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Scott C Weaver - One of the best experts on this subject based on the ideXlab platform.
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enzootic mosquito vector species at Equine Encephalitis transmission foci in the republica de panama
PLOS ONE, 2017Co-Authors: Rolando Torres, Rafael Samudio, Jeanpaul Carrera, Josue Young, Lisbeth Amarilis Hurtado, Luis Fernando Chaves, Scott C Weaver, Robert B. Tesh, R. Márquez, Lorenzo CaceresAbstract:The identification of mosquito vector species present at arboviral enzootic transmission foci is important to understand transmission eco-epidemiology and to propose and implement prevention and control strategies that reduce vector-borne Equine Encephalitis transmission. The goal of this study was to identify mosquito species potentially involved in the transmission of enzootic Equine Encephalitis, in relation to their abundance and diversity at three endemic regions in the Republica de Panama. We sampled adult mosquitoes during the dry and rainy season of Panama. We employed CDC light traps with octanol, EV traps with CO2 and Trinidad 17 traps baited with live hamsters. Traps were deployed in the peridomicile and extradomicile of houses from 18:00 to 6:00 h. We estimated the abundance and diversity of sampled species. We collected a total of 4868 mosquitoes, belonging to 45 species and 11 genera, over 216 sampling nights. Culex (Melanoconion) pedroi, a major Venezuelan Equine Encephalitis vector was relatively rare (< 2.0% of all sampled mosquitoes). We also found Cx. (Mel) adamesi, Cx. (Mel) crybda, Cx. (Mel) ocossa, Cx. (Mel) spissipes, Cx. (Mel) taeniopus, Cx. (Mel) vomerifer, Aedes scapularis, Ae. angustivittatus, Coquillettidia venezuelensis, Cx. nigripalpus, Cx. declarator, Mansonia titillans, M. pseudotitillans and Psorophora ferox all species known to be vectorially competent for the transmission of arboviruses. Abundance and diversity of mosquitoes in the sampled locations was high, when compared with similar surveys in temperate areas. Information from previous reports about vectorial competence / capacity of the sampled mosquito species suggest that sampled locations have all the elements to support enzootic outbreaks of Venezuelan and Eastern Equine encephalitides.
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vaccines for venezuelan Equine Encephalitis
Vaccine, 2009Co-Authors: Slobodan Paessler, Scott C WeaverAbstract:Arboviruses are capable of causing Encephalitis in animals and human population when transmitted by the vector or potentially via infectious aerosol. Recent re-emergence of Venezuelan Equine Encephalitis virus (VEEV) in South America emphasizes the importance of this pathogen to public health and veterinary medicine. Despite its importance no antivirals or vaccines against VEEV are currently available in the USA. Here we review some of the older and newer approaches aimed at generating a safe and immunogenic vaccine as well as most recent data about the mechanistic of protection in animal models of infection.
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PSEUDOTYPED VIRUSES PERMIT RAPID DETECTION OF NEUTRALIZING ANTIBODIES IN HUMAN AND Equine SERUM AGAINST VENEZUELAN Equine Encephalitis VIRUS
American Journal of Tropical Medicine and Hygiene, 2006Co-Authors: Andrey A. Kolokoltsov, Scott C Weaver, Eryu Wang, Tonya M. Colpitts, Robert A. DaveyAbstract:Virus envelope proteins are the primary targets of neutralizing antibody responses. The epitopes recognized differ sufficiently between virus subtypes and species to distinguish viruses and provide an important basis for disease diagnosis. Venezuelan Equine Encephalitis virus (VEEV) causes acute febrile illness in humans and has high mortality in Equines. The most specific detection methods for serum antibodies use live virus in neutralization assays or in blocking enzyme linked immunosorbent assays. However, work with Venezuelan Equine Encephalitis virus requires biosafety level 3 containment and select agent security in the United States. We report two new assays for detection of Venezuelan Equine Encephalitis virus neutralizing antibody responses, based on virus pseudotypes. The first provides detection by marker gene expression after 20 hours and is particularly suited for high-throughput screening; the second uses a new, rapid virus entry assay to give readouts within 1 hour. Both assays are safe, sensitive, and in general recapitulate neutralizing antibody titers obtained by conventional plaque reduction assays. Each is suitable as a rapid primary screen for detection of neutralizing antibodies against Venezuelan Equine Encephalitis virus.
