type 1 and parainfluenza virus types were found in fetal, calf, and adult bovine sera. The prevalence and magnitude of the antibody titers to these viruses increased with the age of the animals examined.

Animals↗

Effect of prostaglandins on cell function and multiplication of parainfluenza 3 viruses in WISH cells.

Cytotoxic effect of prostaglandins E2 and F2alpha on cells grown in vitro and the influence of these compounds on multiplication of myxovirus parainfluenza 3 were investigated. The prostaglandins were added to culture medium (0-01-10 mug/ml) 24 hr before virus infection, or for 2 and 48 hr after inoculation with viruses. WISH cells and monkey kidney cell cultures were used. No direct cytotoxic effect of prostaglandins at concentrations 0-01-1 mug/ml was found (viability, supravital staining, phase-contrast system, Nitro-BT reduction and succinic dehydrogenase tests), whereas the concentration of 10 mug/ml within 48 hr led to reduction and succinic dehydrogenase tests), whereas the concentration of 10 mug/ml within 48 hr led to partial injury of the cell population with symptoms of damage to mitochondria. Prostaglandins E2 and F2alpha inhibited multiplication of parainfluenza 3 virus at concentrations 0-1-10 mug/ml. The inhibitory effect was most pronounced if prostaglandins were added to medium for the whole period of virus multiplication i.e. for 48 hr but little or no effect was found if they were added prior to inoculation or for 2 hr after it. Inhibitory effect of prostaglandins on replication phase of viruses is suggested.

Cell Line↗