PHIDIAS: Pathogen-Host Interaction Data Integration and Analysis System

Table of Contents:

Taxonomy Information
Lifecycle Information
Genome Information
Biosafety Information
Culturing Information
Epidemiology Information
Diagnostic Tests Information
Infected Hosts Information
Phinet: Pathogen-Host Interaction Network
Lab Animal Pathobiology & Management
References
Data Provenance and Curators

Taxonomy Information

Species:
1. Venezuelan Equine Encephalitis virus complex (Website 6):
  1. Common Name: Venezuelan Equine Encephalitis
  2. GenBank Taxonomy No.: 177872
  3. Description: The VEE virus complex consists of six closely related subtypes that manifest different characteristics with respect to ecology, epidemiology, and virulence for humans and equines. The IA/B and C varieties are commonly referred to as epizootic strains. These strains have been responsible for extensive epidemics in North, Central, and South America and are highly pathogenic for humans and equines. All of the epizootic strains are exotic to the United States and have been isolated from natural foci in the world only once since 1973. Subtypes II, III, IV, V, and VI and varieties ID, IE, and IF are referred to as the enzootic strains. Like the epizootic strains, the enzootic strains may cause disease in humans, but they differ from the epizootic strains in their lack of virulence for equines. The enzootic viruses are commonly isolated in specific ecological habitats, where they circulate in transmission cycles primarily involving rodents and Culex mosquitoes of the Melanoconion subgenus(Website 34). Only viruses from subtypes IAB and IC have been implicated in large outbreaks of equine and human encephalitis that have occurred from northern South America to southern Texas. These viruses cause large outbreaks by exploiting equines as highly efficient amplification hosts. The remaining, enzootic subtypes--including ID, IE, and II--circulate in continuous sylvatic foci and do not cause epidemic disease because they replicate poorly in equines. However, two recent outbreaks in Chiapas and Oaxaca, Mexico, in which four isolates of VEEV subtype IE were made from horses, demonstrated for the first time the potential for this subtype to emerge and cause equine disease(Brault et al., 2002).
  4. Variant(s):
    - Venezuelan equine encephalitis virus (Website 1):
      - Common Name: Venezuelan equine encephalitis virus
      - GenBank Taxonomy No.: 11036
      - Parents: Venezuelan Equine Encephalitis virus complex
      - Description: Currently, the VEE complex includes six subtype viruses: VEE (subtype I), Everglades (EVE, subtype II), Mucambo (MUC, subtype III), Pixuna (PIX, subtype IV), CAB (subtype V), and AG80-663 (subype VI). The VEE subtype I viruses have been further subdivided seriologically into IAB, IC, ID, IE, and IF, and the MUC subtype III viruses into IIIA, IIIB (Tonate), and IIIC. However, analysis of the phylogenetic relationships of the VEEV complex viruses gained from sequencing has led to a suggested reclassification of EVE (II) with IAB, IC, ID, and IE, and of IF with Ag80-663(Griffin, 2001).
    - Venezuelan equine encephalitis virus (strain Trinidad Donkey) (Website 7):
      - Common Name: Trinidad Donkey
      - GenBank Taxonomy No.: 11038
      - Parents: Venezuelan Equine Encephalitis virus complex
      - Description: Trinidad Donkey strain was isolated in 1943(Powers et al., 1997). This variant has only been isolated during equine epizootic and is highly pathogenic for equines. It can also cause severe, often fatal infections in humans. The VEE vaccine is derived from variant A of this subtype(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (strain P676) (Website 8):
      - Common Name: P676
      - GenBank Taxonomy No.: 36385
      - Description: Epizootic VEE subtype I-C virus, isolated in 1963 in Miranda St., Venezuela from a horse(Powers et al., 1997). This variant has only been isolated during equine epizootics and is highly pathogenic for equines. It can also cause severe, often fatal infections in humans(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (strain 3880) (Website 9):
      - Common Name: 3880
      - GenBank Taxonomy No.: 36382
      - Description: Enzootic VEE subtype I-D virus was isolated originally from a human in Canito, Panama in 1961(Powers et al., 1997). VEE subtype I-D viruses are maintained in enzootic foci in Panama, Colombia, and Venezuela. This variant is associated with nonequine enzootic cycles and has been shown to be nonpathogenic for equines(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (strain Mena II) (Website 10):
      - Common Name: Mena II
      - GenBank Taxonomy No.: 36384
      - Description: VEE viruses of subtype IE are found in isolated foci in tropical Central America, from Veracruz state in Mexico to northwestern Panama. Culex taeniopus, a common mosquito species in the subtype IE endemic area, has been shown to readily transmit VEE IE(Walton and Grayson, 1989). Mena II was originally isolated in Almirante, Panama from an infected human in 1962(Powers et al., 1997). This variant is associated with nonequine enzootic cycles and has been shown to be nonpathogenic for equines(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (strain 78V3531) (Website 11):
      - Common Name: 78V-3531
      - GenBank Taxonomy No.: 177898
      - Description: This strain was originally isolated from a mosquito in Brazil in 1978(Powers et al., 1997). This variant is associated with nonequine enzootic cycles and has been shown to be nonpathogenic for equines(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (Strain TC-83). (Website 12):
      - Common Name: TC-83
      - GenBank Taxonomy No.: 11037
      - Description: TC-83 is a live attenuated strain that was obtained after 83 passages in fetal guinea pig heart cells(Hart et al., 2001).
    - Venezuelan equine encephalitis virus (strain Everglades FE3-7C). (Website 13):
      - Common Name: Everglades FE3-7C
      - GenBank Taxonomy No.: 36383
      - Description: Everglades (subtype II) virus is an enzootic species that was first isolated in Florida in 1963 from a mosquito(Powers et al., 1997).
    - Venezuelan equine encephalitis virus (strain Mucambo virus). (Website 14):
      - Common Name: Mucambo Virus, BeAn8
      - GenBank Taxonomy No.: 60875
      - Description: Mucambo virus was originally isolated from an infected monkey near Benem, Brazil in 1954(Powers et al., 1997). This variant is associated with nonequine enzootic cycles and has been shown to be nonpathogenic for equines(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (strain Tonate virus). (Website 15):
      - Common Name: Tonate Virus, CaAn410-D
      - GenBank Taxonomy No.: 60877
      - Description: Tonate virus was first isolated from an infected bird in 1973 in Tonate, French Guiana, South America(Powers et al., 1997). There has only been one reported death from this viral subtype, and it is generally considered to give only mild, dengue-like symptoms(Hommel et al., 2000).
    - Venezuelan equine encephalitis virus (strain 71D-1252). (Website 16):
      - Common Name: 71D-1252 (Subtype III Variant C)
      - GenBank Taxonomy No.: 177895
      - Description: Recovered in 1971 from Iquitos, Peru,(Powers et al., 1997). strain 71D1252 contains the only temperature sensitive virions found in nature, and the only natural temperature sensitive strain of VEE virus(Scherer and Chin, 1983).
    - Venezuelan equine encephalitis virus (strain Pixuna). (Website 17):
      - Common Name: Pixuna Virus, BeAn356445
      - GenBank Taxonomy No.: 60876
      - Description: Wild birds are the main host for this virus(Vasconcelos et al., 1991). The symptoms presented by infected people were generally a mild febrile illness. Pixuna virus was originally isolated in 1961 from an infected Anopheles nimbus mosquito near Belem, Brazil(Powers et al., 1997).
    - Venezuelan equine encephalitis virus (strain Cabassou). (Website 18):
      - Common Name: Cabassou Virus (Subtype V)
      - GenBank Taxonomy No.: 60879
      - Description: Cabassou virus was originally isolated in 1974 from a mosquito in French Guiana(Powers et al., 1997).
    - Venezuelan equine encephalitis virus (strain Ag80-663) (Website 19):
      - Common Name: Ag80-663
      - GenBank Taxonomy No.: 166978
      - Description: The virus was originally isolated from a mosquito in Argentina in 1980(Powers et al., 1997). This variant is associated with nonequine enzootic cycles and has been shown to be nonpathogenic for equines(Walton and Grayson, 1989).
    - Venezuelan equine encephalitis virus (strain 3908) (Weaver et al., 1996):
      - Common Name: 3908
      - GenBank Taxonomy No.: U55350
      - Description: The first major VEE outbreak since 1973 occurred in Venezuela and Colombia during 1995, and involved an estimated 75,000 to 100,000 people. Phylogenetic analysis and antigenic characterization indicated that all of the viruses from this outbreak were VEE Subtype I Variant C(Weaver et al., 1996).
    - Venezuelan equine encephalitis virus (strain 6119). (Weaver et al., 1996):
      - Common Name: 6119
      - Description: The first major VEE outbreak since 1973 occurred in Venezuela and Colombia during 1995, and involved an estimated 75,000 to 100,000 people. Phylogenetic analysis and antigenic characterization indicated that all are VEE Subtype I Variant C(Weaver et al., 1996).
    - Venezuelan equine encephalitis virus (strain PMCHo5). (Weaver et al., 1996):
      - Common Name: PMCHo5
      - Description: The first major VEE outbreak since 1973 occurred in Venezuela and Colombia during 1995, and involved an estimated 75,000 to 100,000 people. Phylogenetic analysis and antigenic characterization indicated that all are VEE Subtype I Variant C(Weaver et al., 1996).
    - Venezuelan equine encephalitis virus (strain 83U434) (Weaver et al., 1996):
      - Common Name: 83U434
      - Description: The first major VEE outbreak since 1973 occurred in Venezuela and Colombia during 1995, and involved an estimated 75,000 to 100,000 people. Phylogenetic analysis and antigenic characterization indicated that all are VEE Subtype I Variant C(Weaver et al., 1996).
    - Venezuelan equine encephalitis virus (strain SH3) (Weaver et al., 1996):
      - Common Name: SH3
      - Description: The first major VEE outbreak since 1973 occurred in Venezuela and Colombia during 1995, and involved an estimated 75,000 to 100,000 people. Phylogenetic analysis and antigenic characterization indicated that all are VEE Subtype I Variant C(Weaver et al., 1996).
    - Venezuelan equine encephalitis virus (strain 243937) (Powers et al., 1997):
      - Common Name: 243937
      - Description: Isolated in 1992 from a horse in Trujillo St., Venezuela(Powers et al., 1997).
    - Venezuelan equine encephalitis virus (strain 66457) (Powers et al., 1997):
      - Common Name: 66457
      - Description: Isolated 11/11/81 in Sinamaica, Zulia St., Venezuela from a hamster(Powers et al., 1997).
    - Venezuelan equine encephalitis virus (strain 66637) (Powers et al., 1997):
      - Common Name: 66637
      - Description: Isolated 11/19/81 in Sinamaica, Zulia St., Venezuela from a hamster(Powers et al., 1997).
    - Venezuelan equine encephalitis virus (strain ZPC738) (Wang et al., 1999):
      - Common Name: ZPC738
      - Description: Isolated 9/24/1997 from a sentinel hamster in Zulia St., Venezuela(Wang et al., 1999).

