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Rabies virus

This article is about the virus. For the disease, see Rabies. For other uses, see Rabies (disambiguation).
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Virus classification

The rabies virus is a neurotropic virus that causes rabies in humans and animals. Rabies transmission can occur through the saliva of animals and less commonly through contact with human saliva.

The rabies virus has a cylindrical morphology and is the type species of the Lyssavirus genus of the Rhabdoviridae family. These viruses are enveloped and have a single stranded RNA genome with negative-sense. The genetic information is packaged as a ribonucleoprotein complex in which RNA is tightly bound by the viral nucleoprotein. The RNA genome of the virus encodes five genes whose order is highly conserved. These genes code for nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G) and the viral RNA polymerase (L).[1] The complete genome sequences range from 11,615 to 11,966 nt in length.[2]

All transcription and replication events take place in the cytoplasm inside a specialized “virus factory”, the Negri body (named after Adelchi Negri[3]). These are 2–10 µm in diameter and are typical for a rabies infection and thus have been used as definite histological proof of such infection.[4]


Lyssaviruses have helical symmetry, so their infectious particles are approximately cylindrical in shape. They are characterized by an extremely broad host spectrum ranging from plants to insects and mammals; human-infecting viruses more commonly have cubic symmetry and take shapes approximating regular polyhedra.

The rabies virus has a bullet like shape with a length of about 180 nm and a cross-sectional diameter of about 75 nm. One end is rounded or conical and the other end is planar or concave. The lipoprotein envelope carries knob-like spikes composed of Glycoprotein G. Spikes do not cover the planar end of the virion (virus particle). Beneath the envelope is the membrane or matrix (M) protein layer which may be invaginated at the planar end. The core of the virion consists of helically arranged ribonucleoprotein.

Life cycle

Viral life cycle

After receptor binding, rabies virus enters its host cells through the endosomal transport pathway. Inside the endosome, the low pH value induces the membrane fusion process, thus enabling the viral genome to reach the cytosol. Both processes, receptor binding and membrane fusion, are catalyzed by the glycoprotein G which plays a critical role in pathogenesis (mutant virus without G proteins cannot propagate).[1]

The next step after entry is the transcription of the viral genome by the P-L polymerase (P is an essential cofactor for the L polymerase) in order to make new viral protein. The viral polymerase can only recognize ribonucleoprotein and cannot use free RNA as template. Transcription is regulated by cis-acting sequences on the virus genome and by protein M which is not only essential for virus budding but also regulates the fraction of mRNA production to replication. Later in infection, the activity of the polymerase switches to replication in order to produce full-length positive-strand RNA copies. These complementary RNAs are used as templates to make new negative-strand RNA genomes. They are packaged together with protein N to form ribonucleoprotein which then can form new viruses.[4]


In September 1931, Joseph Lennox Pawan of Trinidad in the West Indies, a Government Bacteriologist, found Negri bodies in the brain of a bat with unusual habits. In 1932, Pawan first discovered that infected vampire bats could transmit rabies to humans and other animals.[5][6] For a brief history of some of the controversies surrounding the early discoveries relating to rabies in Trinidad, see the brief history by James Waterman.[7]

From the wound of entry, the rabies virus travels quickly along the neural pathways of the peripheral nervous system. The retrograde axonal transport of the rabies virus to the CNS (Central Nervous System) is the key step of pathogenesis during natural infection. The exact molecular mechanism of this transport is unknown although binding of the P protein from rabies virus to the dynein light chain protein DYNLL1 has been shown.[8] P also acts as an interferon antagonist, thus decreasing the immune response of the host.

From the CNS, the virus further spreads to other organs. The salivary glands located in the tissues of the mouth and cheeks receive high concentrations of the virus, thus allowing it to be further transmitted due to projectile salivation. Fatality can occur from two days to five years from the time of initial infection.[9] This however depends largely on the species of animal acting as a reservoir. Most infected mammals die within weeks, while strains of a species such as the African Yellow Mongoose (Cynictis penicillata) might survive an infection asymptomatically for years.[10]


Upon viral entry into the body and also after vaccination, the body produces virus neutralizing antibodies which bind and inactivate the virus. Specific regions of the G protein have been shown to be most antigenic in leading to the production of virus neutralizing antibodies. These antigenic sites, or epitopes, are categorized into regions I-IV and minor site a. Previous work has demonstrated that antigenic sites II and III are most commonly targeted by natural neutralizing antibodies.[11] Additionally, a monoclonal antibody with neutralizing functionality has been demonstrated to target antigenic site I.[12] Other proteins, such as the nucleoprotein, have been shown to be unable to elicit production of virus neutralizing antibodies.[13] The epitopes which bind neutralizing antibodies are both linear and conformational.[14]


All extant rabies viruses appear to have evolved within the last 1500 years.[15] There are seven genotypes of rabies virus. In Eurasia cases are due to three of these—genotype 1 (classical rabies) and to a lesser extent genotypes 5 and 6 (European bat lyssaviruses type-1 and -2).[16] Genotype 1 evolved in Europe in the 17th century and spread to Asia, Africa and the Americas as a result of European exploration and colonization.

