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Scott C. Weaver - One of the best experts on this subject based on the ideXlab platform.
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Vector competence of eastern and western forms of Psorophora columbiae (Diptera: Culicidae) mosquitoes for enzootic and Epizootic Venezuelan equine encephalitis virus.
The American journal of tropical medicine and hygiene, 2008Co-Authors: Abelardo C. Moncayo, Wenli Kang, Gregory C. Lanzaro, Arnoldo Orozco, Armando Ulloa, Juan I. Arredondo-jimenez, Scott C. WeaverAbstract:Venezuelan equine encephalitis virus (VEEV) continues to circulate enzootically in Mexico with the potential to re-emerge and cause disease in equines and humans in North America. We infected two geographically distinct mosquito populations of eastern Psorophora columbiae form columbiae (Chiapas, Mexico and Texas, United States) and one mosquito population of western Psorophora columbiae form toltecum (California, United States) with Epizootic and enzootic IE VEEV and Epizootic IAB VEEV. We detected no differences between Epizootic and enzootic IE viruses in their ability to infect any of the mosquito populations analyzed, which suggested that neither species selects for Epizootic IE viruses. Psorophora columbiae f. columbiae (Texas) were significantly less susceptible to infection by Epizootic IE than Ps. columbiae f. columbiae (Mexico). Psorophora columbiae f. toltecum populations were more susceptible than Ps. columbiae f. columbiae populations to Epizootic IE and IAB viruses.
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Susceptibility of Psorophora confinnis (Diptera: Culicidae) to infection with Epizootic (subtype IC) and enzootic (subtype ID) Venezuelan Equine encephalitis viruses.
Journal of medical entomology, 2005Co-Authors: Diana I. Ortiz, Michael Anishchenko, Scott C. WeaverAbstract:Abstract 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, ...
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Envelope Glycoprotein Mutations Mediate Equine Amplification and Virulence of Epizootic Venezuelan Equine Encephalitis Virus
Journal of virology, 2005Co-Authors: Ivorlyne P Greene, Michael Anishchenko, Slobodan Paessler, Laura E. Austgen, Aaron C. Brault, Richard A. Bowen, Scott C. WeaverAbstract:Epidemics of Venezuelan equine encephalitis (VEE) result from high-titer equine viremia of IAB and IC subtype viruses that mediate increased mosquito transmission and spillover to humans. Previous genetic studies suggest that mutations in the E2 envelope glycoprotein allow relatively viremia-incompetent, enzootic subtype ID strains to adapt for equine replication, leading to VEE emergence. To test this hypothesis directly, chimeric VEEV strains containing the genetic backbone of enzootic subtype ID strains and the partial envelope glycoprotein genes of Epizootic subtype IC and IAB strains, as well as reciprocal chimeras, were used for experimental infections of horses. Insertion of envelope genes from two different, closely related enzootic subtype ID strains into the Epizootic backbones resulted in attenuation, demonstrating that the Epizootic envelope genes are necessary for the equine-virulent and viremia-competent phenotypes. The partial Epizootic envelope genes introduced into an enzootic ID backbone were sufficient to generate the virulent, viremia-competent equine phenotype. These results indicate that a small number of envelope gene mutations can generate an equine amplification-competent, Epizootic VEEV from an enzootic progenitor and underscore the limitations of small animal models for evaluating and predicting the Epizootic phenotype.
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Susceptibility of Ochlerotatus taeniorhynchus (Diptera: Culicidae) to infection with Epizootic (subtype IC) and enzootic (subtype ID) Venezuelan equine encephalitis viruses: evidence for Epizootic strain adaptation.
Journal of medical entomology, 2004Co-Authors: Diana I. Ortiz, Scott C. WeaverAbstract:To test the hypothesis that adaptation to Epizootic mosquito vectors mediates emergence of Venezuelan equine encephalitis virus (VEEV) from enzootic progenitors, experimental infection studies were conducted to determine the susceptibility of Ochlerotatus taeniorhynchus (Wiedemann) to Epizootic and enzootic strains. Artificial blood meals containing Epizootic 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 infectivity and transmission potential. Their greater infectivity and replication suggested that adaptation of Epizootic strains to Oc. taeniorhynchus may have enhanced Epizootic transmission during the 1962–1964 and 1995 IC coastal Epizootics. However, strains from the small 1992–1993 Venezuelan outbreak that did not extend to coastal regions do not seem to infect this species better than closely related subtype ID strains. Adaptation of VEEV to Epizootic vectors such as Oc. taeniorhynchus mosquitoes may be a determinant of some but not all VEE emergence events and may influence spread into coastal regions.
