1985
DOI: 10.1128/jvi.56.1.12-18.1985
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Differences in cell-to-cell spread of pathogenic and apathogenic rabies virus in vivo and in vitro

Abstract: Pathogenic parental rabies virus and apathogenic variant virus were shown to differ in their ability to infect neurons in vivo and neuroblastoma cells in vitro. After intracerebral inoculation, the distribution of infected neurons in the brain was similar for both viruses, but the rate of spread throughout the brain, the number of infected neurons, and the degree of cellular necrosis were much lower in the case of apathogenic virus. After adsorption to mouse neuroblastoma cells, apathogenic virus was less rapi… Show more

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Cited by 135 publications
(27 citation statements)
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“…Viral genes encoding outer capsid or envelope proteins have been the most frequently implicated determinants of pathogenicity (e.g., reovirus Si gene [38,42], Sindbis virus El and/or E2 proteins [20,22], lymphocytic choriomeningitis virus S gene [29], mouse hepatitis virus type 4 E2 protein [5], JHM murine coronavirus E2 protein [10], rabies virus glycoprotein [6,7,23,33], mumps virus hemagglutinin/neuraminidase protein [19], influenza virus hemagglutinin protein [2], and poliovirus VP1 protein [21]). However, genes encoding viral proteins with polymerase function (e.g., lymphocytic choriomeningitis L gene [28] and influenza virus PB1, PB2, PA, and NP proteins [31]) as well as noncoding regions of the genome (poliovirus 5' noncoding region [9,17]) have also been indicated as determinants of virulence.…”
Section: Discussionmentioning
confidence: 99%
“…Viral genes encoding outer capsid or envelope proteins have been the most frequently implicated determinants of pathogenicity (e.g., reovirus Si gene [38,42], Sindbis virus El and/or E2 proteins [20,22], lymphocytic choriomeningitis virus S gene [29], mouse hepatitis virus type 4 E2 protein [5], JHM murine coronavirus E2 protein [10], rabies virus glycoprotein [6,7,23,33], mumps virus hemagglutinin/neuraminidase protein [19], influenza virus hemagglutinin protein [2], and poliovirus VP1 protein [21]). However, genes encoding viral proteins with polymerase function (e.g., lymphocytic choriomeningitis L gene [28] and influenza virus PB1, PB2, PA, and NP proteins [31]) as well as noncoding regions of the genome (poliovirus 5' noncoding region [9,17]) have also been indicated as determinants of virulence.…”
Section: Discussionmentioning
confidence: 99%
“…Replacement of Arg333, situated in site III of the G protein, results in the loss of virulence for adult animals (Dietzschold et al ., 1983b; Seif et al ., 1985; Tuffereau et al ., 1989). The mutant virus is still able to infect peripheral neurons but is only transmitted to a few categories of second order neurons in the central nervous system (CNS) (Dietzschold et al ., 1985; Coulon et al ., 1989; Lafay et al ., 1991). We have shown recently that the additional mutation of Lys330, also in site III, abolishes the penetration of the virus into motor and sensory neurons after intramuscular inoculation of the virus (Coulon et al ., 1998).…”
Section: Introductionmentioning
confidence: 99%
“…Variants with an Arg3Glu mutation at position 333 in site III of the G protein are less pathogenic for immunocompetent adult mice than the wild-type parental viruses (5,18). The greatly reduced spread of these antigenic site III mutants within the nervous system (6) indicates that the appropriate G protein structure is absolutely essential for the rapid axonal/transsynaptic spread of rabies virus that leads to a lethal infection in adult animals. Based on these findings, one might expect that site III mutations are the single most important indicator of decreased pathogenicity.…”
mentioning
confidence: 99%