eastern equine encephalitis virus
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IdentityTop of page
Preferred Scientific Name
- eastern equine encephalitis virus
Taxonomic TreeTop of page
- Domain: Virus
- Group: "Positive sense ssRNA viruses"
- Group: "RNA viruses"
- Family: Togaviridae
- Genus: Alphavirus
- Species: eastern equine encephalitis virus
Pathogen CharacteristicsTop of page
The virus of eastern equine encephalitis belongs to the genus Alphavirus, formerly group A arboviruses, in the family Togaviridae. There are 26 confirmed members of the genus Alphavirus, including western equine encephalitis virus and Venezuelan equine encephalitis virus. Serological and phylogenetic analyses of representatives of North and South American eastern equine encephalitis virus varieties, spanning the entire temporal and geographic range available were carried out (Brault et al., 1999). Nucleotide sequencing and phylogenetic analyses revealed additional genetic diversity within the South American variety; 3 major South/Central American lineages were identified including one represented by a single isolate from eastern Brazil, and 2 lineages with more widespread distributions in Central and South America. All North American isolates comprised a single, highly conserved lineage with strains grouped by the time of isolation and partly by location. An eastern equine encephalitis strain isolated during a 1996 equine outbreak in Tamaulipas State, Mexico, was closely related to recent Texas isolates, suggesting southward EEV transportation beyond the presumed enzootic range. Plaque reduction neutralization tests with representatives from the 4 major lineages indicated that each represented a distinct antigenic subtype. As a results, a taxonomic revision of the eastern equine encephalitis complex was proposed. The new nucleotide sequences were deposited in the EMBL/GenBank/DDBJ database under accession numbers AF159550, AF159553-AF159559, AF159561 and AF160169-AF160180.
The viral particles (60-64 nm in diameter) consist of a single-stranded positive-sense RNA genome enclosed within an icosahedral nucleocapsid (30-35 nm in diameter) that is in turn enclosed within a host cell-derived plasma membrane envelope (Biberstein and Zee, 1990). The virion core is composed of a single core protein; the envelope shows peplomers consisting of two glycoproteins (E1 and E2). Glycoprotein E2 appears to carry the major neutralization and haemagglutination epitopes. E1 also has some (probably minor) neutralizing and haemagglutinating epitopes. E1 may also be responsible for generating strain diversity. Razumov et al. (1994), studied the haemagglutination domains of eastern equine encephalitis with 17 HI monoclonal antibodies (MAbs). A highly conserved domain (C domain) forming alphavirus-group-reactive MAbs was identified in the E2 protein of the eastern equine encephalitis virus. Amino acid residues 59 and 232 were shown to be involved in the formation of the C region.
The virus can be propagated in a variety of cell cultures including chick and duck fibroblasts, VERO, BHK, L cells and mosquito cells: cytopathology is often absent in the latter. A variety of lab animals can be experimentally infected, suckling mice being the most common. Embryonated chicken eggs and young chicks may also be susceptible to infection (Biberstein and Zee, 1990).
Pereboev et al. (1993) prepared 33 MAbs interacting with the structural proteins of the virus of eastern equine encephalitis. The mutual arrangement of antigenic sites on E1 and E2 glycoproteins was studied by competitive radioimmunoassay. At least 4 non-overlapping sites were found on E1. The E2 glycoprotein had at least 7 partially overlapping antigenic sites. MAbs to sites E2-2 and E2-3 neutralized viral infectivity and blocked haemagglutination. MAbs to the sites E2-1 blocked haemagglutination. MAbs to the sites E2-2, E2-3 and E2-7 protected mice against lethal infection although the protective sites to E2-2b and E2-7 did not neutralize the virus. Antibodies to the other 3 sites of E2 and to all sites of E1 showed no biological activity. The results demonstrated the dominant role of E2 in antiviral immunity; over 98% of the protective effect was associated with the E2-2 site.
Virus neutralization and haemagglutination inhibition have shown two antigenic variants of eastern equine encephalitis. The alphaviruses are sensitive to lipid solvents, chlorine, phenol and heating to 60ºC for 30 minutes. They are relatively insensitive to trypsin and are stabilized in buffer (pH7.6) in 50% glycerine. Virus can be held indefinitely at 4ºC in the lyophilized state (Biberstein and Zee, 1990).
The arbovirus cycles between vertebrate amplifying hosts and invertebrate vectors. Cooper and Scott (2001) examined the selective pressure associated with virus replication in either host and found that the virus is capable of host specific evolution when assayed in either mosquito or avian cells. Virus lineages grown in alternation between the 2 cell types expressed intermediate phenotypes consistent with dual adaptation to both cellular environments. Alternation of hosts selects for virus populations well adapted for replication in both host systems. Weaver et al. (1999) also examined host evolution and found that alternating host transmission cycles constrain the evolutionary rates of arboviruses but not their fitness for either host alone.
Monoclonal antibodies against western equine encephalitis have been shown to cross react with eastern equine encephalitis (Long et al., 2000). Western equine encephalitis has previously been shown to have arisen by recombination between eastern equine encephalitis and Sindbis-like viruses (Weaver et al., 1997). Nigerian equine encephalitis virus and some alphaviruses, such as western equine encephalitis, eastern equine encephalitis, Semliki Forest virus and Igbo-Ora virus are antigenically similar and related, implying NEEV is also an alphavirus (Adeyefa and Tomori, 1997.)
Host AnimalsTop of page
Vectors and Intermediate HostsTop of page
|Aedes canadensis||Insect||North America|South America|
|Aedes sollicitans||Insect||North America|South America|
ReferencesTop of page
Adeyefa CAO; Tomori O, 1997. Serological analysis of Nigerian equine encephalitis virus. Veterinarski Arhiv, 67(2):77-85.
Biberstein EL; Zee YC, 1990. Review of Veterinary Microbiology. Boston, USA: Blackwell Scientific Publications.
Brault AC; Powers AM; Villarreal Chavez CL; Navarro Lopez R; Fraire Cachón M, 1999. Genetic and antigenic diversity among eastern equine encephalitis viruses from North, Central, and South America. American Journal of Tropical Medicine and Hygiene, 61(4):579-586.
Cooper LA; Scott TW, 2001. Differential evolution of eastern equine encephalitis virus populations in response to host cell type. Genetics, 157(4):1403-1412.
Long MC; Nagata LP; Ludwig GV; Alvi AZ; Conley JD; Bhatti AR; Suresh M, 2000. Construction and characterization of monoclonal antibodies against western equine encephalitis virus. Hybridoma, 19(2):121-127.
Pereboev AV; Agapov EV; Svyatchenko VA; Razumov IA; Protopopova EV; Loktev VB, 1993. Study of the antigenic structure of the virus of eastern equine encephalomyelitis using monoclonal antibodies. Voprosy Virusologii, 38(3):117-122.
Razumov IA; Khusainova AD; Agapov EV; Gaidamovich SY; Pereboev AV; Kolykhalov AA; Netesov SV; Loktev VB, 1994. Intervirology, 37(6):356-360.
Weaver SC; Brault AC; Kang WenLi; Holland JJ, 1999. Genetic and fitness changes accompanying adaptation of an arbovirus to vertebrate and invertebrate cells. Journal of Virology, 73(5):4316-4326.
Weaver SC; Kang WenLi; Shirako Y; Rümenapf T; Strauss EG; Strauss JH, 1997. Recombinational history and molecular evolution of western equine encephalomyelitis complex alphaviruses. Journal of Virology, 71(1):613-623.