Lifecycle Information

VEE virus information
1. Stage Information:
  1. Virion(Website 34):
    - Size: The alphavirus virion is approximately 60 to 65 nm in diameter.
    - Shape: The alphavirus virion, a spherical particle approximately 60 to 65 nm in diameter is typically composed of three different structural proteins enclosing a single molecule of single-stranded RNA.
    - Picture(s):
      - Surface of an Alphavirus (Website 36)
        
        Description: This image is a computer-generated model of the surface of an alphavirus derived by cryoelectron microscopy. The spike-like structures on the virion surface are trimers composed of heterodimers of the virion surface glycoproteins E1 and E2. These spikes are used by the virus to attach to susceptible animal cells. Copyright: CDC.

Genome Summary

Genome of Venezuelan equine encephalitis virus(Website 31)
1. Description: ssRNA positive-strand virus that has no DNA stage(Website 31).
2. Chromosome(Website 31)
  1. GenBank Accession Number: NC_001449, L04653, U55362, U55360, AF00459, AF004472, L01442, AF075259, AF075258, AF075257, AF075256, AF075255, AF075254, AF075253, AF075252, AF075251, AF069903, AF004458, AF100566
  2. Size: 11444 bp(Website 31).
  3. Gene Count: 7 genes(Brault et al., 2002).
  4. Description: The 5' two-thirds of the genome encodes four nonstructural proteins (nsP1 to 4) that are involved in viral replication. After virus entry into the cytoplasm of cells, a nonstructural polyprotein is translated and utilized in the production of full-length negative-sense RNA. The negative-sense RNA is used for the generation of genomic RNA as well as a subgenomic mRNA (26S) that is homologous to the 3' one-third of the genome. The subgenomic RNA is translated directly into a structural polyprotein that is proteolytically cleaved into the capsid, E2, and E1 envelope glycoproteins(Brault et al., 2002). The product of protein NP_040822.1 is a putative nonstructural polyprotein precursor. The product of protein NP_040823.1 is a nonstructural polyprotein precursor. The product of protein NP_040824.1 is a structural polyprotein precursor that is post-translationally cleaved to form the capsid protein, the E3 protein, the E2 envelope glycoprotein, and the envelope glycoprotein(Website 31).

