Japanese encephalitis virus (JEV): potentiation of lethality in mice by microwave radiation.
Identifieur interne : 003557 ( PubMed/Corpus ); précédent : 003556; suivant : 003558Japanese encephalitis virus (JEV): potentiation of lethality in mice by microwave radiation.
Auteurs : D G Lange ; J. SedmakSource :
- Bioelectromagnetics [ 0197-8462 ] ; 1991.
English descriptors
- KwdEn :
- Animals, Blood-Brain Barrier (radiation effects), Capillary Permeability (radiation effects), Encephalitis Virus, Japanese (pathogenicity), Endothelium, Vascular (cytology), Endothelium, Vascular (microbiology), Hypercapnia (complications), Male, Mice, Microwaves (adverse effects), Virulence (radiation effects).
- MESH :
- adverse effects : Microwaves.
- complications : Hypercapnia.
- cytology : Endothelium, Vascular.
- microbiology : Endothelium, Vascular.
- pathogenicity : Encephalitis Virus, Japanese.
- radiation effects : Blood-Brain Barrier, Capillary Permeability, Virulence.
- Animals, Male, Mice.
Abstract
The expression of Japanese Encephalitis Virus (JEV) lethality in mice requires entry of the virus into the central nervous system. This entry is presumably through the capillary endothelial cells (CEC), because entry between CECs is inhibited by bands of circumferential tight-junctions. A viremic stage occurs during the first 4 to 5 days after JEV administration in mice, and both microwave radiation (2.45-GHz, continuous wave, 10-min exposure) and hypercarbia were employed to increase CEC permeability to JEV. Exposure to microwaves at power densities of 10-50 mW/cm2 resulted in a dose-dependent increase in JEV-induced lethality. Mice did not become tolerant or sensitized to microwave potentiation of JEV-induced mortality because 4 daily exposures at 10 or 50 mW/cm2 (SARS, approximately 24-98 W/kg) did not alter the lethality pattern to subsequent microwave radiation of JEV-exposed animals. Similarly, hypercarbia (5, 10, and 20% CO2) was observed to produce a dose-dependent increase in JEV-induced lethality. Both microwave radiation and hypercarbia are thought to promote pinocytosis in CNS capillary endothelial cells. This may be one mechanism by which they enhance JEV-induced lethality in adult Swiss-Cox mice.
DOI: 10.1002/bem.2250120603
PubMed: 1750827
Links to Exploration step
pubmed:1750827Le document en format XML
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<author><name sortKey="Lange, D G" sort="Lange, D G" uniqKey="Lange D" first="D G" last="Lange">D G Lange</name>
<affiliation><nlm:affiliation>Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Sedmak, J" sort="Sedmak, J" uniqKey="Sedmak J" first="J" last="Sedmak">J. Sedmak</name>
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<author><name sortKey="Lange, D G" sort="Lange, D G" uniqKey="Lange D" first="D G" last="Lange">D G Lange</name>
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<term>Blood-Brain Barrier (radiation effects)</term>
<term>Capillary Permeability (radiation effects)</term>
<term>Encephalitis Virus, Japanese (pathogenicity)</term>
<term>Endothelium, Vascular (cytology)</term>
<term>Endothelium, Vascular (microbiology)</term>
<term>Hypercapnia (complications)</term>
<term>Male</term>
<term>Mice</term>
<term>Microwaves (adverse effects)</term>
<term>Virulence (radiation effects)</term>
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<keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Microwaves</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hypercapnia</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelium, Vascular</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Endothelium, Vascular</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Encephalitis Virus, Japanese</term>
</keywords>
<keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Blood-Brain Barrier</term>
<term>Capillary Permeability</term>
<term>Virulence</term>
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<front><div type="abstract" xml:lang="en">The expression of Japanese Encephalitis Virus (JEV) lethality in mice requires entry of the virus into the central nervous system. This entry is presumably through the capillary endothelial cells (CEC), because entry between CECs is inhibited by bands of circumferential tight-junctions. A viremic stage occurs during the first 4 to 5 days after JEV administration in mice, and both microwave radiation (2.45-GHz, continuous wave, 10-min exposure) and hypercarbia were employed to increase CEC permeability to JEV. Exposure to microwaves at power densities of 10-50 mW/cm2 resulted in a dose-dependent increase in JEV-induced lethality. Mice did not become tolerant or sensitized to microwave potentiation of JEV-induced mortality because 4 daily exposures at 10 or 50 mW/cm2 (SARS, approximately 24-98 W/kg) did not alter the lethality pattern to subsequent microwave radiation of JEV-exposed animals. Similarly, hypercarbia (5, 10, and 20% CO2) was observed to produce a dose-dependent increase in JEV-induced lethality. Both microwave radiation and hypercarbia are thought to promote pinocytosis in CNS capillary endothelial cells. This may be one mechanism by which they enhance JEV-induced lethality in adult Swiss-Cox mice.</div>
</front>
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<Abstract><AbstractText>The expression of Japanese Encephalitis Virus (JEV) lethality in mice requires entry of the virus into the central nervous system. This entry is presumably through the capillary endothelial cells (CEC), because entry between CECs is inhibited by bands of circumferential tight-junctions. A viremic stage occurs during the first 4 to 5 days after JEV administration in mice, and both microwave radiation (2.45-GHz, continuous wave, 10-min exposure) and hypercarbia were employed to increase CEC permeability to JEV. Exposure to microwaves at power densities of 10-50 mW/cm2 resulted in a dose-dependent increase in JEV-induced lethality. Mice did not become tolerant or sensitized to microwave potentiation of JEV-induced mortality because 4 daily exposures at 10 or 50 mW/cm2 (SARS, approximately 24-98 W/kg) did not alter the lethality pattern to subsequent microwave radiation of JEV-exposed animals. Similarly, hypercarbia (5, 10, and 20% CO2) was observed to produce a dose-dependent increase in JEV-induced lethality. Both microwave radiation and hypercarbia are thought to promote pinocytosis in CNS capillary endothelial cells. This may be one mechanism by which they enhance JEV-induced lethality in adult Swiss-Cox mice.</AbstractText>
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