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Host strain-dependent difference in susceptibility in a rat model of herpes simplex type 1 encephalitis.

Bereczky-Veress, Biborka (author)
Karolinska Institutet
Lidman, Olle (author)
Karolinska Institutet
Sabri, Farideh (author)
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Bednar, Ivan (author)
Granath, Fredrik (author)
Karolinska Institutet
Bergström, Tomas, 1950 (author)
Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för infektionssjukdomar,Institute of Biomedicine, Department of Infectious Medicine
Spenger, Christian (author)
Grandien, Alf (author)
Karolinska Institutet
Olsson, Tomas (author)
Karolinska Institutet
Piehl, Fredrik (author)
Karolinska Institutet
Diez, Margarita (author)
Karolinska Institutet
Sk?ldenberg, Birgit (author)
Karolinska Institutet
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 (creator_code:org_t)
Springer Science and Business Media LLC, 2008
2008
English.
In: Journal of neurovirology. - : Springer Science and Business Media LLC. - 1538-2443 .- 1355-0284. ; 14:2, s. 102-18
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Herpes simplex encephalitis (HSE) is characterized by severe focal brain inflammation leading to substantial loss of nervous tissue. The authors established a model of Herpes simplex virus type 1 (HSV)-1-induced acute encephalitis in the rat by injecting into the whiskers' area a virus strain isolated from a fatal human HSE case. The model might resemble natural propagation of HSV-1 in humans; spreading from the mouth and lips via the trigeminal nerve to trigeminal ganglia and subsequently entering the central nervous system (CNS). HSV-1 infected Dark Agouti (DA) rats developed a well-synchronized disease and died 5 days after inoculation. HSV-1 detection by quantitative polymerase chain reaction (qPCR), virus isolation and immunohistochemistry, magnetic resonance imaging, and histopathological examination verified dramatic encephalitis mainly in the brainstem, but also in the olfactory bulb and other segments of the brain of diseased rats. In contrast, Piebald Virol Glaxo (PVG) rats were completely resistant to disease, displaying a more rapid clearance of peripheral infection and no evidence of virus entering into neither the trigeminal ganglia nor the CNS. These results suggest a regulation of susceptibility to HSV-1-induced encephalitis at the level of peripheral infection and subsequent neuronal uptake/transport of the virus. This provides a basis for future positioning of genetic polymorphisms regulating HSE and for dissection of important pathogenetic mechanisms of this severe human disease.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

Keyword

Animals
Brain Stem
metabolism
DNA
Viral
analysis
Disease Models
Animal
Disease Susceptibility
Encephalitis
Herpes Simplex
genetics
immunology
microbiology
pathology
Herpesvirus 1
Human
isolation & purification
Humans
Rats
Trigeminal Ganglion
microbiology

Publication and Content Type

ref (subject category)
art (subject category)

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