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Postepizootic Persistence of Venezuelan Equine Encephalitis Virus, Venezuela
Emerging Infectious Diseases, 2005Co-Authors: Juan Carlos Navarro, Eryu Wang, Gladys Medina, Clovis Vasquez, Lark L. Coffey, Alexander Suárez, Hernán Biord, Marlene Salas, Scott C WeaverAbstract:Five years after the apparent end of the major 1995 Venezuelan Equine Encephalitis (VEE) epizootic/epidemic, focal outbreaks of Equine Encephalitis occurred in Carabobo and Barinas States of western Venezuela. Virus isolates from horses in each location were nearly identical in sequence to 1995 isolates, which suggests natural persistence of subtype IC VEE virus (VEEV) strains in a genetically stable mode. Serologic evidence indicated that additional outbreaks occurred in Barinas State in 2003. Field studies identified known Culex (Melanoconion) spp. vectors and reservoir hosts of enzootic VEEV but a dearth of typical epidemic vectors. Cattle serosurveys indicated the recent circulation of enzootic VEEV strains, and possibly of epizootic strains. Persistence of VEEV subtype IC strains and infection of horses at the end of the rainy season suggest the possibility of an alternative, cryptic transmission cycle involving survival through the dry season of infected vectors or persistently infected vertebrates.
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venezuelan Equine Encephalitis
Annual Review of Entomology, 2003Co-Authors: Scott C Weaver, Cristina Ferro, Roberto Barrera, Jorge Boshell, Juan Carlos NavarroAbstract:Venezuelan Equine Encephalitis virus (VEEV) remains a naturally emerging disease threat as well as a highly developed biological weapon. Recently, progress has been made in understanding the complex ecological and viral genetic mechanisms that coincide in time and space to generate outbreaks. Enzootic, Equine avirulent, serotype ID VEEV strains appear to alter their serotype to IAB or IC, and their vertebrate and mosquito host range, to mediate repeated VEE emergence via mutations in the E2 envelope glycoprotein that represent convergent evolution. Adaptation to Equines results in highly efficient amplification, which results in human disease. Although epizootic VEEV strains are opportunistic in their use of mosquito vectors, the most widespread outbreaks appear to involve specific adaptation to Ochlerotatus taeniorhynchus, the most common vector in many coastal areas. In contrast, enzootic VEEV strains are highly specialized and appear to utilize vectors exclusively in the Spissipes section of the Culex (Melanoconion) subgenus.
Marc Fischer - One of the best experts on this subject based on the ideXlab platform.
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eastern Equine Encephalitis virus in the united states 2003 2016
American Journal of Tropical Medicine and Hygiene, 2018Co-Authors: Nicole P Lindsey, Erin J Staples, Marc FischerAbstract:Eastern Equine Encephalitis virus (EEEV), a mosquito-borne alphavirus, is one of the most severe arboviral encephalitides in North America.1 Eastern Equine Encephalitis virus is primarily maintained in an enzootic cycle between birds and Culiseta melanura mosquitoes, which breed in freshwater hardwood swamp environments.2 Spread of EEEV to mammals typically requires bridging mosquitoes (e.g., Aedes or Coquillettidia species) that feed on both birds and mammals.1,2 There is some evidence that alternative enzootic and epizootic cycles exist.3–6 Humans are considered dead-end hosts because they generally do not develop high enough viremia levels to allow virus transmission to feeding mosquitoes. Most persons infected with EEEV have no apparent illness.7 An estimated < 5% of persons infected with EEEV develop meningitis or Encephalitis.2,7 Systemic infection is characterized by acute onset of fever, chills, malaise, myalgia, and arthralgia.1 Signs and symptoms in patients with neuroinvasive disease include fever, headache, altered mental status, and seizures.8–10 Eastern Equine Encephalitis virus neuroinvasive disease is estimated to have a 30% case fatality rate and results in neurologic sequelae in more than 50% of survivors.8,11–13 Although veterinary EEEV vaccines are available for use in horses, there are no licensed vaccines or effective treatment of humans. The first human EEEV disease cases were recognized during a 1938 outbreak in southeastern Massachusetts.8 Human EEEV disease cases have occurred sporadically and in small clusters, primarily along the Atlantic and Gulf coasts of the United States.9,11,14 The largest recorded EEEV outbreak occurred in New Jersey in 1959, with 32 laboratory-confirmed human cases during an 8-week period.11 From 1997 through 2007, a median of eight neuroinvasive disease cases were reported to the Centers for Disease Control and Prevention annually.15 This report summarizes the national EEEV surveillance data for 2003 through 2016, including human disease cases and nonhuman infections.
