Rabies virus selectively alters 5-HT1 receptors subtypes in rat brain

Ceccaldi, Pierre‐Emmanuel; Fillion, Marie‐Paule; Ermine, Alain; Tsiang, H; Fillion, G.

doi:10.1016/0922-4106(93)90120-x

Cited by 58 publications

(30 citation statements)

References 32 publications

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“…For example, animals infected with rabies virus exhibit elevated aggression (Macrae, 1973), which may be caused by neural cell death in regions associated with aggression (i.e. amygdala, hippocampus, and hypothalamus) as well as suppression of 5-HT neurotransmission (Ceccaldi et al, 1993;Dietzschold et al, 2001). Male mice infected with tick-borne encephalitis (TBE) virus have elevated concentrations of circulating testosterone and are more aggressive than uninfected mice (Moshkin et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Infection with viruses, including rabies virus and hantaviruses, increases aggression and, presumably, transmission within host populations (Klein, 2003). Parasites may alter the behavior of vertebrates by infecting and killing neurons in the brain (Dietzschold et al, 2001), altering neurotransmission (Ceccaldi, et al, 1993;Lancaster et al, 2007), or influencing the synthesis of steroids in peripheral organs (Larralde et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Elevated testosterone and reduced 5-HIAA concentrations are associated with wounding and hantavirus infection in male Norway rats

Easterbrook

Kaplan

Glass

et al. 2007

Hormones and Behavior

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Among rodents that carry hantaviruses, males are more likely to engage in aggression and to be infected than females. One mode of hantavirus transmission is via the passage of virus in saliva during wounding. The extent to which hantaviruses cause physiological changes in their rodent host that increase aggression and, therefore, virus transmission has not been fully documented. To assess whether steroid hormones and neurotransmitters contribute to the correlation between aggression and Seoul virus infection, Norway rats were trapped in Baltimore, Maryland and wounding, infection status, steroid hormones, and concentrations of neurotransmitters, including norepinephrine (NE), dopamine (DA), 3,4-dihydroxyphenol acetic acid (DOPAC), serotonin (5-HT), and 5-hydroxyindole-3-acetic acid (5-HIAA) in select brain regions were examined. Older males and males with high-grade wounds were more likely to have anti-Seoul virus IgG and viral RNA in organs than either juveniles or adult males with less severe wounds. Wounded males had higher circulating testosterone, lower hypothalamic 5-HIAA, and lower NE in the amygdala than males with no wounds. Infected males had higher concentrations of testosterone, corticosterone, NE in the hypothalamus, and DOPAC in the amygdala than uninfected males, regardless of wounding status. In the present study, wounded males that were infected with Seoul virus had elevated testosterone and reduced 5-HIAA concentrations, suggesting that these neuroendocrine mechanisms may contribute to aggression and the likelihood of transmission of hantavirus in natural populations of male Norway rats.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Elevated testosterone and reduced 5-HIAA concentrations are associated with wounding and hantavirus infection in male Norway rats

Easterbrook

Kaplan

Glass

et al. 2007

Hormones and Behavior

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“…These findings have given support to the concept that neuronal dysfunction must play an important role in producing the disease. 24 A variety of experimental studies in rabies virus infection have investigated potential abnormalities in neurotransmission involving acetylcholine, [25][26][27] serotonin, 28,29 and γ-amino-n-butyric acid. 30 Abnormalities of uncertain significance were found, but no fundamental defects were demonstrated that explain neuronal dysfunction in rabies.…”

Section: Mechanisms For Neuronal Dysfunction and Deathmentioning

confidence: 99%

Update on rabies

Jackson¹

2011

RRTM

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Human rabies is almost invariably fatal, and globally it remains an important public health problem. Our knowledge of rabies pathogenesis has been learned mainly from studies performed in experimental animal models, and a number of unresolved issues remain. In contrast with the neural pathway of spread, there is still no credible evidence that hematogenous spread of rabies virus to the central nervous system plays a significant role in rabies pathogenesis. Although neuronal dysfunction has been thought to explain the neurological disease in rabies, recent evidence indicates that structural changes involving neuronal processes may explain the severe clinical disease and fatal outcome. Endemic dog rabies results in an ongoing risk to humans in many resource-limited and resource-poor countries, whereas rabies in wildlife is important in North America and Europe. In human cases in North America, transmission from bats is most common, but there is usually no history of a bat bite and there may be no history of contact with bats. Physicians may not recognize typical features of rabies in North America and Europe. Laboratory diagnostic evaluation for rabies includes rabies serology plus skin biopsy, cerebrospinal fluid, and saliva specimens for rabies virus antigen and/or RNA detection. Methods of postexposure rabies prophylaxis, including wound cleansing and administration of rabies vaccine and human rabies immune globulin, are highly effective after recognized exposure. Although there have been rare survivors of human rabies, no effective therapy is presently available. Therapeutic coma (midazolam and phenobarbital), ketamine, and antiviral therapies (known as the "Milwaukee protocol") were given to a rabies survivor, but this therapy was likely not directly responsible for the favorable outcome. New therapeutic approaches for human rabies need to be developed. A better understanding of basic mechanisms involved in rabies pathogenesis may be helpful in the development of potential new therapies for the future.

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“…Among the dysfunctions which have been reported are alterations in electroencephalographic recordings and sleep (Gourmelon et al, 1986), and changes in the binding, uptake and release of neurotransmitters in synaptosomal preparations and cell cultures (Ceccaldi et al, 1993 ;Ladogana et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Alteration of the actin-based cytoskeleton by rabies virus.

Ceccaldi

Valtorta

Braud

et al. 1997

Journal of General Virology

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We investigated the effect of rabies virus infection on the actin cytoskeleton using various techniques. Confocal microscopic examination of rabies virusinfected neuroblastoma cells at late stages of infection revealed a dramatic decrease in F-actin staining. The results of a fluorimetric assay with pyrenylated actin indicated that purified rabies virus nucleocapsid has no direct action on the kinetics of actin polymerization and only a weak effect on the final extent of polymerization. Videomicroscopy experiments with purified components showed that rabies virus nucleocapsid inhibits the actin-bundling effect induced by dephospho-synapsin I, a neuron-specific protein which is known to exert a control on the actin-based cytoskeleton. Thus, the observed decrease in F-actin staining in infected cells might be ascribed to an indirect action of rabies nucleocapsid on the effects of actinbinding proteins such as synapsin I.

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Rabies virus selectively alters 5-HT1 receptors subtypes in rat brain

Cited by 58 publications

References 32 publications

Elevated testosterone and reduced 5-HIAA concentrations are associated with wounding and hantavirus infection in male Norway rats

Elevated testosterone and reduced 5-HIAA concentrations are associated with wounding and hantavirus infection in male Norway rats

Update on rabies

Alteration of the actin-based cytoskeleton by rabies virus.

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