Biosafety Information

Biosafety information for Venezuelan equine encephalitis virus
1. Level: Biosafety level 3.
2. Precautions: Biosafety Level 3 practices, safety equipment, and facilities are recommended for activities using potentially infectious clinical materials and infected tissue cultures, animals, or arthropods. For Venezuelan equine encephalomyelitis, investigational (IND) vaccine TC-83 provides excellent protection against many epizootic strains. This protection may extend to other VEE strains of the complex, including Everglades, Mucambo, Tonate, and Cabassou viruses. TC-83 vaccine should be used as part of a comprehensive safety program and may be particularly important in protecting those working with infected animals and virus concentrates. The administration of the vaccine and the use of its inactivated counterpart (C-84) should be determined by personnel experienced in the use of these vaccines within the constraints of the IND(Website 29).
3. Disposal: Decontaminate before disposal, steam sterilization, and incineration(Website 29).

Culturing Information

Cell culture :
1. Description: VEE viruses, like other alphaviruses, replicates readily in various cell culture systems and laboratory animal hosts. The cell lines of choice vary among laboratories, but include primary chick and duck embryo fibroblasts, VERO (African green monkey kidney) cells, fetal hamster (BHK-21) and guinea pig kidney cells, fetal guinea pig heart cells, and mouse fibroblast (L) cells. After infection, cytopathic changes occur rapidly, within 24 hours. The VEE viruses readily form plaques under agar or gum tragacanth. Plaque morphology in VERO cells under agar can be used to differentiate epizootic variants from sylvatic variants and subtypes(Walton and Grayson, 1989).

Epidemiology Information:

Outbreak Locations:
1. VEE viruses have been isolated and identified only in the Western Hemisphere. Epizootic VEE virus variants have been isolated in Venezuela, Colombia, Ecuador, Peru, Trinidad, Argentina, Costa Rica, Nicaragua, El Salvador, Honduras, Guatemala, Belize, Mexico, and the US(Walton and Grayson, 1989).
Transmission Information:
1. From: Human(Griffin, 2001). , To: Mosquito(Griffin, 2001). (Griffin, 2001)
  Mechanism: The ability of alphaviruses to infect mosquitoes efficiently with spread to and replication in the salivary glands is essential for maintaining the natural cycle of transmission. Not all mosquitoes taking a blood meal from a viremic host will become infected, and not all infected mosquitoes develop salivary gland infection and the ability to transmit the virus(Griffin, 2001).
2. From: Mosquito(Griffin, 2001). , To: Human(Griffin, 2001). (Griffin, 2001)
  Mechanism: The primary mode of alphavirus transmission to vertebrates is through the bite of an infected mosquito. Mosquitoes salivate during feeding and deposit virus-infected saliva extravascularly. Saliva virus titers are highest early after the mosquito is infected and decline, along with transmission rates, after 1 to 2 weeks, but mosquitoes remain infected for life(Griffin, 2001).
3. From: Horse(Griffin, 2001). , To: Mosquito(Griffin, 2001). (Griffin, 2001)
  Mechanism: Horse-mosquito-horse transmission is important in epizootics of VEE. During epizootics, horses are an important amplifying species, and availability of susceptible equines provides a means for virus spread(Griffin, 2001).
4. From: Mosquito(Griffin, 2001). , To: Horse(Griffin, 2001). (Griffin, 2001)
  Mechanism: Horse-mosquito-horse transmission is important in epizootics of VEE. During epizootics, horses are an important amplifying species, and availability of susceptible equines provides a means for virus spread(Griffin, 2001).
5. From: Bird(Walton and Grayson, 1989). , To: Mosquito(Walton and Grayson, 1989). (Walton and Grayson, 1989)
  Mechanism: The cycle of enzootic VEE appears to involve virus transmission to small rodents and birds by mosquitoes(Walton and Grayson, 1989).
6. From: Mosquito(Walton and Grayson, 1989). , To: Birds(Walton and Grayson, 1989). (Walton and Grayson, 1989)
  Mechanism: Birds are exposed to VEEV when they are bitten by an infected mosquito. Birds undeniably serve an integral part in the epidemiology of sylvatic VEE virus, but do not appear to be involved in epizootics of VEE(Walton and Grayson, 1989).
7. From: Rodent(Walton and Grayson, 1989). , To: Mosquito(Walton and Grayson, 1989). (Walton and Grayson, 1989)
  Mechanism: The cycle of enzootic VEE appears to involve virus transmission to small rodents and birds by mosquitoes(Walton and Grayson, 1989).
8. From: Mosquitoes(Walton and Grayson, 1989). , To: Rodents(Walton and Grayson, 1989). (Walton and Grayson, 1989)
  Mechanism: Rodents are exposed to VEEV when they are bitten by an infected mosquito. Wild rodents undeniably serve an integral part in the epidemiology of sylvatic VEE virus, but do not appear to be involved in epizootics of VEE(Walton and Grayson, 1989).
9. From: Human(Website 30). , To: Human(Website 30). (Website 30)
  Mechanism: At present time, direct human-to-human transmission is not proven scientifically but is suspected(Website 30). Fetal abnormalities, spontaneous abortions, and stillbirths may occur with infection during pregnancy. Congenitally infected infants show severe neurological damage, with widespread necrosis, hemorrhage, and hypoplasia resulting, in the most severe cases, in hydranencephaly(Griffin, 2001).
10. From: Rodent(Walton and Grayson, 1989). , To: Human(Walton and Grayson, 1989). (Walton and Grayson, 1989)
  Mechanism: Laboratory related illness can be acquired after handling infected rodents(Walton and Grayson, 1989).
11. From: VEEV(Walton and Grayson, 1989). , To: Human(Walton and Grayson, 1989). (Walton and Grayson, 1989)
  Mechanism: Laboratory related illnesses can be acquired by aerosol infection(Walton and Grayson, 1989, Website 30). An analysis of laboratory incidents suggests that the aerosol form of VEE is highly infectious(Website 30).
Environmental Reservoir:
1. Small rodents(Walton and Grayson, 1989):
  1. Description: The cycle of enzootic VEE appears to involve virus transmission to small rodents and birds by mosquitoes(Walton and Grayson, 1989).
2. Birds(Walton and Grayson, 1989):
  1. Description: The cycle of enzootic VEE appears to involve virus transmission to small rodents and birds by mosquitoes(Walton and Grayson, 1989).
3. Bats(Website 30, Ubico and MacLean, 1995, Seymour et al., 1978):
  1. Description: VEE has a zoonotic reservoir in bats(Website 30). Antibodies against VEE have been found in neotropical bats in Guatemala,(Ubico and MacLean, 1995). and data suggest that bats regularly are infected by VEE virus, and may possibly serve as alternate hosts to maintain virus circulation if most terrestrial animals become immune(Seymour et al., 1978).
Intentional Releases:
1. Intentional Release Information:
  1. Description: Although other encephalitic viruses could be considered as potential weapons (eg, the tick-borne encephalitis viruses), few possess as many of the required characteristics for strategic or tactical weapons development as the alphaviruses. These viruses can be produced in large amounts in inexpensive and unsophisticated systems; They are relatively stable and highly infectious for humans as aerosols; Strains are available that produce either incapacitating or lethal infections; and the existence of multiple serotypes of VEE and EEE viruses, as well as the inherent difficulties of inducing efficient mucosal immunity, confound defensive vaccine development(Website 34). The virus that causes VEE is quite susceptible to genetic manipulation. This has proven useful in the laboratory in the development of more effective vaccines, however, it also could be exploited to produce more effective biological weapons(Website 30).
  2. Emergency Contact: Contact an infectious disease specialist if VEE is suggested. In addition, involve the local county health department(Website 30).
  3. Delivery Mechanism: Aerosol transmission of VEE has occurred as a result of laboratory accidents or lack of laboratory precautions(Website 30). The equine encephalomyelitis viruses remain as highly credible threats today, and intentional release as a small-particle aerosol, from a single airplane, could be expected to infect a high percentage of individuals within an area of at least 10,000 km(2)(Website 34).

