Arbovirus Investigations in Argentina, 1977–1980
C. H. CalisherT. P. MonathM. S. SabattiniJ. KerschnerC. J. MitchellJ. S. LazuickC. B. CroppAnn R. Hunt
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Abstract:
Forty viruses isolated from mosquitoes between 1977 and 1980 in Argentina have been identified and characterized. Nineteen strains of VEE virus, identical by neutralization (N) tests, were shown by hemagglutination-inhibition tests with anti-E2 glycoprotein sera to represent a new subtype VI of the VEE complex. RNA oligonucleotide fingerprints of this virus were distinct from subtype I viruses. The virus was not lethal for English short-haired guinea pigs, indicating that it is probably not equine-virulent. Three strains of a member of the WEE virus complex were shown to differ by N tests in 1 direction from prototype WEE virus. The new WEE subtype was also found to be distinct by RNA oligonucleotide mapping. Its vector relationships indicate that it is an enzootic virus, and it has not been associated with equine disease. A new member of the Anopheles A serogroup was identified, shown to be most closely related to Lukuni and Col An 57389 viruses, and given the name Las Maloyas virus. A strain of Para virus (Bunyaviridae, Bunyavirus) was identified. Six isolates, representing 3 new viruses morphologically resembling bunyaviruses are described; the names Antequera, Barranqueras, and Resistencia are proposed for these agents, which were all isolated from Culex (Melanoconion) delpontei in Chaco Province. No serologic relationships between these viruses and other bunyaviruses were found. Since they are antigenically interrelated, they form a new (Antequera) serogroup. Eight Gamboa serogroup viruses and 2 strains of St. Louis encephalitis virus were also identified.Keywords:
Enzootic
Orbivirus
Encephalitis Viruses
Togaviridae
Venezuelan equine encephalitis is caused by a virus in the family Togaviridae, genus Alphavirus (Fig. 1 and 2). It is an enveloped virus with an icosahedral capsid 60 to 70 nm in diameter with a linear, single-stranded positive-sense RNA nonsegmented genome of approximately 11.4 kilobases (1). These images are electron micrographs of virus growing in Aedes albopictus C6/36 cells 8 days postinfection and negatively stained with 2% phosphotungstate from an outbreak in Gualaca, Panama, in 1971. Venezuelan equine encephalitis viruses occur in South and Central America and in the Florida Everglades of the United States (2). Venezuelan equine encephalitis virus exists in two settings: (i) a continuous cycle maintained between Culex mosquito vectors and rodents (enzootic) and (ii) epidemics that involve several mosquito species that feed on mammals (epizootic).
See also:
Venezuelan Equine Encephalitis (VEE) Infection in Horses
References.
1. Griffin, D. E. 2001. Alphaviruses. p. 917–962. In D. M. Knipe and P. M. Howley (ed.), Fields virology. Lippincott Williams and Wilkins, Philadelphia, Pa.
2. Roberts, W. A., and G. A. Carter. 1976. Essentials of veterinary virology, p. 107. Michigan State University Press, East Lansing, Mich.
Enzootic
Togaviridae
Epizootic
Aedes albopictus
Alphavirus infection
Encephalitis Viruses
Veterinary virology
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Of more than 500 arboviruses recognized worldwide, five were first isolated in Canada and 58 were first isolated in the USA. Six of these viruses are human pathogens: western equine encephalitis (WEE) and eastern equine encephalitis (EEE) viruses (family Togaviridae, genus Alphavirus), St. Louis encephalitis (SLE) and Powassan (POW) viruses (Flaviviridae, Flavivirus), LaCrosse (LAC) virus (Bunyaviridae, Bunyavirus) and Colorado tick fever (CTF) virus (Reoviridae, Coltivirus). Their scientific histories, geographic distributions, virology, epidemiology, vectors, vertebrate hosts, transmission, pathogenesis, clinical and differential diagnoses, control, treatment and laboratory diagnosis are reviewed. In addition, mention is made of the Venezuelan equine encephalitis (VEE) complex viruses (family Togaviridae, genus Alphavirus), which periodically cause human and equine disease in North America.