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Eastern Equine Encephalitis Virus in the United States, 2003–2016
American Journal of Tropical Medicine and Hygiene, 2018Co-Authors: Nicole P Lindsey, J. Erin Staples, Marc FischerAbstract:Eastern Equine Encephalitis virus (EEEV), a mosquito-borne alphavirus, is one of the most severe arboviral encephalitides in North America.1 Eastern Equine Encephalitis virus is primarily maintained in an enzootic cycle between birds and Culiseta melanura mosquitoes, which breed in freshwater hardwood swamp environments.2 Spread of EEEV to mammals typically requires bridging mosquitoes (e.g., Aedes or Coquillettidia species) that feed on both birds and mammals.1,2 There is some evidence that alternative enzootic and epizootic cycles exist.3–6 Humans are considered dead-end hosts because they generally do not develop high enough viremia levels to allow virus transmission to feeding mosquitoes. Most persons infected with EEEV have no apparent illness.7 An estimated < 5% of persons infected with EEEV develop meningitis or Encephalitis.2,7 Systemic infection is characterized by acute onset of fever, chills, malaise, myalgia, and arthralgia.1 Signs and symptoms in patients with neuroinvasive disease include fever, headache, altered mental status, and seizures.8–10 Eastern Equine Encephalitis virus neuroinvasive disease is estimated to have a 30% case fatality rate and results in neurologic sequelae in more than 50% of survivors.8,11–13 Although veterinary EEEV vaccines are available for use in horses, there are no licensed vaccines or effective treatment of humans. The first human EEEV disease cases were recognized during a 1938 outbreak in southeastern Massachusetts.8 Human EEEV disease cases have occurred sporadically and in small clusters, primarily along the Atlantic and Gulf coasts of the United States.9,11,14 The largest recorded EEEV outbreak occurred in New Jersey in 1959, with 32 laboratory-confirmed human cases during an 8-week period.11 From 1997 through 2007, a median of eight neuroinvasive disease cases were reported to the Centers for Disease Control and Prevention annually.15 This report summarizes the national EEEV surveillance data for 2003 through 2016, including human disease cases and nonhuman infections.
Nicole P Lindsey - One of the best experts on this subject based on the ideXlab platform.
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eastern Equine Encephalitis virus in the united states 2003 2016
American Journal of Tropical Medicine and Hygiene, 2018Co-Authors: Nicole P Lindsey, Erin J Staples, Marc FischerAbstract:Eastern Equine Encephalitis virus (EEEV), a mosquito-borne alphavirus, is one of the most severe arboviral encephalitides in North America.1 Eastern Equine Encephalitis virus is primarily maintained in an enzootic cycle between birds and Culiseta melanura mosquitoes, which breed in freshwater hardwood swamp environments.2 Spread of EEEV to mammals typically requires bridging mosquitoes (e.g., Aedes or Coquillettidia species) that feed on both birds and mammals.1,2 There is some evidence that alternative enzootic and epizootic cycles exist.3–6 Humans are considered dead-end hosts because they generally do not develop high enough viremia levels to allow virus transmission to feeding mosquitoes. Most persons infected with EEEV have no apparent illness.7 An estimated < 5% of persons infected with EEEV develop meningitis or Encephalitis.2,7 Systemic infection is characterized by acute onset of fever, chills, malaise, myalgia, and arthralgia.1 Signs and symptoms in patients with neuroinvasive disease include fever, headache, altered mental status, and seizures.8–10 Eastern Equine Encephalitis virus neuroinvasive disease is estimated to have a 30% case fatality rate and results in neurologic sequelae in more than 50% of survivors.8,11–13 Although veterinary EEEV vaccines are available for use in horses, there are no licensed vaccines or effective treatment of humans. The first human EEEV disease cases were recognized during a 1938 outbreak in southeastern Massachusetts.8 Human EEEV disease cases have occurred sporadically and in small clusters, primarily along the Atlantic and Gulf coasts of the United States.9,11,14 The largest recorded EEEV outbreak occurred in New Jersey in 1959, with 32 laboratory-confirmed human cases during an 8-week period.11 From 1997 through 2007, a median of eight neuroinvasive disease cases were reported to the Centers for Disease Control and Prevention annually.15 This report summarizes the national EEEV surveillance data for 2003 through 2016, including human disease cases and nonhuman infections.