Diagnostic Tests Information

Organism Detection Test:
1. Microscopy (Valero-Fuenmayor et al., 1997):
  1. Description: A transmission electron microscopy study was used to detect the presence of Togavirus particles from the cerebrospinal fluid of patients with clinical symptoms and signs of encephalitis, and compared to serum from healthy patients or with serum from sick equines. The presence of Togavirus particles were detected in 100% of the virologically positive cases(Valero-Fuenmayor et al., 1997).
2. Inoculation of neonatal mice :
  1. Description: Isolation of alphaviruses from vertebrate sera during acute disease or from postmortem brain samples, as well as isolation from invertebrate hosts, has been accomplished most often by intracerebral inoculation of neonatal mice, an animal model that is extremely susceptible to most, if not all, alphaviruses. Because alphaviruses produce an extensive cytopathic effect in almost all common vertebrate cell cultures examined, this also is an effective means of isolation(Johnston and Peters, 1996).
Immunoassay Test:
1. Hemagglutination :
  1. Description: Hemagglutination inhibition, although cross-reactive throughout the alphavirus genus, nonetheless retains sufficient specificity to define six antigen complexes or serotypes, which include the antigenic complexes of Western equine encephalitis, Venezuelan equine encephalitis, Eastern equine encephalitis, Semilik forest, Middleburg, Nduma, and Barmah Forest. Identification of a specific virus or subtype usually requires neutralization tests or modified hemagglutination tests. The kinetic hemagglutination inhibition test, for example, is extremely useful in differentiating subtypes of Venezuelan equine encephalitis virus as well as geographic varieties of eastern equine encephalitis and Ross river virus(Johnston and Peters, 1996).
2. Identification of VEE subtypes by Immunoassasys :
  1. Description: Identification of the VEE subtype of an isolate involved can be accomplished by cross-neutralization tests, hemagglutination inhibition, enzyme-linked immunosorbent assay (ELISA), or plaque reduction neutralization (PRN) antibodies appear as viremia diminishes. Since patients with encephalitis typically come to evaluation later in the course of clinical illness, virus is recovered less often from them, and they usually have serum antibody by the time of clinical presentation(Website 34).
3. Complement Fixation :
  1. Description: In a diagnostic laboratory, the preferred tests for VEE virus are the complement fixation (CF), hemagglutination inhibition (HI), and plaque reduction neutralization (N) tests. CF and HI antibodies are detectable at 7 to 10 days after infection(Walton and Grayson, 1989). Identification of the VEE subtype of an isolate involved can be accomplished by cross-neutralization tests, HI, enzyme-linked immunosorbent assay (ELISA), or plaque reduction neutralization (PRN) antibodies appear as viremia diminishes. Complement-fixing (CF) antibodies make their appearance later during convalescence(Website 34).
4. IgM capture ELISA also known as MAC-ELISA :
  1. Description: Identification of the VEE subtype of an isolate involved can be accomplished by cross-neutralization tests. HI, enzyme-linked immunosorbent assay (ELISA), or plaque reduction neutralization (PRN) antibodies appear as viremia diminishes. VEE IgM antibodies are present in acute phase sera, and it has been reported that the VEE IgM tests do not react with sera from patients with EEE or WEE. Since patients with encephalitis typically come to evaluation later in the course of clinical illness, virus is recovered less often from them, and they usually have serum antibody by the time of clinical presentation(Website 34). Human and equine sera are tested for serologic evidence of recent VEE virus infection by IgM capture ELISA, also known as MAC-ELISA(Weaver et al., 1996).
5. IgM capture ELISA :
  1. Description: Identification of the VEE subtype of an isolate involved can be accomplished by cross-neutralization tests, HI, enzyme-linked immunosorbent assay (ELISA), or plaque reduction neutralization (PRN) antibodies appear as viremia diminishes. VEE IgM antibodies are present in acute phase sera, and it has been reported that the VEE IgM tests do not react with sera from patients with EEE or WEE. Since patients with encephalitis typically come to evaluation later in the course of clinical illness, virus is recovered less often from them, and they usually have serum antibody by the time of clinical presentation(Website 34). IgM capture ELISA is usually sufficiently specific and gives a rapid inexpensive assessment of recent infection using a single early convalescent serum sample(Johnston and Peters, 1996).
6. mAB-based Epitope Blocking Assay :
  1. Time to Perform: unknown
  2. Description: An epitope blocking assay using an EEEV glycoprotein E1-expressing recombinant Sindbis virus and virus-specific monoclonal antibodies (mAbs) binding to the E1 of EEEV (strain NJ/60) and the E1 of Sindbis virus was established using automated flow cytometry. The test was evaluated using sera of infected and vaccinated rabbits. A cut-off value of 30% inhibition for antigenic complex-specific seroconversion was found to be sufficient for the detection of the respective infection. By using three different mAbs in parallel, we were able to detect alphavirus genus-, EEEV- and WEEV-complex-specific serum antibodies. As this test is based on the inhibition of binding of virus-specific mAbs, sera of every origin other than mouse can be tested. Thus, this assay may prove useful in the serological screening of a variety of animal species during an outbreak investigation(Passler and Pfeffer, 2003).
7. Neutralization test :
  1. Description: Identification of a specific virus or subtype usually requires neutralization tests or modified hemagglutination tests. The neutralization test has continued to provide the highest specificity for the infecting virus species(Johnston and Peters, 1996).
8. Indirect fluorescent antibody test :
  1. Description: Serum samples obtained from acutely ill patients were inoculated into cultures of monkey kidney (Vero) and mosquito (C6/36) cells. Vero cell cultures were examined daily for evidence of viral cytopathic effect. Cells from selected positive cultures were examined by indirect fluorescent antibody test (IFAT) for evidence of VEE viral antigen with a VEE mouse polyclonal immune ascitic fluid(Weaver et al., 1996).
Nucleic Acid Detection Test:
1. Dissociation-Enhanced Lanthanide Fluorescent Immunoassy (DELFIA) (Website 34):
  1. Description: The DELFIA was a rapid and highly sensitive method of detection, which shows great promise in clinical diagnostic applications. Like the ELISA, it can detect analytes in a number of different sample matrices, though at much lower concentrations. Currently, the many special requirements (equipment and technical) and frequent hot wells make these assays cumbersome to perform and hard to interpret, especially for junior laboratory personnel(Smith et al., 2001).