Togaviridae
Flavivirus
Tick-borne encephalitis
Encephalitis Viruses
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Venezuelan equine encephalitis (VEE) is caused by a virus in the family Togaviridae genus Alphavirus. It is an enveloped virus with an icosahedral capsid 60 to 70 nm in diameter with a linear, single-stranded positive-sense RNA nonsegmented genome of approximately 11.4 kilobases (4). VEE periodically occurs in South and Central America and occurred in Texas in 1971 (6). VEE viruses exist in two settings: (i) a continuous cycle maintained between Culex mosquito vectors and rodents (enzootic), and (ii) epidemics that involve several mosquito species that feed on mammals (epizootic). Epizootic VEE virus varients occur in irregular epizootic cycles and cause clinical disease and deaths in equines only during those cycles. Sylvatic or enzootic VEE viruses may be found at any time in enzootic cycles involving rodents; equine disease is rarely associated with infection by sylvatic VEE viruses. Aedes taeniorhynchus is thought to be the main mosquito vector (1); however, other mosquitoes are thought to play a role, and during an epidemic in horses in 1969 to 1971 Aedes aegypti, Culex tarsalis, Deinocerites pseudes, and Psorophora confinnis mosquitoes were shown to be infected. This epidemic began in 1969 in northern South America and by the time it ended in 1971, it had resulted in the deaths of hundreds of thousands of horses throughout Central America, Mexico, and Texas (3). Female mosquitoes ingest the virus when bloodfeeding on infected rodents or horses to obtain protein for egg production and after a 7 to 20 day extrinsic incubation period can transmit the virus when feeding on a new host. The mosquitoes remain infected for life. The principal mosquito vector for human infections is thought to be Culex pipiens although more than 30 other species have been implicated (5)
Usually 0.5 to 5 days after being bitten by an infected mosquito, horses begin to show signs. Infections range from asymptomatic, to mild (anorexia, fever), or severe either with fatality or without. Horses with a severe response show a distinctive lack of coordination that leads to a leaning stance and circling due to the swelling of the brain (Fig. 1–3). Other signs include fever, lack of appetite with rapid weight loss, and depression, and may include seizures. The sylvatic virus is endemic in northern South America, Trinidad, Central America, Mexico, and Florida. Epizootic virus appears sporadically in epizootics mostly in Mexico, Central and South America. The photos shown here were taken in Gualaca, Panama. Prognosis is poor for horses infected with epizootic viruses (50 to 90% mortality). Horses often die from trauma induced during seizures. Figure 4 shows a horse that has died, and shows lesions on the eyes and face incurred during seizures. Also note the lack of vegetation around the head, which is caused as the horse's head swings back and forth during the seizures. Similar defoliation is also often noted near the legs of horses that die of VEE as their legs will swing in a paddling motion. Upon necropsy the brain shows signs of encephalitis (swelling of the brain) and hemorrhaging that is actually caused by head trauma during the seizures rather than viral damage (Fig. 5). Horses are often euthanatized before they reach this point, as recovery in cases this severe is rare (3, 6). There is a vaccine to control this disease that should be administered yearly and also contains western and eastern encephalitis viruses along with VEE viruses.
Similar to western and eastern encephalitis, humans can become infected with VEE. In humans, signs of VEE infection include fever, exhaustion, back pain, nausea, vomiting, and headache; children are at greatest risk for developing central nervous system infections. The overall mortality rate in epidemics is 0.5 to 1%. In patients who develop encephalitis, the mortality rate is about 20%, in the absence of adequate medical care this can approach 25 to 30%. Encephalitis is clinically diagnosed in only 1 to 4% of adults and 3 to 5% of children. There is no vaccination for humans (3).
