Sendai virus infected

Sendai virus infection potentiates neurogenic inflammation in the rat trachea. J. Appl. Physiol. 68, 754-760. 

McWilliam, A. S., Marsh, A. M., and Holt, P. G. (1997) Inflammatory infiltration of the upper airway epithelium during Sendai virus infection involvement of epithelial dendritic cells. J. Virol. 71, 226-236. 

Iida et al. (1987) and Nishimura et al. (1984) have reported that if chitin is partially deacetylated, especially at 70%, it has the ability to stimulate nonspecific host resistance against E. coli and Sendai virus infection in mice. Meanwhile, chitin and chitosan have the ability to increase the number of mouse peritoneal exudate cells that generate reactive oxygen intermediates and then display candidacidal activities (Suzuki et al., 1984). Suzuki et al. (1986) reported that chitin hexamer (GlcNAc)6 had a strong candidacidal activity. 

Percy DH, Auger DC, Croy BA. Signs and lesions of experimental Sendai virus infection in two genetically distinct strains of SCID/beige mice. Vet Pathol 1994 31 67-73. 

A detailed analysis of the involvement of microtubules in cytopathic effects was made by Ebina et al. (1978) who infected cells with poliovirus, Sendai virus, adenovirus, and herpesvirus in order to examine the effect of each virus on the formation of microtubular par-acrystals induced by vinblastine sulfate in HeLa-S3 cells. In polio-virus-infected cells, the cytopathic effect (cell rounding) and inhibition of paracrystal formation were both noted at 4 hr postinfection, proceeding in parallel. In the case of Sendai virus infection, no effect on paracrystal formation could be noted despite a syncytial cytopathic effect. In adenovirus- and herpesvirus-infected cells, inhibition of paracrystal formation occurred well before the cytopathic effect and was not blocked by UV irradiation or nucleic acid analogues but was by inhibition of protein synthesis. These findings led Ebina et al. (1978) to the hypothesis that early viral proteins are responsible for inhibition of microtubule formation and the cytopathic effect (cell rounding) except that Sendai virus did not cause this type of cytopathology. 

Blair, C. D., and Brennan, P. J., 1972, Effect of Sendai virus infection on lipid metabolism in chich embryo fibroblasts, J. Virol. 9 813. 

In 1957 Isaacs and Lindemann noted that virally infected cells produced a protein that conferred viral resistance to naive cells [Ij.They called the substance interferon. The properties of interferons immediately captured the imagination of virologists. However, clinical research was limited by the inability to produce interferon in sufficient quantity and to adequately purify the protein. The first major step in overcoming these problems was the discovery by Grosser that human leukocytes could produce interferons when stimulated in culture by Sendai virus [2]. 

The immunostimulating activity of chitosan has also been reported. A 70% DD chitosan showed immunostimulating effects by activating macrophages and natural killer cells in rats when infected with . coli and Sendai virus (Nishimura et al., 1984). Chang et al. (2004) also reported the immune-enhancing effects of chitosan as a novel adjuvant to an inactivated influenza vaccine, and the antibody content in serum remarkably increased the antiviral defenses of mice. 

To maintain maximum infectivity of Sendai virus it is essential that the virus be stored and handled properly. The virus is best stored either in liquid nitrogen or at -80°C. Under these conditions, the virus will remain viable for several years. 

It should be noted that Sendai virus is extremely infectious for rodents and very difficult to eradicate from a rodent housing facility once established. Animals infected with Sendai should not be housed in the same facility as other rodents used for experimental purposes and personnel handling. Sendai should be restricted from entering any rodent housing facility. Appropriate precautions should also be taken when disposing of virus-contaminated material. 

Castleman, W. L. (1983) Respiratory tract lesions in weanling outbred rats infected with Sendai virus. Am. J. Vet. Res. 44, 1024-1031. 

The presence of informosomelike RNPs has been demonstrated also in the case of Ehrlich ascites carcinoma cells infected with Sendai virus (Volkova et al., 1969). The cytoplasmic extracts of the cells labeled for 30 minutes with uridine contain virus-specific RNA in the form of particles with a sedimentation coefficient 45S (the sedimentation coefficient of the complete virus equals 57S). The buoyant density of the RNP peak in CsCI equals 1.43 to 1.44 g/cm. Although these properties are compatible with the idea that they are informosome, the particles, and in particular their protein component, should be characterized in more detail before reaching a definite conclusion. Recently SOS virus RNA-containing particles with p = 1.40 g/cm have been found in HeLa cells infected with poliovirus (Huang and Baltimore, 1970), although the authors have some doubts about the reality of these complexes. 

Volkova, M. Y., V. M. Zaides, and V. G. Zaslavsky. 1969. Slowly sedimenting particles present in cytoplasmic extract of Ehrlich ascites cells infected by Sendai virus. Molec. Biol. (U.S.S.R.), 3 635-638. 

At least two environmental factors may contribute to the development of HP as a promoting factor viral infections and inhalation injury. Experimental models of HP have shown that animals challenged with respiratory syncytial virus or Sendai virus exhibit a more severe inflammatory response to subsequent Saccharopolyspora rectivirgula exposure, which may persist long after the viral infection has declined (11,12). Also, studies in humans have revealed that common respiratory vimses, primarily Influenza A, are often present in the lower airways of patients with HP (13). The reasons why viral infections may potentiate HP are unknown, but it may be related to vims-induced mucociliary dysfunction, increased expression of costimulatory molecules by alveolar macrophages, and increased secretion of chemokines, enhancing the recruitment of lymphocytes to the lungs (13,14). 

The paramyxoviruses, largely because of their profound cell-fusing activity, have served as an important model of membrane perturbation by viruses. During Sendai virus-mediated fusion of mouse ascites cells, Pasternak and Micklem (1973) detected loss of intracellular metabolites coincident with inhibition of their accumulation from the medium. This failure to maintain selective permeability did not occur at 0°C and was unaffected by cytochalasin B which inhibits fusion by the virus. Chick embryo fibroblasts infected with Newcastle disease virus were found to release cellular enzymes, such as lactate dehydrogenase, glutamic oxaloacetic transaminase, and lysosomal enzymes (Katzman and Wilson, 1974). These cells also became... 

Scheid, A., and Choppin, P. W., 1974, Identification of biological activities of paramyxovirus glycoproteins. Activation of cell fusion, hemolysis and infectivity by proteolytic cleavage of an inactive precursor protein of Sendai virus. Virology 57 475. 

Common viral infections may affect the outcome of carcinogenicity studies by altering survival or tumor incidence. Nevertheless, viral infections did not cause consistent adverse effects on survival or tumor prevalence in control F344 rats from 28 NCI-NTP studies, though body weights were reduced by Sendai and pneumonia viruses of mice (Rao et al., 1989). The probability of such infections can be minimized by using viral-antibody-free animals, which are readily available. 

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