Infected Hosts Information

Humans
1. Taxonomy Information:
  1. Species:
    1. Homo sapiens (Website 20):
      - Common Name: Homo sapiens
      - GenBank Taxonomy No.: 9606
      - Description: Most commonly, human involvement occurs following intrusion into geographical regions where natural transmission cycles are in progress, or following perturbation of those cycles by environmental changes or the addition of other vectors. Seroprevalence rates among human populations living in or near endemic VEE areas vary but can approach 100%, suggesting that continuous transmission occurs(Website 34).
    2. Equus caballus (Website 21):
      - Common Name: Equus caballus
      - GenBank Taxonomy No.: 9796
      - Description: Due to the magnitude of the viremias and their large body surface area, equines are considered the primary amplifiers of epizootic VEE virus activity. Humans and domestic animals are tangentially infected by the bites of mosquitoes which acquire their infections from equines(Walton and Grayson, 1989).
    3. Culex spp (Website 22):
      - Common Name: Culex spp
      - GenBank Taxonomy No.: 53527
      - Description: At least 41 species from 11 genera of mosquitoes have been reported to be naturally infected with sylvatic VEE viruses. Of these, 20 species are found in the genus Culex(Walton and Grayson, 1989).
    4. Culex subgenus Melanoconion (Website 23):
      - Common Name: Culex subgenus Melanoconion
      - GenBank Taxonomy No.: 53535
      - Description: At least 41 species from 11 genera of mosquitoes have been reported to be naturally infected with sylvatic VEE viruses. Of these, 20 species are found in the genus Culex and 13 in the subgenus Melanconion(Walton and Grayson, 1989). Enzootic VEE virus subtypes are maintained quite efficiently in transmission cycles involving mainly mosquitoes belonging to the subgenus Melanoconion. These mosquitoes often occur in very humid localities with abundant open spaces such as sunny, swampy pastures cut by slowly flowing streams. The mosquitoes are ground feeders, seldom found higher than 8 m above ground, and prefer feeding on mammals rather than birds(Website 34).
    5. Culicidae (Website 24):
      - Common Name: Culicidae
      - GenBank Taxonomy No.: 7157
      - Description: Infection rates of greater than 72% and transmission rates of greater than 17% were reported for those species commonly considered as VEE vectors: Psorophora confinnis, Aedes sollicitans, Aedes aegypti, Mansonia titillans, Anopheles freeborni, and Mansonia indubitans(Walton and Grayson, 1989).
    6. Rodentia (Website 26):
      - Common Name: Rodentia
      - GenBank Taxonomy No.: 9989
      - Description: The cycle of enzootic VEE appears to involve virus transmission to small rodents and birds by mosquitoes(Walton and Grayson, 1989).
    7. Aves (Website 27):
      - Common Name: Aves
      - GenBank Taxonomy No.: 8782
      - Description: The cycle of enzootic VEE appears to involve virus transmission to small rodents and birds by mosquitoes(Walton and Grayson, 1989).
    8. Chiroptera (Website 28):
      - Common Name: Chiroptera
      - GenBank Taxonomy No.: 9397
      - Description: Epizootic VEE virus has been isolated from vampire bats and experimental infections have demonstrated that virus is present in the oral cavities of these mammals after infection. The possible role of vampire bats in the transmission of epizootic VEE virus is not known, but it can be inferred that transmission could occur when the bats feed(Walton and Grayson, 1989).
    9. Primates (Website 5):
      - Common Name: Primates
      - GenBank Taxonomy No.: 9443
      - Description: Infection of rhesus macaques with epizootic strains of the virus elicits a biphasic febrile response: the first phase is coincident with the viremia, and the second phase with termination of viremia. Symptoms are usually mild, consisting of anorexia, loose stools, irritability, and occasionally tremor or myoclonus at the time of fever(Griffin, 2001).
    10. Cavia (Website 4):
      - Common Name: Cavia
      - GenBank Taxonomy No.: 10140
      - Description: Experimental infection of small laboratory animals with VEEV produces a variety of disease patterns. After subcutaneous inoculation of guinea pigs, rabbits, or hamsters with virulent strains of VEEV, there is viremia, and virus replicates in bone marrow, lymph nodes, spleen, and brain. There is a rapid destruction of myeloid and lymphoid cells in lymph nodes, spleen, thymus, intestinal and conjunctival lymphoid tissue, and bone marrow, and damage to the intestinal wall and pancreas. Hamsters also develop cerebral hemorrhage and neuronal cell death. Death occurs 2 to 4 days after infection and may be associated with ileal necrosis, bacteremia, and endotoxemia(Griffin, 2001).
    11. Hamsters (Website 3):
      - Common Name: Hamsters
      - GenBank Taxonomy No.: 10026
      - Description: Experimental infection of small laboratory animals with VEEV produces a variety of disease patterns. After subcutaneous inoculation of guinea pigs, rabbits, or hamsters with virulent strains of VEEV, there is viremia, and virus replicates in bone marrow, lymph nodes, spleen, and brain. There is a rapid destruction of myeloid and lymphoid cells in lymph nodes, spleen, thymus, intestinal and conjunctival lymphoid tissue, and bone marrow, and damage to the intestinal wall and pancreas. Hamsters also develop cerebral hemorrhage and neuronal cell death. Death occurs 2 to 4 days after infection and may be associated with ileal necrosis, bacteremia, and endotoxemia(Griffin, 2001).
    12. Oryctolagus cuniculus (Website 2):
      - Common Name: Oryctolagus cuniculus
      - GenBank Taxonomy No.: 9986
      - Description: Experimental infection of small laboratory animals with VEEV produces a variety of disease patterns. After subcutaneous inoculation of guinea pigs, rabbits, or hamsters with virulent strains of VEEV, there is viremia, and virus replicates in bone marrow, lymph nodes, spleen, and brain. There is a rapid destruction of myeloid and lymphoid cells in lymph nodes, spleen, thymus, intestinal and conjunctival lymphoid tissue, and bone marrow, and damage to the intestinal wall and pancreas. Hamsters also develop cerebral hemorrhage and neuronal cell death. Death occurs 2 to 4 days after infection and may be associated with ileal necrosis, bacteremia, and endotoxemia(Griffin, 2001).
2. Infection Process:
  1. Infectious Dose: 1 viral subunit administered subcutaneously is infectious(Website 32),
  2. Description: The virus gains access to the bloodstream of a human after he or she is bitten by an infected mosquito. VEE is lipid- and glycoprotein-enveloped; it contains RNA of approximately 12 kilobase pairs in length. The virus initially enters lymphatic and bone marrow cells by receptor-mediated endocytosis. After the virus replicates and releases itself into the bloodstream, it infects other cells, causing fever and the other symptoms typical of febrile illnesses. In a subset of patients, the virus gains entrance into the CNS, where it continues to replicate, resulting in acute encephalitis(Website 30),
3. Disease Information:
  1. Encephalitis(i.e., Encephalitis) :
    1. Incubation: The incubation period ranges from 1 day to 1 week(Website 30),
    2. Prognosis:
    3. Symptom Information :
      - Syndrome -- Venezuelan equine encephalitis :
        
