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Results for “VIRAL INTERFERENCE”

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At least 1,207 records · Page 67Linked to original sources
PubMed1981

Persistent infection with mouse hepatitis virus, JHM strain in DBT cell culture.

After inoculation with JHM strain into DBT cell monolayers, a persistently infected DBT cell culture was established without producing typical cytopathic changes after about 15th passages. By immunofluorescence virus specific antigen was demonstrated in 10 to 15% DBT cells. This persistently infected culture (JHM-CC) was resistant to superinfection with parental JHM, but such resistance was not shown against vesicular stomatitis virus. JHM-CC virus produced small plaques on DBT cell monolayers. Temperature sensitive (TS) mutant, defective interfering (DI) particle or interferon was not detected in the JHM-CC. To intracerebral inoculation with JHM-CC virus, cortisone treated ICR mice survived without showing clinical signs, however, demyelinating lesions were produced in the brain and spinal cord of them.

Animals↗
PubMed1976

Murine influenza virus encephalomyelitis. III. Effect of defective interfering virus particles.

Defective interfering influenza virus particles lessened the yield of infective virus recovered from brain after intracerebral challange of 3-week old mice, but failed to affect the appearance of disease or lethality. In 7-week old mice, the presence of defective interfering influenza virus particles reduced both lethality and virus yield. Viral inocula containing significant numbers of defective particles appeared to diminish later inflammatory changes, nerve cell degeneration and the appearance of viral antigen in deeper cerebral regions. The protective effect exerted by defective virus particles does not appear related to interferon production in brain.

Age Factors↗
PubMed1975

A study on the influence of papovavirus upon encephalitis caused by SSPE agent.

To investigate a possible interaction between the SSPE agent and papovaviruses, histopathological and statistical evaluations were made of encephalitis induced in hamsters by intracerberal inoculation with isolates from SSPE and PML patients, and with BK virus, alone or in combination. With SSPE virus alone, hamster brains showed a reduction of susceptibility to encephalitis with increasing age. A modification of the pathology of SSPE encephalitis was observed after administration of the PML isolate or BK virus: encephalitis was either enhanced or inhibited depending on the time the papovaviruses were administered. A possible mechanism of interaction between SSPE and papovaviruses is briefly discussed.

Age Factors↗
PubMed1989

Cell-membrane phospholipase C is involved in inducing the antiviral effect of interferon.

A monospecific inhibitory antibody directed to phospholipase C (phosphoinositidase C) blocked the antiviral effect of human interferons alpha and beta when tested on human quiescent fibroblasts challenged with the vesicular stomatitis virus. This action was due to specific inhibition of polyphosphoinositide hydrolysis because (a) the F(ab')2 fragment of the antibody molecule was also inhibitory; (b) excess antibodies directed to phospholipase A2 and to a phosphatidylcholine-preferring phospholipase C did not have any inhibitory effect, and (c) the combination of 12-O-tetradecanoyl-phorbol-acetate and calcium ionophore A23187 had an interferon-like antiviral effect which was not influenced by the inhibitory anti-phospholipase C antibodies. To avoid an interferon-like effect due to induction of interferon by second messengers, Vero cells, which lack interferon biosynthesis, were also used. Liposomes containing inositol 1,4,5-triphosphate and 1-oleoyl-2-acetyl-rac-glycerol protected Vero cells against the infection with the vesicular stomatitis virus. These results taken together show that phosphoinositide-derived second messengers are involved in triggering the antiviral effect of interferons alpha and beta.

Antibodies↗