83 virus as a modulator of virulent influenza virus infection

83 virus as a modulator of virulent influenza virus infection

165 ELECTROPHYSIOLOGICAL ALTERATIONS IN FIXED AND STREET RABIES VIRUSES Gourmelon P., Briet D., Court L., Tsiang H. CRSSA,Clamart & Institut Pasteu...

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165 ELECTROPHYSIOLOGICAL

ALTERATIONS

IN FIXED AND STREET RABIES VIRUSES

Gourmelon P., Briet D., Court L., Tsiang H. CRSSA,Clamart & Institut Pasteur, Paris.

The brain electrical activities were investigated in mice and cats. Chronically implanted electrodes allowed a continuous recording of EEG. Quantification of the brain electrical activity and sleep organization periods were evaluated using spectral analysis techniques. During fixed rabies virus infection, a drastic collapse in the organization of sleep stages was observed before the onset of clinical signs. EEG disturbancies were also found to occur. The main features of these abnormalities were: l/the disappearance of rapid eye movement sleep (REM), 2/ the continuous slowing of the EEG activities (2-4 c/s), 3/ the occurrence of paroxystic events. In all the cases, the cerebral death precede the cardiac arrest of about 30 minutes. During street rabies virus infection, the EEG was remarquably preserved until the terminal stage both in mice and cats. Paroxystic elements were prevalent and contrasted with the absence of disorganization of the brain electrical activity. Sleep alterations were consistently observed. REM modifications and a general sleep stages decrease was accompagnied by an increase of the waking stages ressembling total insomnia. These data stress the physiological differences for fixed and street rabies viruses. They also indicate that during street rabies virus infection, although the infected neuron is capable to generate electrical signals, some regulatory or integrative activities of the brain are altered.

(This investigation CRE 846019).

was supported

by grants

from MRI N"82L1107

and INSERM,

166 ROLE OF AVIRULENT VIRULENT INFLUENZA

INFLUENZA A/CHICK/PENNSYLVANIA/83 VIRUS INFECTION

VIRUS

AS A MODULATOR

OF

THOMAS M. CHAMBERS AND ROBERT G. WEBSTER Children's Research Hospital, St. Jude Department of Virology/Molecular Biology, 332 North Lauderdale, P.O. Box 318, Memphis, Tennessee 38101. The A/Chick/Pennsylvania/l/83 influenza virus is an avirulent H5N2 virus containing subgenomic RNAs. We have reported that preparations of this virus contain a high proportion of defective-interfering particles (Chambers and Webster, J. Virol. 61:1517-1523, 1987). A biological role of influenza defective-interfering particles in nature has never been established. Chickens co-infected with this virus and lethal amounts of virulent influenza viruses exhibited greatly reduced morbidity and mortality. This protective effect extended to virulent viruses of both H5N2 and H7N7 subtype. Inhibition of virulent virus dissemination in co-infected chickens was detected as early as 48 hrs after infection. Although direct inhibition of virulent virus replication at the intracellular level in chickens remains unproven, we shall discuss evidence that Chicken/Pennsylvania virus, but not unrelated avirulent viruses, may be a strong inducer of an early non-specific antiviral response in infected chickens.

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