Sendai virus injected intracerebrally into 3-week-old mice caused infection of ependymal and choroid plexus epithelial cells. Budding of mature viruses occurred only from the apical surfaces of these cells. The viral peplomere proteins, haemagglutinin-neuraminidase and fusion, were concentrated on the apical portion of the ependymal cells, while the nucleocapsid-associated polymerase protein was dispersed throughout the cytoplasm. This indicates that intracellular routing of the virus envelope glycoproteins to the cell surface may be one of the factors that determines the site of virus budding. Vesicular stomatitis and vaccinia viruses, on the other hand, budded or egressed predominantly from the baso-lateral cell surfaces.

Animals↗

PubMedDate not supplied

Selective infections of olfactory and respiratory epithelium by vesicular stomatitis and Sendai viruses.

Following intranasal instillation of vesicular stomatitis virus (VSV) in mice there was an extensive infection of the olfactory epithelium in contrast to a minimal involvement of the respiratory epithelium. Sendai virus (SV), on the other hand, caused an extensive infection of the respiratory epithelium and only minimal infection of the olfactory mucous membrane. VSV budded from basolateral surfaces of supporting cells and olfactory neurons, but not from their apical surfaces or the ciliated bulbous endings of the olfactory neuron dendrites. This asymmetric release of VSV favoured neuroinvasion. The virus spread along the olfactory nerves to the glomeruli in the olfactory bulbs after which it propagated transneuronally into the rest of the brain. SV budded only from the apical surface of respiratory epithelial cells, was released into the air passages, and there were no signs of invasion into the olfactory bulbs. Inoculation of the olfactory mucous membrane is a useful procedure for studies on selectivity of attack on peripheral neurons by viruses and on mechanisms of virus invasion of the nervous system in vivo.

Animals↗

PubMedDate not supplied

Nasal epithelium in woodworkers in the furniture industry. A histological and cytological study.

The incidence of nasal adenocarcinoma is greatly increased in wood dust exposed furniture workers. The background is discussed and histological and cytological examinations are performed in 45 workers. The histological findings are compared with different kinds of cytological methods, May-Grünwald-Giemsa and Papanicolau. It was a significant increase in cuboidal cell metaplasia revealed by histology and Papanicolau stained cytology. MGG, on the other hand, revealed significantly raised occurrence of goblet cell hyperplasia. These findings are discussed in relation to a morphogenetical model which could explain some features in the development of premalignant changes which could precede nasal adenocarcinomas.

Adenocarcinoma↗

PubMedDate not supplied

Experimental studies on carcinogenesis in the nasal mucosa.

Of 24 Syrian golden hamsters exposed to wood dust in a concentration in the air of 30 mg/m3 for 6 h per day, 5 days a week, for a period of 40 weeks, one animal got dysplasia and one a malignant tumour in the nasal mucosa. In a group of 24 animals given 3 mg of diethylnitrosamine subcutaneously once a week for 12 weeks, a high frequency of benign and malignant tumours (mainly adenocarcinoma) of the nasal mucosa was found, but a group of similar size exposed to both wood dust and diethylnitrosamine did not show a higher frequency of nasal tumours than those given this latter substance alone.

Adenocarcinoma↗

PubMedDate not supplied

Effects of wood dust exposure and diethylnitrosamine. A pilot study in Syrian golden hamsters.

Fine wood dust is epidemiologically associated with human nasal cancer. The aim of the present study was to elaborate an animal model for inhalation studies of the effects of fine wood dust on the upper and lower airways. Syrian golden hamsters were used. After 10 months one animal in the group which was exposed only to wood dust, had developed a malignant nasal tumour and another animal in the same group had nasal dysplasia. Spontaneous nasal tumours in this laboratory animal is not known. Many tumours of the nose, larynx and trachea arose in animals treated with a carcinogen (diethylnitrosamine). There was no increase in tumours in animals with combined exposure to diethylnitrosamine and wood dust.

Adenocarcinoma↗