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Lance A Durden - One of the best experts on this subject based on the ideXlab platform.
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experimental transmission of langat tick borne encephalitis virus complex virus by the soft tick ornithodoros sonrai acari argasidae
Journal of Medical Entomology, 1994Co-Authors: Michael J. Turell, Lance A DurdenAbstract:Laboratory studies determined that the soft tick Ornithodoros sonrai Sautet & Witkowski is a competent vector of Langat (tick-borne encephalitis virus complex) virus. When ticks fed on suckling mice having a mean Viremia of 10(7.2) plaque-forming units per ml, 52% (n = 208) became infected, and 84% (n = 87) of the infected ticks transmitted virus by bite when fed individually on suckling mice > or = 27 d after the infectious blood meal. Overall, 79 of 184 (43%) of ticks exposed to the original viremic mice individually transmitted virus by bite when tested up to 351 d after the infectious blood meal. In addition, ticks transmitted virus both transstadially and transovarially. Some ticks that transmitted virus during their first transmission attempt were retested. These ticks transmitted virus during 81 (99%) of 82 refeeding attempts, including ticks that transmitted virus 512 d after the initial infectious meal. Therefore, Ornithodoros spp. should be considered as potential vectors of Langat and other tick-borne encephalitis viruses.
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laboratory transmission of eastern equine encephalomyelitis virus to chickens by chicken mites acari dermanyssidae
Journal of Medical Entomology, 1993Co-Authors: Lance A Durden, Kenneth J Linthicum, Thomas P MonathAbstract:: Pools of adult female chicken mites, Dermanyssus gallinae (De Geer), were allowed to feed on chicks that had been inoculated with eastern equine encephalomyelitis (EEE) virus and that had a Viremia level of 10(6.2)-10(6.6) plaque-forming units per milliliter of blood. Virus remained detectable by plaque assay in samples of these mites for 30 d after the infectious blood meal. Virus was not recovered from any of 151 progeny of virus-exposed female mites. Mites that had fed on viremic chicks were allowed to feed on naive chicks 3, 7, 11, 15, or 30 d later. EEE virus was transmitted to chicks by these mites on days 3 (one transmission in four trials) and 7 (one transmission in four trials). Both transmissions were confirmed by the presence of virus in chick blood 24-72 h after mites had fed, and by plaque-reduction neutralization assays of 21-d convalescent chick sera against the original viral strain.
Michael J. Turell - One of the best experts on this subject based on the ideXlab platform.
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experimental transmission of eastern equine encephalitis virus by ochlerotatus j japonicus diptera culicidae
Journal of Medical Entomology, 2002Co-Authors: Michael R. Sardelis, David J Dohm, Benedict Pagac, Richard G Andre, Michael J. TurellAbstract:Abstract We evaluated the potential for Ochlerotatus j. japonicus (Theobald), a newly recognized invasive mosquito species in the United States, to transmit eastern equine encephalitis (EEE) virus. Aedes albopictus (Skuse) and Culex pipiens (L.) were similarly tested for comparison. Ochlerotatus j. japonicus and Ae. albopictus became infected and transmitted EEE virus by bite after feeding on young chickens 1 d after they had been inoculated with EEE virus (Viremias ranging from 107.0–8.7 plaque-forming units [PFU]/ml of blood). No Cx. pipiens (n = 20) had detectable levels of virus 14 d after feeding on an EEE-virus infected chicken with a Viremia of 108.1 PFU per ml of blood. Depending on the viral titer in the donor chicken, infection rates ranged from 55–100% for Oc. j. japonicus and 93–100% for Ae. albopictus. In these two species, dissemination rates were identical to or nearly identical to infection rates. Depending on the viral titer in the blood meal, estimated transmission rates ranged from 15 t...
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eastern equine encephalitis virus in birds relative competence of european starlings sturnus vulgaris
American Journal of Tropical Medicine and Hygiene, 1999Co-Authors: Nicholas Komar, Michael J. Turell, David J Dohm, Andrew SpielmanAbstract:To determine whether eastern equine encephalitis (EEE) virus infection in starlings may be more fulminant than in various native candidate reservoir birds, we compared their respective intensities and durations of Viremia. Viremias are more intense and longer lasting in starlings than in robins and other birds. Starlings frequently die as their Viremia begins to wane; other birds generally survive. Various Aedes as well as Culiseta melanura mosquitoes can acquire EEE viral infection from infected starlings under laboratory conditions. The reservoir competence of a bird is described as the product of infectiousness (proportion of feeding mosquitoes that become infected) and the duration of infectious Viremia. Although starlings are not originally native where EEE is enzootic, a starling can infect about three times as many mosquitoes as can a robin.
