Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Search research articles

Related Experiment Videos

Pathogenesis of rabies.

B Dietzschold¹, M Schnell, H Koprowski

¹Department of Microbiology, Center for Neurovirology, Thomas Jefferson University, Philadelphia, PA, USA. Bernhard.dietzschold@jefferson.edu

Current Topics in Microbiology and Immunology

|June 29, 2005

Summary

Rabies virus (RV) causes fatal central nervous system disease by infecting neurons and inhibiting essential protein synthesis. Viral proteins like G and P play roles in neuroinvasion and pathogenesis, contributing to lethal outcomes.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

The phenotype of the RABV glycoprotein determines cellular and global virus load in the brain and is decisive for the pace of the disease.

Virology·2017

Same author

Immunogenicity and safety of recombinant rabies viruses used for oral vaccination of stray dogs and wildlife.

Zoonoses and public health·2009

Same author

Role of virus-induced neuropeptides in the brain in the pathogenesis of rabies.

Developments in biologicals·2008

Same author

Second-generation rabies virus-based vaccine vectors expressing human immunodeficiency virus type 1 gag have greatly reduced pathogenicity but are highly immunogenic.

Journal of virology·2002

Same author

Immunopathology and immunoprotection in CNS virus infections: mechanisms of virus clearance from the CNS.

Current topics in microbiology and immunology·2002

Same author

Silver-haired bat rabies virus variant does not induce apoptosis in the brain of experimentally infected mice.

Journal of neurovirology·2001

Area of Science:

Neuroscience
Virology
Molecular Biology

Background:

Rabies is a fatal neurological disease caused by the rabies virus (RV), a negative-stranded RNA virus.
RV pathogenesis is complex, involving viral genetic factors and host-pathogen interactions within the central nervous system (CNS).
Neuroinvasiveness, particularly transsynaptic neuronal spread, is a hallmark of RV infection.

Purpose of the Study:

To elucidate the viral factors and mechanisms contributing to rabies virus pathogenesis and neuroinvasiveness.
To understand the role of specific RV proteins, such as G and P, in viral spread and disease outcome.
To identify the key molecular events leading to the lethal neurological dysfunction observed in rabies.

Main Methods:

Analysis of RV genetic elements, including the G and L genes, in relation to pathogenesis.
Investigation of viral protein functions, specifically the G protein in transsynaptic spread and the P protein in axonal transport.
Examination of molecular mechanisms underlying neuronal dysfunction during RV infection.

Main Results:

Viral elements regulating gene expression, particularly the L gene, are implicated in RV pathogenesis.
The RV G protein mediates the spread of the virus from post-synaptic to pre-synaptic sites.
The RV P protein may be crucial for retrograde axonal transport within neurons.
Inhibition of protein synthesis essential for neuronal function is a primary cause of lethal neurological disease.

Conclusions:

RV pathogenesis is a multigenic trait influenced by viral proteins like G and P.
Understanding RV neuroinvasion and mechanisms of neuronal dysfunction is critical for combating rabies.
Targeting viral factors involved in gene expression, neuronal spread, and protein synthesis inhibition may offer therapeutic strategies.

Related Experiment Videos