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generation and characterization of closely related Epizootic and enzootic infectious cdna clones for studying interferon sensitivity and emergence mechanisms of venezuelan equine encephalitis virus
Journal of Virology, 2004Co-Authors: Michael Anishchenko, Anne Sophie Carrara, Ivorlyne P Greene, Slobodan Paessler, Patricia V Aguilar, Scott C. WeaverAbstract:Venezuelan equine encephalitis virus (VEEV) is a reemerging pathogen and a continuing threat to humans and equines in the Americas. Identification of the genetic determinants that enable Epizootic VEEV strains to arise and exploit equines as amplification hosts to cause widespread human disease is pivotal to understanding VEE emergence. The sensitivity to murine alpha/beta interferon-mediated antiviral activity was previously correlated to the Epizootic phenotype of several VEEV strains. Infectious cDNA clones were generated from an Epizootic subtype IC VEEV strain (SH3) isolated during the 1992 Venezuelan outbreak and a closely related enzootic, sympatric subtype ID strain (ZPC738). These VEEV strains had low-cell-culture-passage histories and differed by only 12 amino acids in the nonstructural and structural proteins. Rescued viruses showed similar growth kinetics to their parent viruses in several cell lines, and murine infections resulted in comparable viremia and disease. Unlike what was found in other studies of Epizootic and enzootic VEEV strains, the sensitivities to murine alpha/beta interferon did not differ appreciably between these Epizootic versus enzootic strains, calling into question the reliability of interferon sensitivity as a marker of Epizootic potential.
Rosa Alba Salas - One of the best experts on this subject based on the ideXlab platform.
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Emergence of a new epidemic/Epizootic Venezuelan equine encephalitis virus in South America
Proceedings of the National Academy of Sciences of the United States of America, 1995Co-Authors: Rebeca Rico-hesse, Scott C. Weaver, Julieta De Siger, Gladys Medina, Rosa Alba SalasAbstract:One of the most important questions in arbovirology concerns the origin of epidemic Venezuelan equine encephalitis (VEE) viruses; these viruses caused periodic, extensive epidemics/Epizootics in the Americas from 1938-1973 (reaching the United States in 1971) but had recently been presumed extinct. We have documented the 1992 emergence of a new epidemic/Epizootic VEE virus in Venezuela. Phylogenetic analysis of strains isolated during two outbreaks indicated that the new epidemic/Epizootic virus(es) evolved recently from an enzootic VEE virus in northern South America. These results suggest continued emergence of Epizootic VEE viruses; surveillance of enzootic viruses and routine vaccination of equines should therefore be resumed.
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emergence of a new epidemic Epizootic venezuelan equine encephalitis virus in south america
Proceedings of the National Academy of Sciences of the United States of America, 1995Co-Authors: Rebeca Ricohesse, Scott C. Weaver, Julieta De Siger, Gladys Medina, Rosa Alba SalasAbstract:One of the most important questions in arbovirology concerns the origin of epidemic Venezuelan equine encephalitis (VEE) viruses; these viruses caused periodic, extensive epidemics/Epizootics in the Americas from 1938-1973 (reaching the United States in 1971) but had recently been presumed extinct. We have documented the 1992 emergence of a new epidemic/Epizootic VEE virus in Venezuela. Phylogenetic analysis of strains isolated during two outbreaks indicated that the new epidemic/Epizootic virus(es) evolved recently from an enzootic VEE virus in northern South America. These results suggest continued emergence of Epizootic VEE viruses; surveillance of enzootic viruses and routine vaccination of equines should therefore be resumed.
Michael Anishchenko - One of the best experts on this subject based on the ideXlab platform.
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Susceptibility of Psorophora confinnis (Diptera: Culicidae) to infection with Epizootic (subtype IC) and enzootic (subtype ID) Venezuelan Equine encephalitis viruses.
Journal of medical entomology, 2005Co-Authors: Diana I. Ortiz, Michael Anishchenko, Scott C. WeaverAbstract:Abstract 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, ...