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Eastern Equine Encephalitis Virus in the United States, 2003–2016
American Journal of Tropical Medicine and Hygiene, 2018Co-Authors: Nicole P Lindsey, J. Erin Staples, Marc FischerAbstract:Eastern Equine Encephalitis virus (EEEV), a mosquito-borne alphavirus, is one of the most severe arboviral encephalitides in North America.1 Eastern Equine Encephalitis virus is primarily maintained in an enzootic cycle between birds and Culiseta melanura mosquitoes, which breed in freshwater hardwood swamp environments.2 Spread of EEEV to mammals typically requires bridging mosquitoes (e.g., Aedes or Coquillettidia species) that feed on both birds and mammals.1,2 There is some evidence that alternative enzootic and epizootic cycles exist.3–6 Humans are considered dead-end hosts because they generally do not develop high enough viremia levels to allow virus transmission to feeding mosquitoes. Most persons infected with EEEV have no apparent illness.7 An estimated < 5% of persons infected with EEEV develop meningitis or Encephalitis.2,7 Systemic infection is characterized by acute onset of fever, chills, malaise, myalgia, and arthralgia.1 Signs and symptoms in patients with neuroinvasive disease include fever, headache, altered mental status, and seizures.8–10 Eastern Equine Encephalitis virus neuroinvasive disease is estimated to have a 30% case fatality rate and results in neurologic sequelae in more than 50% of survivors.8,11–13 Although veterinary EEEV vaccines are available for use in horses, there are no licensed vaccines or effective treatment of humans. The first human EEEV disease cases were recognized during a 1938 outbreak in southeastern Massachusetts.8 Human EEEV disease cases have occurred sporadically and in small clusters, primarily along the Atlantic and Gulf coasts of the United States.9,11,14 The largest recorded EEEV outbreak occurred in New Jersey in 1959, with 32 laboratory-confirmed human cases during an 8-week period.11 From 1997 through 2007, a median of eight neuroinvasive disease cases were reported to the Centers for Disease Control and Prevention annually.15 This report summarizes the national EEEV surveillance data for 2003 through 2016, including human disease cases and nonhuman infections.
Juan Carlos Navarro - One of the best experts on this subject based on the ideXlab platform.
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Postepizootic Persistence of Venezuelan Equine Encephalitis Virus, Venezuela
Emerging Infectious Diseases, 2005Co-Authors: Juan Carlos Navarro, Eryu Wang, Gladys Medina, Clovis Vasquez, Lark L. Coffey, Alexander Suárez, Hernán Biord, Marlene Salas, Scott C WeaverAbstract:Five years after the apparent end of the major 1995 Venezuelan Equine Encephalitis (VEE) epizootic/epidemic, focal outbreaks of Equine Encephalitis occurred in Carabobo and Barinas States of western Venezuela. Virus isolates from horses in each location were nearly identical in sequence to 1995 isolates, which suggests natural persistence of subtype IC VEE virus (VEEV) strains in a genetically stable mode. Serologic evidence indicated that additional outbreaks occurred in Barinas State in 2003. Field studies identified known Culex (Melanoconion) spp. vectors and reservoir hosts of enzootic VEEV but a dearth of typical epidemic vectors. Cattle serosurveys indicated the recent circulation of enzootic VEEV strains, and possibly of epizootic strains. Persistence of VEEV subtype IC strains and infection of horses at the end of the rainy season suggest the possibility of an alternative, cryptic transmission cycle involving survival through the dry season of infected vectors or persistently infected vertebrates.