        Description: Venezuelan equine encephalitis (VEE) is a mosquito borne acute viral disease characterized by fever and one or more of the following: chills, headache, back pain, myalgias, prostration, nausea, and vomiting. The disease may progress to encephalitis(Website 30).
        
        Observed:
        VEE is rare in the United States(Website 30),
      - Symptom -- Fever :
        
        Description: Fever: Persons with the mild form of illness may describe only minimal flu-like symptoms of low-grade fever, myalgias, or headache. Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat(Website 30).
      - Symptom -- Myalgia :
        
        Description: Myalgia: Persons with the mild form of illness may describe only minimal flu-like symptoms of low-grade fever, myalgias, or headache. Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat(Website 30).
      - Symptom -- Headache :
        
        Description: Headache: Persons with the mild form of illness may describe only minimal flu-like symptoms of low-grade fever, myalgias, or headache. Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat (Website 30). Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Chills :
        
        Description: Intermittent chills: Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat(Website 30).
      - Symptom -- Back pain :
        
        Description: Back pain: Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat(Website 30).
      - Symptom -- Photophobia :
        
        Description: Photophobia: Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat. Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Vomiting :
        
        Description: Vomiting: Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat. Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Hypesthesia :
        
        Description: Hypesthesia: Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat(Website 30).
      - Symptom -- Sore throat :
        
        Description: Sore throat: Typical symptoms of moderate disease found on history include a fever, intermittent chills, myalgias, back pain, a headache, photophobia, vomiting, and/or hypesthesia. Less common complaints include a sore throat(Website 30).
      - Symptom -- Acute-onset high fever :
        
        Description: Acute-onset high fever: Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Severe myalgia :
        
        Description: Severe myalgia: Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Severe back pain :
        
        Description: Severe back pain: Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Weakness :
        
        Description: Weakness: Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Prostration :
        
        Description: Prostration: Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30).
      - Symptom -- Confusion :
        
        Description: Confusion: Patients with the severe form present with an acute-onset high fever (39-40 C), severe myalgias, severe back pain, a headache, photophobia, vomiting, weakness, prostration, and confusion(Website 30). In the 1995 VEE outbreak in South America, convulsions, disorientation, drowsiness, and mental depression were often seen in patients seeking medical care(Weaver et al., 1996).
      - Symptom -- Diarrhea :
        
        Description: Diarrhea: Patients seeking medical care for VEE sometimes present with diarrhea(Weaver et al., 1996).
      - Symptom -- Convulsions :
        
        Description: Convulsions: In the 1995 VEE outbreak in South America, convulsions, disorientation, drowsiness, and mental depression were often seen in patients seeking medical care(Weaver et al., 1996).
      - Symptom -- Depression :
        
        Description: Mental depression: In the 1995 VEE outbreak in South America, convulsions, disorientation, drowsiness, and mental depression were often seen in patients seeking medical care(Weaver et al., 1996).
      - Symptom -- Leukopenia :
        
        Description: Leukopenia: A count of less than 4,500 white blood cells per cubic millimeter(Bowen et al., 1976).
        
        Observed:
        Leukopenia was observed in 75 per cent of the patients examined(Bowen et al., 1976),
      - Symptom -- Central nervous involvement :
        
        Description: Mild to moderate central nervous involvement(Bowen et al., 1976).
        
        Observed:
        Evidence of mild to moderate central nervous system involvement was found in 10 out of 25 children and young people under 17 years of age, and in six out of 54 adults(Bowen et al., 1976), In one epidemic, it was estimated that the ratio of encephalitis to infections is less than 0.5% in adults, although possibly as high as 4% in children(Website 34),
      - Symptom -- Seizures :
        
        Description: Seizures: Seizures, ataxia, paralysis, or coma herald more severe CNS involvement(Website 34). In children with overt encephalitis, case fatalities range as high as 35% compared with 10% for adults(Bowen et al., 1976).
      - Symptom -- Ataxia :
        
        Description: Ataxia: Seizures, ataxia, paralysis, or coma herald more severe CNS involvement(Website 34). In children with overt encephalitis, case fatalities range as high as 35% compared with 10% for adults(Bowen et al., 1976).
      - Symptom -- Coma :
        
        Description: Coma: Seizures, ataxia, paralysis, or coma herald more severe CNS involvement(Website 34). In children with overt encephalitis, case fatalities range as high as 35% compared with 10% for adults(Website 34, Bowen et al., 1976).
      - Symptom -- Paralysis :
        
        Description: Paralysis: Seizures, ataxia, paralysis, or coma herald more severe CNS involvement(Website 34). Two children still had residual paralysis six weeks after onset of illness, but by 10 months these sequelae had disappeared(Bowen et al., 1976).
      - Symptom -- Death :
        
        Description: Death(Website 30, Weaver et al., 1996, Bowen et al., 1976).
        
        Observed:
        The overall mortality rate from epidemics is 0.5-1%. In patients who develop encephalitis, the mortality rate is in the range of 20%(Website 30), In the 1995 outbreak in South America, a case-fatality rate of 0.7% was reported, although precise numbers could not be determined(Weaver et al., 1996), In children with overt encephalitis, case fatalities range as high as 35% compared with 10% for adults(Bowen et al., 1976),
    4. Treatment Information:
      - Supportive : No specific treatment other than supportive care is available(Website 30).
        