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Envelope Glycoprotein Mutations Mediate Equine Amplification and Virulence of Epizootic Venezuelan Equine Encephalitis Virus
Journal of virology, 2005Co-Authors: Ivorlyne P Greene, Michael Anishchenko, Slobodan Paessler, Laura E. Austgen, Aaron C. Brault, Richard A. Bowen, Scott C. WeaverAbstract:Epidemics of Venezuelan equine encephalitis (VEE) result from high-titer equine viremia of IAB and IC subtype viruses that mediate increased mosquito transmission and spillover to humans. Previous genetic studies suggest that mutations in the E2 envelope glycoprotein allow relatively viremia-incompetent, enzootic subtype ID strains to adapt for equine replication, leading to VEE emergence. To test this hypothesis directly, chimeric VEEV strains containing the genetic backbone of enzootic subtype ID strains and the partial envelope glycoprotein genes of Epizootic subtype IC and IAB strains, as well as reciprocal chimeras, were used for experimental infections of horses. Insertion of envelope genes from two different, closely related enzootic subtype ID strains into the Epizootic backbones resulted in attenuation, demonstrating that the Epizootic envelope genes are necessary for the equine-virulent and viremia-competent phenotypes. The partial Epizootic envelope genes introduced into an enzootic ID backbone were sufficient to generate the virulent, viremia-competent equine phenotype. These results indicate that a small number of envelope gene mutations can generate an equine amplification-competent, Epizootic VEEV from an enzootic progenitor and underscore the limitations of small animal models for evaluating and predicting the Epizootic phenotype.
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generation and characterization of closely related Epizootic and enzootic infectious cdna clones for studying interferon sensitivity and emergence mechanisms of venezuelan equine encephalitis virus
Journal of Virology, 2004Co-Authors: Michael Anishchenko, Anne Sophie Carrara, Ivorlyne P Greene, Slobodan Paessler, Patricia V Aguilar, Scott C. WeaverAbstract:Venezuelan equine encephalitis virus (VEEV) is a reemerging pathogen and a continuing threat to humans and equines in the Americas. Identification of the genetic determinants that enable Epizootic VEEV strains to arise and exploit equines as amplification hosts to cause widespread human disease is pivotal to understanding VEE emergence. The sensitivity to murine alpha/beta interferon-mediated antiviral activity was previously correlated to the Epizootic phenotype of several VEEV strains. Infectious cDNA clones were generated from an Epizootic subtype IC VEEV strain (SH3) isolated during the 1992 Venezuelan outbreak and a closely related enzootic, sympatric subtype ID strain (ZPC738). These VEEV strains had low-cell-culture-passage histories and differed by only 12 amino acids in the nonstructural and structural proteins. Rescued viruses showed similar growth kinetics to their parent viruses in several cell lines, and murine infections resulted in comparable viremia and disease. Unlike what was found in other studies of Epizootic and enzootic VEEV strains, the sensitivities to murine alpha/beta interferon did not differ appreciably between these Epizootic versus enzootic strains, calling into question the reliability of interferon sensitivity as a marker of Epizootic potential.
Diana I. Ortiz - One of the best experts on this subject based on the ideXlab platform.
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Susceptibility of Psorophora confinnis (Diptera: Culicidae) to infection with Epizootic (subtype IC) and enzootic (subtype ID) Venezuelan Equine encephalitis viruses.
Journal of medical entomology, 2005Co-Authors: Diana I. Ortiz, Michael Anishchenko, Scott C. WeaverAbstract:Abstract 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, ...
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Susceptibility of Ochlerotatus taeniorhynchus (Diptera: Culicidae) to infection with Epizootic (subtype IC) and enzootic (subtype ID) Venezuelan equine encephalitis viruses: evidence for Epizootic strain adaptation.
Journal of medical entomology, 2004Co-Authors: Diana I. Ortiz, Scott C. WeaverAbstract:To test the hypothesis that adaptation to Epizootic mosquito vectors mediates emergence of Venezuelan equine encephalitis virus (VEEV) from enzootic progenitors, experimental infection studies were conducted to determine the susceptibility of Ochlerotatus taeniorhynchus (Wiedemann) to Epizootic and enzootic strains. Artificial blood meals containing Epizootic 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 infectivity and transmission potential. Their greater infectivity and replication suggested that adaptation of Epizootic strains to Oc. taeniorhynchus may have enhanced Epizootic transmission during the 1962–1964 and 1995 IC coastal Epizootics. However, strains from the small 1992–1993 Venezuelan outbreak that did not extend to coastal regions do not seem to infect this species better than closely related subtype ID strains. Adaptation of VEEV to Epizootic vectors such as Oc. taeniorhynchus mosquitoes may be a determinant of some but not all VEE emergence events and may influence spread into coastal regions.