The virus is cultivated typically in
cell culture and quantified using plaque assays; virus is serially diluted and plated on the African green monkey kidney cell line Vero V76 cells and cytopathic effect is quantified. Diagnosis is usually attempted using paired serums (acute and convalescent; 2 weeks apart) assaying for a four-fold increase in serum neutralizing antibody titers. This assay detects antibodies in the serum, if animals have had an immune response. However, this is problematic as many animals die before the second, 2 week, convalescent sample can be obtained (6).
See also:
Venezuelan Equine Encephalitis Virus
References.
1. Brault, A. C., A. M. Powers, and S. C. Weaver. 2002. Vector infection determinants of Venezuelan equine encephalitis virus reside within the E2 envelope glycoprotein. J. Virol. 76
:6387–6392.
2. Committee on Foreign Animal Diseases of the United States Animal Health Association. 1998, revision date. The Gray book of foreign animal diseases, 6th ed. United States Animal Health Association, Richmond, Va. [Online.] http://www.vet.uga.edu/VPP/gray_book/FAD/index.htm.
3. Fenner, F., P. A. Bachmann, E. P. J. Gibbs, F. A. Murphy, M. J. Studdert, and D. O. White. 1987. Veterinary virology, p. 460–462. Academic Press, Inc., Orlando, Fla.
4. Griffin, D. E. 2001. Alphaviruses, p. 917–962. In D. M. Knipe and P. M. Howley (ed.), Fields virology. Lippincott Williams and Wilkins, Philadelphia, Pa.
5. Nasci, R. S., and B. R. Miller. Culicine mosquitoes and the agents they transmit, p. 85–97. In B. J. Beaty and W. C. Marquardt (ed.), The biology of disease vectors. University Press of Colorado, Niwot, Colo.
6. Roberts, W. A., and G. A. Carter. 1976. Essentials of veterinary virology, p. 107. Michigan State University Press, East Lansing, Mich.
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Togaviridae
Alphavirus infection
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Colônias de células de mosquito Aedes albopictus C6/36 foram infectadas com 23 arbovirus, sendo 19 destes existentes no Brasil, pertencentes às famílias Togaviridae, Flaviviridae, Bunyaviridae e Rhabdoviridae. A Replicação virai foi detectada por imunofluorescência indireta com todos os vírus estudados enquanto que o efeito citopático foi observado durante a infecção por alguns destes. No teste de imunofluorescência indireta utilizou-se fluidos ascíticos imunes de camundongos, específicos para os vírus estudados. A replicação virai caracterizada por grande produção de antígeno recomenda a utilização de células C6/36 na propagação e em tentativas de isolamento desses arbovirus. A técnica de imunofluorescência ofereceu importantes subsídios na classificação e identificação de vírus que replicam nestas células.
Togaviridae
Cytopathic effect
Aedes albopictus
Immunofluorescence
Tospovirus
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African horse sickness
Enzootic
Orbivirus
Culicoides
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Rift Valley Fever
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Western equine encephalitis (WEE) was once prevalent and routinely isolated from mosquitoes in Colorado; however, isolations of Western equine encephalitis virus (WEEV) have not been reported from mosquito pools since the early 1990s. The objective of the present study was to test pools of Culex tarsalis (Coquillett) mosquitoes sampled from Weld County, CO, in 2016 for evidence of WEEV infection. Over 7,000 mosquitoes were tested, but none were positive for WEEV RNA. These data indicate that WEEV either was not circulating enzootically in Northern Colorado, was very rare, and would require much more extensive mosquito sampling to detect, or was heterogeneously distributed spatially and temporally and happened to not be present in the area sampled during 2016. Even though the reported incidence of WEE remains null, screening for WEEV viral RNA in mosquito vectors offers forewarning toward the detection and prevention of future outbreaks.