        Success Rate: Recovery from the illness occurs in 99% of adults and 97-98% of children(Website 30). For those who survive encephalitic involvement, neurological recovery is usually complete(Website 34).
4. Prevention:
  1. Vector control(Walton and Grayson, 1989)
    - Description: Mosquito control and personal protective measures against mosquito bites are effective means to prevent equines and humans from being infected(Walton and Grayson, 1989), Aerial applications of malathion or dibron have proven highly effective in killing adult mosquitoes and is the method of choice(Walton and Grayson, 1989), Applying larvicides to mosquito-breeding sites has been shown to be an effective control method(Griffin, 2001),
    - Efficacy:
      - Rate: When properly applied from an elevation of 30 to 90 m, a single treatment will kill more than 95% of adult mosquitoes(Walton and Grayson, 1989).
      - Duration:
    - Complication: At high doses, malathion, like other organophosphates, can over stimulate the nervous system causing nausea, dizziness, or confusion. Severe high-dose poisoning with any organophosphate can cause convulsions, respiratory paralysis, and death(Website 35),
  1. Vaccination of horses(Walton and Grayson, 1989)
    - Description: TC-83, a vaccine derived by serial passage of epizootic I-AB variant in fetal guinea pig heart cell cultures, has been used to vaccinate horses in the Americas. Vaccination of equines will protect humans from infection with epizootic VEE virus(Walton and Grayson, 1989),
    - Efficacy:
      - Rate: Immunity in horses develops approximately 3 days after vaccination and horse deaths cease by 8 to 9 days after vaccination(Walton and Grayson, 1989).
      - Duration: Protection to challenge immunity lasts at least 19 months, and neutralizing antibody persists for at least 30 months(Walton and Grayson, 1989).
    - Contraindicator: Formalin-treated vaccines derived from virulent VEE virus subtypes should never be manufactured or used in equines or humans(Walton and Grayson, 1989), Foals under 2 weeks of age and pregnant mares should not be vaccinated(Website 33),
  1. Vaccination of humans(Pittman et al., 1996)
    - Description: Two vaccines developed for protection against the IA/IB subtypes of VEE virus are used under investigational new drug (IND) status to vaccinate at-risk personnel. TC-83 is a live attenuated strain that was obtained after 83 passages in fetal guinea pig heart cells. C-84 is a formaldehyde-inactivated vaccine(Hart et al., 2001),
    - Efficacy:
      - Rate: Eighty-two per cent of vaccinees responded to TC-83 with an 80% plaque reduction neutralization titer (PRNT80) of > or = 1:20(Pittman et al., 1996).
      - Duration: Kaplan-Meier analysis showed a 60% probability of TC-83 vaccinees maintaining a PRNT80 of > or = 1:20 for 5.5-8 years. However, 18% of recipients have insufficient titers of virus-neutralizing antibodies in their serum 1 month after vaccination. We conclude that, although TC-83 is reactogenic, when administered as the primary vaccine and C-84 is administered as a boost, these vaccines provide good long-term immunity and are safe in humans(Pittman et al., 1996). In mice, TC-83 or C-84 vaccination induces long-term (1 year) immunity to the virulent VEE IA/IB Trinidad donkey virus administered subcutaneously. TC-83 vaccination also protects mice from aerosol challenge for at least 1 year after vaccination . However, C-84 vaccination fails to protect most mice against aerosol challenge 6 months after vaccination(Hart et al., 2001).
    - Contraindicator: TC-83 should not be used during pregnancy(Casamassima et al., 1987),
    - Complication: TC-83 induces fever, headache, malaise and myalgias in approximately 23% of vaccinated people(Pittman et al., 1996),
  1. Environment modification(Walton and Grayson, 1989)
    - Description: With knowledge of the breeding sites of vector species of mosquitoes, it is possible to disturb these breeding sites on a limited scale. This can be done by draining breeding sites, by killing the vegetation with which the vector is associated, and by eliminating artificial breeding sites(Walton and Grayson, 1989),
5. Model System:
  1. Primate
    1. Model Host: Primates.
      Primate(Griffin, 2001),
    2. Model Pathogens: VEEV complex(Griffin, 2001).
    3. Description: Infection of rhesus macaques with epizootic strains of the virus elicits a biphasic febrile response: the first phase is coincident with the viremia, and the second phase with termination of viremia. Symptoms are usually mild, consisting of anorexia, loose stools, irritability, and occasionally tremor or myoclonus at the time of fever(Griffin, 2001),
  1. Mouse
    1. Model Host: .
      Mus musculus(Johnston and Peters, 1996),
    2. Model Pathogens: VEEV complex(Johnston and Peters, 1996).
    3. Description: Isolation of alphaviruses from vertebrate sera during acute disease or from postmortem brain samples, as well as isolation from invertebrate hosts, has been accomplished most often by intracerebral inoculation of neonatal mice, an animal model that is extremely susceptible to most, if not all, alphaviruses(Johnston and Peters, 1996), Mice are increasingly used for studies of VEEV pathogenesis. In addiition to myeloid and lymphoid necrosis, mice develop encephalomyelitis, leading to death in 6 to 7 days(Griffin, 2001),
  1. Guinea pig
    1. Model Host: .
      Guinea pig(Griffin, 2001),
    2. Model Pathogens: VEEV complex(Griffin, 2001).
    3. Description: Experimental infection of small laboratory animals with VEEV produces a variety of disease patterns. After subcutaneous inoculation of guinea pigs, rabbits, or hamsters with virulent strains of VEEV, there is viremia, and virus replicates in bone marrow, lymph nodes, spleen, and brain. There is a rapid destruction of myeloid and lymphoid cells in lymph nodes, spleen, thymus, intestinal and conjunctival lymphoid tissue, and bone marrow, and damage to the intestinal wall and pancreas. Hamsters also develop cerebral hemorrhage and neuronal cell death. Death occurs 2 to 4 days after infection and may be associated with ileal necrosis, bacteremia, and endotoxemia(Griffin, 2001),
  1. Hamster
    1. Model Host: .
      Hamster(Griffin, 2001),
    2. Model Pathogens: VEEV complex(Griffin, 2001).
    3. Description: Experimental infection of small laboratory animals with VEEV produces a variety of disease patterns. After subcutaneous inoculation of guinea pigs, rabbits, or hamsters with virulent strains of VEEV, there is viremia, and virus replicates in bone marrow, lymph nodes, spleen, and brain. There is a rapid destruction of myeloid and lymphoid cells in lymph nodes, spleen, thymus, intestinal and conjunctival lymphoid tissue, and bone marrow, and damage to the intestinal wall and pancreas. Hamsters also develop cerebral hemorrhage and neuronal cell death. Death occurs 2 to 4 days after infection and may be associated with ileal necrosis, bacteremia, and endotoxemia(Griffin, 2001),
  1. Rabbit
    1. Model Host: Oryctolagus cuniculus.
      Rabbit(Griffin, 2001),
    2. Model Pathogens: VEEV complex(Griffin, 2001).
    3. Description: Experimental infection of small laboratory animals with VEEV produces a variety of disease patterns. After subcutaneous inoculation of guinea pigs, rabbits, or hamsters with virulent strains of VEEV, there is viremia, and virus replicates in bone marrow, lymph nodes, spleen, and brain. There is a rapid destruction of myeloid and lymphoid cells in lymph nodes, spleen, thymus, intestinal and conjunctival lymphoid tissue, and bone marrow, and damage to the intestinal wall and pancreas. Hamsters also develop cerebral hemorrhage and neuronal cell death. Death occurs 2 to 4 days after infection and may be associated with ileal necrosis, bacteremia, and endotoxemia(Griffin, 2001),