Bat rabies in North America appears to have been present since 1281 CE (95% confidence interval: 906–1577 CE).[17]


Rabies virus is used in research for viral neuronal tracing to establish synaptic connections and directionality of synaptic transmission. [18]

See also


  1. ^ a b Finke S, Conzelmann KK (August 2005). "Replication strategies of rabies virus". Virus Res. 111 (2): 120–131. PMID 15885837. doi:10.1016/j.virusres.2005.04.004. 
  2. ^ "Rabies complete genome". NCBI Nucleotide Database. Retrieved 29 May 2013. 
  3. ^ synd/2491 at Who Named It?
  4. ^ a b Albertini AA, Schoehn G, Weissenhorn W, Ruigrok RW (January 2008). "Structural aspects of rabies virus replication". Cell. Mol. Life Sci. 65 (2): 282–294. PMID 17938861. doi:10.1007/s00018-007-7298-1. 
  5. ^ Pawan, J. L. (1936). "Transmission of the Paralytic Rabies in Trinidad of the Vampire Bat: Desmodus rotundus murinus Wagner, 1840". Annals of Tropical Medicine and Parasitology 30: 137–156. ISSN 0003-4983. 
  6. ^ Pawan, J. L. (1936). "Rabies in the vampire bat of Trinidad, with special reference to the clinical course and the latency of infection". Ann Trop Med Parasitol 30: 101–129. ISSN 0003-4983. 
  7. ^ Waterman, James A. (1965). "The History of the Outbreak of Paralytic Rabies in Trinidad Transmitted by Bats to Human beings and Lower animals from 1925". Caribbean Medical Journal 26 (1–4): 164–169. ISSN 0374-7042. 
  8. ^ Raux H, Flamand A, Blondel D (November 2000). "Interaction of the rabies virus P protein with the LC8 dynein light chain". J. Virol. 74 (21): 10212–10216. PMC 102061. PMID 11024151. doi:10.1128/JVI.74.21.10212-10216.2000. 
  9. ^ "Rabies". University of Northern British Columbia. Retrieved 2008-10-10. 
  10. ^ Taylor PJ (December 1993). "A systematic and population genetic approach to the rabies problem in the yellow mongoose (Cynictis penicillata)". Onderstepoort J. Vet. Res. 60 (4): 379–87. PMID 7777324. 
  11. ^ Benmansour A (1991). "Antigenicity of rabies virus glycoprotein". Journal of Virology 65 (8): 4198–4203. PMC 248855. PMID 1712859. 
  12. ^ Marissen, WE.; Kramer, RA.; Rice, A.; Weldon, WC.; Niezgoda, M.; Faber, M.; Slootstra, JW.; Meloen, RH. et al. (Apr 2005). "Novel rabies virus-neutralizing epitope recognized by human monoclonal antibody: fine mapping and escape mutant analysis". J Virol 79 (8): 4672–8. PMC 1069557. PMID 15795253. doi:10.1128/JVI.79.8.4672-4678.2005. 
  13. ^ Wiktor, TJ.; György, E.; Schlumberger, D.; Sokol, F.; Koprowski, H. (Jan 1973). "Antigenic properties of rabies virus components". J Immunol 110 (1): 269–76. PMID 4568184. 
  14. ^ Bakker, AB.; Marissen, WE.; Kramer, RA.; Rice, AB.; Weldon, WC.; Niezgoda, M.; Hanlon, CA.; Thijsse, S. et al. (Jul 2005). "Novel human monoclonal antibody combination effectively neutralizing natural rabies virus variants and individual in vitro escape mutants". J Virol 79 (14): 9062–8. PMC 1168753. PMID 15994800. doi:10.1128/JVI.79.14.9062-9068.2005. 
  15. ^ Nadin-Davis, S. A.; Real, L. A. (2011). "Molecular phylogenetics of the lyssaviruses--insights from a coalescent approach". Adv Virus Res. Advances in Virus Research 79: 203–238. ISBN 9780123870407. PMID 21601049. doi:10.1016/B978-0-12-387040-7.00011-1. 
  16. ^ McElhinney, L. M.; Marston, D. A.; Stankov, S; Tu, C.; Black, C.; Johnson, N.; Jiang, Y.; Tordo, N.; Müller, T.; Fooks, A. R. (2008). "Molecular epidemiology of lyssaviruses in Eurasia". Dev Biol (Basel) 131: 125–131. PMID 18634471. 
  17. ^ Kuzmina, N. A.; Kuzmin, I. V.; Ellison, J. A.; Taylor, S. T.; Bergman, D. L.; Dew, B.; Rupprecht, C. E. (2013). "A reassessment of the evolutionary timescale of bat rabies viruses based upon glycoprotein gene sequences". Virus Genes. Forthcoming (2): 305. doi:10.1007/s11262-013-0952-9. 
  18. ^ Ginger, M., Haberl M., Conzelmann K.-K., Schwarz M. and Frick A. (2013). Revealing the secrets of neuronal circuits with recombinant rabies virus technology. Front. Neural Circuits. doi:10.3389/fncir.2013.00002

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