Rabies Virus

Abstract

Rabies is an acute fatal encephalomyelitis, caused by a group of genetically related lyssaviruses. The primary sources of rabies are major animal reservoirs in the orders Chiroptera and Carnivora, although this deadly zoonosis may affect all mammals, including humans.

Keywords: rabies; hydrophobia; rhabdovirus; lyssavirus; mad dog

Figure 1.

Rabies virions are bullet‐shaped and measure approximately 180 nm in length and 75 nm in diameter. The outer surface is covered by 10‐nm spike‐like glycoprotein peplomers. The basic structure and composition is depicted in the longitudinal diagram. The internal construction of the virion is portrayed in the cross‐sectional diagram.

Figure 2.

The cycle of replication and infection in lyssaviruses involves: (1) adsorption; (2) penetration; (3) uncoating; (4) transcription; (5) translation; (6) processing; (7) replication; (8) assembly; and (9) budding.

Figure 3.

The rabies virus genome is single‐stranded, antisense, nonsegmented RNA of approximately 12 kb. There is a leader (LDR) of 50 nucleotides followed by N, NS, M, G and L genes, which code for the five structural proteins. The intergenic nontranslated regions (NC) are considered variable, especially between G and L genes. The numbers below each gene are the length, in nucleotides, of the mRNA transcripts for each gene.

Figure 4.

The distribution of the predominate terrestrial maintenance hosts for rabies in the USA are indicated on this map (Arctic/Red Fox, Arizona (AZ) Grey Fox, North–Central (NC) Skunk, Texas (TX) Coyote, Texas Grey Fox, South–Central Skunk, Raccoon). Epidemiologically separate variants can be defined by limited nucleotide (nt) sequence analysis of 200 nt of the rabies N gene, and are indicated by different shading patterns. The relationships between the rabies virus variants are demonstrated in the phylogram on the right. The genetic distance is proportional to horizontal branch lengths. The percent homology is given at the major branch nodes.

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Further Reading

Bourhy H, Kissy B and Tordo N (1993) Molecular diversity of lyssavirus genes. Virology 194: 70–81.

Centers for Disease Control and Prevention (1999) Human rabies prevention: United States, 1999: Recommendations of the Advisory Committee on Immunization Practices (ACIP) 48 (RR‐1): 1–21.

Charlton KM (1994) The pathogenesis of rabies and other lyssaviral infections: recent studies. Current Topics in Microbiology and Immunology 187: 95–119.

Hanlon CA and Rupprecht CE (1998) The reemergence of rabies. In: Scheld WM, Armstrong D and Hughes JM (eds) Emerging Infections I, pp. 59–80. Washington, DC: ASM Press.

Murphy FA, Harrison K, Winn WC and Bauer SP (1973) Comparative pathogenesis of rabies and rabies‐like viruses: infection of the central nervous system and centrifugal spread of virus to peripheral tissues. Laboratory Investigations 29: 1–16.

Noah DL, Drenzek CL, Smith JS et al. (1998) Epidemiology of human rabies in the United States, 1980–1996. Annals of Internal Medicine 128: 922–930.

Rupprecht CE and Smith JS (1994) Raccoon rabies. Virology 5: 155–164.

Smith JS (1989) Rabies virus epitopic variation: use in ecologic studies. Advances in Virus Research 36: 215–253.

Smith JS (1996) New aspects of rabies with emphasis on epidemiology, diagnosis, and prevention of the disease in the United States. Clinical Microbiology Reviews 9: 166–176.

Steele JH and Fernandez PJ (1991) History of rabies and global aspects. In: Baer GM (ed.) Natural History of Rabies, 2nd edn. Boca Raton, FL: CRC Press.

Wunner WH, Larson JK, Dietzschold B and Smith CL (1988) The molecular biology of rabies viruses. Reviews of Infectious Diseases 10: S771–S784.

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How to Cite close
Hanlon, Cathleen A, and Orciari, Lillian A(Apr 2001) Rabies Virus. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1038/npg.els.0000427]