Phinet: Pathogen-Host Interaction Network

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Lab Animal Pathobiology & Management

References:

Bowen et al., 1976: Bowen GS, Fashinell TR, Dean PB, Gregg. Clinical aspects of human Venezuelan equine encephalitis in Texas. Bull Pan Am Health Organ. 1976; 10(1); 46-57. [PubMed: 949558].

Brault et al., 2002: Brault AC, Powers AM, Holmes EC, Woelk CH, Weaver SC. Positively charged amino acid substitutions in the E2 envelope glycoprotein are associated with the emergence of venezuelan equine encephalitis virus. Journal of Virology. 2002; 76(4); 1718-1730. [PubMed: 11799167].

Casamassima et al., 1987: Casamassima AC, Hess LW, Marty A. TC-83 Venezuelan equine encephalitis vaccine exposure during pregnancy. Teratology. 1987; 36(3); 287-289. [PubMed: 3424216].

Griffin, 2001: Griffin DE. Alphaviruses. 917-962. In: . Field's Virology Fourth Edition Volume 1. 2001. Lippincott Williams and Wilkins, Philadelphia Pa.

Hart et al., 2001: Hart MK, Lind C, Bakken R, Robertson M, Tammariello R, Ludwig GV. Onset and duration of protective immunity to IA/IB and IE strains of Venezuelan equine encephalitis virus in vaccinated mice. Vaccine. 2001; 20(3-4); 616-622. [PubMed: 11672929].

Johnston and Peters, 1996: Johnston RE, Peters CJ. Alphaviruses. 843-898. In: . Field's Virology Third Edition Volume 1. 1996. Lippincott-Raven Publishers, Philadelphia PA.

Passler and Pfeffer, 2003: Passler S, Pfeffer M. Detection of antibodies to alphaviruses and discrimination between antibodies to eastern and western equine encephalitis viruses in rabbit sera using a recombinant antigen and virus-specific monoclonal antibodies. J Vet Med B Infect Dis Vet Public Health. 2003; 50(6); 265-269. [PubMed: 14628996].

Pittman et al., 1996: Pittman PR, Makuch RS, Mangiafico JA, Cannon TL, Gibbs PH, Peters CJ. Long-term duration of detectable neutralizing antibodies after administration of live-attenuated VEE vaccine and following booster vaccination with inactivated VEE vaccine. Vaccine. 1996; 14(4); 337-343. [PubMed: 8744562].

Seymour et al., 1978: Seymour C, Dickerman RW, Martin MS. Venezuelan encephalitis virus infection in neotropical bats. I. Natural infection in a Guatemalan enzootic focus. American Journal of Tropical Medicine and Hygiene. 1978; 27(2); 290-296. [PubMed: 646021].

Smith et al., 2001: Smith DR, Rossi CA, Kijek TM, Henchal EA, Ludwig GV. Comparison of Dissociation-Enhanced Lanthanide Fluorescent Immunoassays to Enzyme-Linked Immunosorbent Assays for Detection of Staphylococcal Enterotoxin B, Yersinia pestis-Specific F1 Antigen, and Venezuelan Equine Encephalitis Virus. Clinical and Diagnostic Laboratory Immunology. 2001; 38(4); 1527-1535. [PubMed: 11687442].

Ubico and MacLean, 1995: Ubico SR, MacLean RG. Serologic survey of neotropical bats in Guatemala for virus antibodies. Journal of Wildlife Diseases. 1995; 31(1); 1-9. [PubMed: 7563415].

Valero-Fuenmayor et al., 1997: Valero-Fuenmayor N, Garcia-Tamayo J, Escorihuela-Garcia S, Caleiras E, Parada D. Importance of transmission electron microscopy in the diagnosis of a Venezuelan equine encephalitis outbreak in 1995 in the Venezuelan Guajira. Invest Clin. 1997; 38(2); 73-82. [PubMed: 9296642].

Walton and Grayson, 1989: Walton TE, Grayson MA. Venezuelan Equine Encephalitis. 203-231. In: . The Arboviruses: Epidemiology and Ecology Volume IV. 1989. CRC Press, Boca Raton, Florida.

Weaver et al., 1996: Weaver SC, Salas R, Rico-Hesse R, Ludwig GV, Oberste MS, Boshell J, Tesh RB. Re-emergence of epidemic Venezuelan equine encephalomyelitis in South America. The Lancet. 1996; 348(9025); 436-440. [PubMed: 8709783].

Website 2: Oryctolagus cuniculus

Website 20: Homo sapiens

Website 21: Equus caballus

Website 22: Culex

Website 23: Melanoconion

Website 24: Culicidae

Website 26: Rodentia

Website 27: Aves

Website 28: Chiroptera

Website 29: BMBL Section VII. Arboviruses and Arenaviruses Assigned to Biosafety Level 3

Website 3: Cricetinae

Website 30: Venezuelan Equine Encephalitis

Website 31: Venezuelan equine encephalitis virus, complete genome

Website 32: MATERIAL SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

Website 33: VENEZUELAN EQUINE ENCEPHALOMYELITIS

Website 34: Viral Encephalitides

Website 35: Malathion For Mosquito Control

Website 36: Division of Vector-Borne Infectious Diseases, CDC

Website 4: Cavia

Website 5: Primates

Data Provenance and Curators:

PathInfo: Rebecca Wattam

HazARD: (for the section of Lab Animal Pathobiology & Management)

PHIDIAS: Yongqun "Oliver" He

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