Kenneth L Gage - One of the best experts on this subject based on the ideXlab platform.
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Adaptive strategies of Yersinia pestis to persist during inter-Epizootic and Epizootic periods
Veterinary research, 2008Co-Authors: Rebecca J. Eisen, Kenneth L GageAbstract:Plague is a flea-borne zoonotic bacterial disease caused by Yersinia pestis. It has caused three historical pandemics, including the Black Death which killed nearly a third of Europe's population in the 14th century. In modern times, plague Epizootics can extirpate entire susceptible wildlife populations and then disappear for long time periods. Understanding how Y. pestis is maintained during inter-Epizootic periods and the factors responsible for transitioning to Epizootics is important for preventing and controlling pathogen transmission and ultimately reducing the burden of human disease. In this review, we focus primarily on plague in North American foci and discuss the potential adaptive strategies Y. pestis might employ to ensure not only its survival during inter-Epizootic periods but also the rapid Epizootic spread and invasion of new territories that are so characteristic of plague and have resulted in major pandemics and establishment of plague foci throughout much of the world.
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Exposure of Small Rodents to Plague during Epizootics in Black-tailed Prairie Dogs
Journal of wildlife diseases, 2008Co-Authors: Paul Stapp, Kenneth L Gage, Rebecca J. Eisen, Daniel J. Salkeld, Ryan Pappert, John Young, Leon G. Carter, Daniel W. Tripp, Michael F. AntolinAbstract:Plague, caused by the bacterium Yersinia pestis, causes die-offs of colonies of prairie dogs (Cynomys ludovicianus). It has been argued that other small rodents are reservoirs for plague, spreading disease during Epizootics and maintaining the pathogen in the absence of prairie dogs; yet there is little empirical support for distinct enzootic and Epizootic cycles. Between 2004 and 2006, we collected blood from small rodents captured in colonies in northern Colorado before, during, and for up to 2 yr after prairie dog Epizootics. We screened 1,603 blood samples for antibodies to Y. pestis, using passive hemagglutination and inhibition tests, and for a subset of samples we cultured blood for the bacterium itself. Of the four species of rodents that were common in colonies, the northern grasshopper mouse (Onychomys leucogaster) was the only species with consistent evidence of plague infection during Epizootics, with 11.1-23.1% of mice seropositive for antibody to Y. pestis during these events. Seropositive grasshopper mice, thirteen-lined ground squirrels (Spermophilus tridecemlineatus), and deer mice (Peromyscus maniculatus) were captured the year following Epizootics. The appearance of antibodies to Y. pestis in grasshopper mice coincided with periods of high prairie dog mortality; subsequently, antibody prevalence rates declined, with no seropositive individuals captured 2 yr after Epizootics. We did not detect plague in any rodents off of colonies, or on colonies prior to Epizootics, and found no evidence of persistent Y. pestis infection in blood cultures. Our results suggest that grasshopper mice could be involved in Epizootic spread of Y. pestis, and possibly, serve as a short-term reservoir for plague, but provide no evidence that the grasshopper mouse or any small rodent acts as a long-term, enzootic host for Y. pestis in prairie dog colonies.
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estimation of vector infectivity rates for plague by means of a standard curve based competitive polymerase chain reaction method to quantify yersinia pestis in fleas
American Journal of Tropical Medicine and Hygiene, 1998Co-Authors: B J Hinnebusch, Kenneth L Gage, Tom G SchwanAbstract:The prevalence of infectivity within a vector population is a critical factor in arthropod-borne disease epidemiology but it is difficult to estimate. In the case of bubonic plague, infective flea vectors contain large numbers of Yersinia pestis within a bacterial mass that blocks the flea's foregut, and only such blocked fleas are important for biologic transmission. A bacterial quantitation method could therefore be used to assess the prevalence of plague-infective (blocked) fleas in a population. We developed a standard, curve-based, competitive polymerase chain reaction (PCR) procedure to quantitate Y. pestis in individual fleas. The quantitative PCR (Q-PCR) method equaled a colony count reference method in accuracy and precision when evaluated using mock samples and laboratory-infected fleas. The Q-PCR was more reliable than colony count, however, for field-collected fleas and for blocked fleas collected after their death. In a sample of fleas collected from a prairie dog colony in the aftermath of a plague Epizootic, 48% were infected but less than 2% contained numbers of Y. pestis indicative of blockage. The method provides a means to monitor plague Epizootics and associated risks of flea-borne transmission to humans, and is applicable to the study of other vector-borne diseases.