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venezuelan Equine Encephalitis
Annual Review of Entomology, 2003Co-Authors: Scott C Weaver, Cristina Ferro, Roberto Barrera, Jorge Boshell, Juan Carlos NavarroAbstract:Venezuelan Equine Encephalitis virus (VEEV) remains a naturally emerging disease threat as well as a highly developed biological weapon. Recently, progress has been made in understanding the complex ecological and viral genetic mechanisms that coincide in time and space to generate outbreaks. Enzootic, Equine avirulent, serotype ID VEEV strains appear to alter their serotype to IAB or IC, and their vertebrate and mosquito host range, to mediate repeated VEE emergence via mutations in the E2 envelope glycoprotein that represent convergent evolution. Adaptation to Equines results in highly efficient amplification, which results in human disease. Although epizootic VEEV strains are opportunistic in their use of mosquito vectors, the most widespread outbreaks appear to involve specific adaptation to Ochlerotatus taeniorhynchus, the most common vector in many coastal areas. In contrast, enzootic VEEV strains are highly specialized and appear to utilize vectors exclusively in the Spissipes section of the Culex (Melanoconion) subgenus.
Slobodan Paessler - One of the best experts on this subject based on the ideXlab platform.
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Pathogenesis of Venezuelan Equine Encephalitis.
Veterinary microbiology, 2013Co-Authors: Katherine G Taylor, Slobodan PaesslerAbstract:Equine encephalids have high mortality rates and represent a significant zoonotic public health threat. Of these the most pathogenic viruses to equids are the alphaviruses in the family Togaviridae. The focus of this review Venezualen Equine Encephalitis virus (VEEV) has caused the most widespread and recent epidemic outbreaks of disease. Circulation in naturally occuring rodent-mosquito cycles, results in viral spread to both human and Equine populations. However, Equines develop a high titer viremia and can transmit the virus back to mosquito populations. As such, the early recognition and control of viral infection in Equine populations is strongly associated with prevention of epidemic spread of the virus and limiting of disease incidence in human populations. This review will address identification and pathogenesis of VEEV in equids vaccination and treatment options, and current research for drug and vaccine development.
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vaccines for venezuelan Equine Encephalitis
Vaccine, 2009Co-Authors: Slobodan Paessler, Scott C WeaverAbstract:Arboviruses are capable of causing Encephalitis in animals and human population when transmitted by the vector or potentially via infectious aerosol. Recent re-emergence of Venezuelan Equine Encephalitis virus (VEEV) in South America emphasizes the importance of this pathogen to public health and veterinary medicine. Despite its importance no antivirals or vaccines against VEEV are currently available in the USA. Here we review some of the older and newer approaches aimed at generating a safe and immunogenic vaccine as well as most recent data about the mechanistic of protection in animal models of infection.
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noncytopathic replication of venezuelan Equine Encephalitis virus and eastern Equine Encephalitis virus replicons in mammalian cells
Journal of Virology, 2005Co-Authors: Olga Petrakova, Slobodan Paessler, Evgeniya Volkova, Rodion Gorchakov, Richard M Kinney, Ilya FrolovAbstract:Venezuelan Equine Encephalitis (VEE) and eastern Equine Encephalitis (EEE) viruses are important, naturally emerging zoonotic viruses. They are significant human and Equine pathogens which still pose a serious public health threat. Both VEE and EEE cause chronic infection in mosquitoes and persistent or chronic infection in mosquito-derived cell lines. In contrast, vertebrate hosts infected with either virus develop an acute infection with high-titer viremia and Encephalitis, followed by host death or virus clearance by the immune system. Accordingly, EEE and VEE infection in vertebrate cell lines is highly cytopathic. To further understand the pathogenesis of alphaviruses on molecular and cellular levels, we designed EEE- and VEE-based replicons and investigated their replication and their ability to generate cytopathic effect (CPE) and to interfere with other viral infections. VEE and EEE replicons appeared to be less cytopathic than Sindbis virus-based constructs that we designed in our previous research and readily established persistent replication in BHK-21 cells. VEE replicons required additional mutations in the 5′ untranslated region and nsP2 or nsP3 genes to further reduce cytopathicity and to become capable of persisting in cells with no defects in alpha/beta interferon production or signaling. The results indicated that alphaviruses strongly differ in virus-host cell interactions, and the ability to cause CPE in tissue culture does not necessarily correlate with pathogenesis and strongly depends on the sequence of viral nonstructural proteins.