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Eastern equine encephalitis virus in birds: relative competence of European starlings (Sturnus vulgaris
1999Co-Authors: Nicholas Komar, Michael J. Turell, David J Dohm, Andrew SpielmanAbstract:Abstract. To determine whether eastern equine encephalitis (EEE) virus infection in starlings may be more ful-minant than in various native candidate reservoir birds, we compared their respective intensities and durations of Viremia. Viremias are more intense and longer lasting in starlings than in robins and other birds. Starlings frequently die as their Viremia begins to wane; other birds generally survive. Various Aedes as well as Culiseta melanura mosquitoes can acquire EEE viral infection from infected starlings under laboratory conditions. The reservoir com-petence of a bird is described as the product of infectiousness (proportion of feeding mosquitoes that become infected) and the duration of infectious Viremia. Although starlings are not originally native where EEE is enzootic, a starling can infect about three times as many mosquitoes as can a robin. Precise knowledge of the identity of the avian reservoir of eastern equine encephalitis (EEE) virus may facilitate ef-forts to protect the public health. Serologic evidence sug-gests that numerous species of birds are exposed to this vi-rus, particularly those residing near swamps in which the Culiseta melanura vector mosquito breeds.1–3 This virus has been isolated from a similarly broad array of hosts. Indeed
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experimental transmission of langat tick borne encephalitis virus complex virus by the soft tick ornithodoros sonrai acari argasidae
Journal of Medical Entomology, 1994Co-Authors: Michael J. Turell, Lance A DurdenAbstract:Laboratory studies determined that the soft tick Ornithodoros sonrai Sautet & Witkowski is a competent vector of Langat (tick-borne encephalitis virus complex) virus. When ticks fed on suckling mice having a mean Viremia of 10(7.2) plaque-forming units per ml, 52% (n = 208) became infected, and 84% (n = 87) of the infected ticks transmitted virus by bite when fed individually on suckling mice > or = 27 d after the infectious blood meal. Overall, 79 of 184 (43%) of ticks exposed to the original viremic mice individually transmitted virus by bite when tested up to 351 d after the infectious blood meal. In addition, ticks transmitted virus both transstadially and transovarially. Some ticks that transmitted virus during their first transmission attempt were retested. These ticks transmitted virus during 81 (99%) of 82 refeeding attempts, including ticks that transmitted virus 512 d after the initial infectious meal. Therefore, Ornithodoros spp. should be considered as potential vectors of Langat and other tick-borne encephalitis viruses.
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Viremia IN THREE ORDERS OF BIRDS (ANSERIFORMES, GALLIFORMES AND PASSERIFORMES) INOCULATED WITH OCKELBO VIRUS
Journal of wildlife diseases, 1993Co-Authors: Jan O. Lundström, Michael J. Turell, Bo NiklassonAbstract:One-hundred six birds of 14 species were inoculated with approximately 1027 plaqueforming units of Ockelbo virus and bled daily for 5 days to determine Viremia levels. Virus was detected in birds of all 14 species tested (four Anseriformes, one Galliformes and nine Passeriformes). The onset of Viremia occurred earlier and viral titers were higher in very young anseriforms and galliforms than in older birds. Adult passeriforms had Ockelbo Viremias of higher titer and longer duration than did adult anseriforms. Viremia titers in adult birds of all three orders tested were sufficient to induce high transmission rates in enzootic mosquito vectors, and Viremias in passeriforms could induce high transmission rates in bridging vectors as well. Passeriforms of the genera Turdus and Fringilla could serve as amplification hosts for Ockelbo virus based on the presently demonstrated Viremia of high titer and long duration in these birds, and the previously demonstrated high prevalence of Ockelbo virus neutralizing an...
Michael P Busch - One of the best experts on this subject based on the ideXlab platform.