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Togaviridae
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To test the hypothesis that adaptation to epizootic mosquito vectors mediates the emergence of Venezuelan equine encephalitis virus (family Togaviridae, genus Alphavirus, VEEV) from enzootic progenitors, the susceptibility of the epizootic vector Psorophora confinnis (Lynch-Arribalzaga) to epizootic versus enzootic strains was evaluated. Artificial bloodmeals containing subtype IC strains isolated during the 1962–1964, 1992–1993, and 1995 Venezuelan/Colombian epizootics and closely related Venezuelan enzootic subtype ID strains were used to compare mosquito infectivity and transmission potential. Strains from the smaller 1992–1993 epizootic showed lower or equal infectivity and replication compared with enzootic viruses and to strains isolated during the larger 1962–1964 and 1995 epizootics. These experiments failed to provide evidence that Ps. confinnis selects for epizootic VEEV viruses with higher infectivity, as has been shown for Aedes (Ochlerotatus) taeniorhynchus (Wiedemann). Nonetheless, its high susceptibility, abundance in enzootic and epizootic regions, and feeding behavior suggest that Ps. confinnis is an important bridge vector for both enzootic and epizootic VEEV.
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Togaviridae
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The decrease in western equine encephalomyelitis virus (WEEV; Togaviridae, Alphavirus) activity in North America over the past 20–30 years has prompted research to determine if there have been concurrent declines in virulence. Six (WEEV) strains isolated from Culex tarsalis mosquitoes from California during each of the six preceding decades failed to show a consistent declining temporal trend in virus titer using mosquito (C6/36), avian (duck embryo fibroblast), or mammalian (Vero) cells, results similar to our recent in vivo studies using birds and mosquitoes. Titers measured by Vero cell plaque assay were consistently highest on mosquito cell culture, followed by avian and mammalian cell cultures. Similar to previous in vivo results in house sparrows and mice, titers for the IMP181 strain isolated in 2005 were significantly lower in both avian and mammalian cells. Real-time monitoring of changes in cell growth measured by electrical impedance showed consistent differences among cell types, but not WEEV strains. Collectively, these in vitro results failed to explain the decrease in WEEV enzootic and epidemic activity. Results with the IMP181 strain should be verified by additional sequencing, cell growth, and pathogenesis studies using concurrent or 2006 isolates of WEEV from California.
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Vero cell
Sindbis virus
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SUMMARY Venezuelan equine encephalitis (VEE) belongs to the Alphavirus of the new world. This virus is considered an emerging disease in equines, humans and others wild animals, that is transmitted between vertebrate hosts by infected mosquitoes. Sporadic outbreaks occurred from the begging of the 20 th century caused neurological syndrome in equines and humans. VEE complex alphavirus are classified into six distinct antigenic subtypes each with varieties. The antigenic subtypes IAB and IC, have been responsible for all epizootics. There are two main hypotheses for the origin of epizootic VEE viruses: First, use of inadequately inactivated vaccines using epizootic VEE IAB virus and second, evolution from closely related enzootic VEE strains like subtype ID strains. This enzootic subtype circulates in tropical lowland forest between Colombia and Venezuela. Their circulating and outbreaks epidemics needs control measure, like vectors control, mobilization between borders, and vaccination with safe and effective vaccines.
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Epizootic
Togaviridae
Alphavirus infection
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Arboviruses belong to various families of viruses that are transmitted by arthropods, mainly mosquitoes and ticks. Arboviruses that cause human encephalitis in the United States are members of 3 main virus families: Togaviridae, Flaviviridae, and Bunyaviridae; they include St. Louis encephalitis (SLE), Western equine encephalitis (WEE), Eastern equine encephalitis (EEE), La Crosse virus (LAC), and other California serogroup viruses. In the United States, the incidence is usually 150 to 3,000 cases per year. Most infections are asymptomatic or may result in a nonspecific flu-like syndrome, but if clinical cases do occur, the consequences may be serious. Diseases caused by arboviruses include encephalitis, febrile diseases, and hemorrhagic fevers. Rapid serologic assays such as IgM-capture ELISA (MAC-ELISA) and IgG ELISA can be used soon after infection for diagnosis. There is no specific treatment and therapy is mainly supportive. Prevention includes vector control, educating the public to avoid high-risk areas, wearing protective clothing, and using DEET-containing insect repellents.
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Encephalitis Viruses
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