Characterization of modulation of western equine encephalomyelitis virus by Culex tarsalis (Diptera: Culicidae) maintained at 32 degrees C following parenteral infection

Two lines of Culex tarsalis Coquillett genetically selected for low or high western equine encephalomyelitis (WEE) virus production (low viral producer [LVP] or high viral producer [HVP], respectively) modulated WEE (i.e., decreased the concentration of virus to 10(4) plaque-forming units after intr...

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Veröffentlicht in:Journal of medical entomology 1998-05, Vol.35 (3), p.289-295
Hauptverfasser: Kramer, L.D. (University of California, Davis, CA.), Hardy, J.L, Presser, S.B
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container_issue 3
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container_title Journal of medical entomology
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creator Kramer, L.D. (University of California, Davis, CA.)
Hardy, J.L
Presser, S.B
description Two lines of Culex tarsalis Coquillett genetically selected for low or high western equine encephalomyelitis (WEE) virus production (low viral producer [LVP] or high viral producer [HVP], respectively) modulated WEE (i.e., decreased the concentration of virus to 10(4) plaque-forming units after intrathoracic inoculation). The LVP line modulated WEE more than HVP, and modulation was most pronounced at 32 degrees C. At 15 degrees C, viral replication to high titers occurred in both lines. When infected LVP were transferred to 15 degrees C after 4 d extrinsic incubation at 32 degrees C, replication of WEE to high titers did not occur. Mosquitoes transferred from 15 degrees C after replication to high titers occurred, to 32 degrees C did significantly modulate WEE titer. Incubation at 32 degrees C prior to infection had no effect on the degree or timing of WEE modulation in both LVP and HVP lines. Most LVP infected following feeding on a high dose of WEE had salivary gland infection barriers. Viral modulation by Cx. tarsalis was an alphavirus phenomenon, and was not restricted to WEE
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Incubation at 32 degrees C prior to infection had no effect on the degree or timing of WEE modulation in both LVP and HVP lines. Most LVP infected following feeding on a high dose of WEE had salivary gland infection barriers. 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(University of California, Davis, CA.)</creatorcontrib><creatorcontrib>Hardy, J.L</creatorcontrib><creatorcontrib>Presser, S.B</creatorcontrib><title>Characterization of modulation of western equine encephalomyelitis virus by Culex tarsalis (Diptera: Culicidae) maintained at 32 degrees C following parenteral infection</title><title>Journal of medical entomology</title><addtitle>J Med Entomol</addtitle><description>Two lines of Culex tarsalis Coquillett genetically selected for low or high western equine encephalomyelitis (WEE) virus production (low viral producer [LVP] or high viral producer [HVP], respectively) modulated WEE (i.e., decreased the concentration of virus to 10(4) plaque-forming units after intrathoracic inoculation). The LVP line modulated WEE more than HVP, and modulation was most pronounced at 32 degrees C. At 15 degrees C, viral replication to high titers occurred in both lines. When infected LVP were transferred to 15 degrees C after 4 d extrinsic incubation at 32 degrees C, replication of WEE to high titers did not occur. Mosquitoes transferred from 15 degrees C after replication to high titers occurred, to 32 degrees C did significantly modulate WEE titer. Incubation at 32 degrees C prior to infection had no effect on the degree or timing of WEE modulation in both LVP and HVP lines. Most LVP infected following feeding on a high dose of WEE had salivary gland infection barriers. 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(University of California, Davis, CA.)</creatorcontrib><creatorcontrib>Hardy, J.L</creatorcontrib><creatorcontrib>Presser, S.B</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of medical entomology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kramer, L.D. 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The LVP line modulated WEE more than HVP, and modulation was most pronounced at 32 degrees C. At 15 degrees C, viral replication to high titers occurred in both lines. When infected LVP were transferred to 15 degrees C after 4 d extrinsic incubation at 32 degrees C, replication of WEE to high titers did not occur. Mosquitoes transferred from 15 degrees C after replication to high titers occurred, to 32 degrees C did significantly modulate WEE titer. Incubation at 32 degrees C prior to infection had no effect on the degree or timing of WEE modulation in both LVP and HVP lines. Most LVP infected following feeding on a high dose of WEE had salivary gland infection barriers. Viral modulation by Cx. tarsalis was an alphavirus phenomenon, and was not restricted to WEE</abstract><cop>England</cop><pmid>9615548</pmid><doi>10.1093/jmedent/35.3.289</doi><tpages>7</tpages></addata></record>
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source MEDLINE; Oxford University Press Journals All Titles (1996-Current)
subjects ALPHAVIRUS
ANIMAL VIRUSES
Animals
ARBOVIRUSES
Arboviruses - growth & development
BIOLOGICAL DIFFERENCES
Culex - genetics
Culex - virology
CULEX TARSALIS
DIFERENCIAS BIOLOGICAS
DIFFERENCE BIOLOGIQUE
DISEASE VECTORS
Encephalitis Virus, Western Equine - growth & development
Encephalitis Virus, Western Equine - isolation & purification
ENVIRONMENTAL TEMPERATURE
EXPERIMENTAL INFECTION
Female
GLANDE SALIVAIRE
GLANDULAS SALIVALES
INFECCION EXPERIMENTAL
INFECTION EXPERIMENTALE
Insect Vectors - virology
LINE DIFFERENCES
REPLICACION
REPLICATION
SALIVARY GLANDS
Salivary Glands - virology
SELECCION
SELECTION
Selection, Genetic
TEMPERATURA AMBIENTAL
Temperature
TEMPERATURE AMBIANTE
VECTEUR DE MALADIE
VECTOR COMPETENCE
VECTORES
VECTORS
VIRAL REPLICATION
VIRUS DE LOS ANIMALES
VIRUS DES ANIMAUX
VIRUS MODULATION
Virus Replication
WESTERN EQUINE ENCEPHALITIS VIRUS
title Characterization of modulation of western equine encephalomyelitis virus by Culex tarsalis (Diptera: Culicidae) maintained at 32 degrees C following parenteral infection
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