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virus and antibody dynamics in acute west nile virus infection
The Journal of Infectious Diseases, 2008Co-Authors: Steven Kleinman, Michael P Busch, Leslie H Tobler, Hany Kamel, Philip J Norris, Irina Walsh, Jose L MatudAbstract:Background. The dynamics of the early stages of West Nile virus (WNV) infection can be assessed by follow-up studies of viremic blood donors. Methods. A total of 245 donors with WNV Viremia were followed up weekly for 4 weeks and then monthly for up to 6 additional months or until seroconversion. Plasma samples were tested for WNV RNA by transcription-mediated amplification (TMA) and for WNV-specific IgM and IgG antibodies. RNA persistence was investigated by 6 replicate TMA tests; samples that were viremic for >40 days were tested for WNV-neutralizing activity. Follow up of 35 additional viremic donors for up to 404 days was conducted to evaluate persistence of WNV-specific antibody. Results. The median time from RNA detection to IgM seroconversion was 3.9 days; to IgG seroconversion, 7.7 days; to RNA negativity by single-replicate TMA, 13.2 days; and to RNA negativity by 6-replicate TMA, 6.1 additional days after results of single-replicate TMA are negative. For 4 donors in whom RNA persisted for >40 days after the index donation, all samples obtained after this threshold were also positive for WNV IgG and neutralizing activity. The mean times to IgM and IgA negativity were 156 and 220 days, respectively. Conclusions. IgM and IgG develop rapidly after Viremia and before RNA levels become undetectable, which occurred a mean of 13.2 days after the index donation among donors in this study. WNV RNA detection by replicate TMA rarely persists for >40 days after the index donation and is accompanied by WNV-specific neutralizing antibody, consistent with an absence of WNV transmission via transfusion of seropositive blood components.
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dynamics of Viremia in early hepatitis c virus infection
Transfusion, 2005Co-Authors: Simone A Glynn, David Wright, Steven Kleinman, Dale F Hirschkorn, Charles M Heldebrant, Richard Smith, Cristina Giachetti, James Gallarda, Michael P BuschAbstract:BACKGROUND: It is important to characterize viral dynamics in early hepatitis C virus (HCV) infection to further our understanding of viral pathogenesis and the potential for secondary transmission in acute infection through blood transfusion or other routes. STUDY DESIGN AND METHODS: Serial units given by 77 source plasma donors who had evolved from HCV RNA–negative to HCV RNA–positive by nucleic acid amplification technology (NAT) screening with 512-unit pool-NAT or were followed from RNA detection to antibody conversion were tested by individual NAT and quantitative RNA assays. RESULTS: During the ramp-up phase when exponential growth occurs, HCV viral load doubled every 10.8 hours (95% confidence interval [CI], 9.9-12.0). Intermittent Viremia was observed before the ramp-up phase in 37 of 50 panels with the earliest detectable viremic bleed occurring 63 days before the estimated onset of ramp-up. The plateau phase or high-titer viremic period that occurs between ramp-up and seroconversion was estimated to last 56.3 days (95% CI, 44.8-67.8). CONCLUSIONS: Intermittent low-level HCV Viremia can occur as much as 2 months before the periods of exponential increase in viral load and the high-titer plateau-phase Viremia that usually precede seroconversion. Animal inoculation studies are in progress to evaluate if transfusion of low-level viremic plasma can transmit HCV infection.
Thomas P Monath - One of the best experts on this subject based on the ideXlab platform.
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recombinant chimeric yellow fever dengue type 2 virus is immunogenic and protective in nonhuman primates
Journal of Virology, 2000Co-Authors: Farshad Guirakhoo, R Weltzin, Thomas J Chambers, Zhenxi Zhang, Kenneth F Soike, Marion S Ratterree, Juan Pablo Arroyo, K Georgakopoulos, John Catalan, Thomas P MonathAbstract:A chimeric yellow fever (YF)-dengue type 2 (dengue-2) virus (ChimeriVax-D2) was constructed using a recombinant cDNA infectious clone of a YF vaccine strain (YF 17D) as a backbone into which we inserted the premembrane (prM) and envelope (E) genes of dengue-2 virus (strain PUO-218 from a case of dengue fever in Bangkok, Thailand). The chimeric virus was recovered from the supernatant of Vero cells transfected with RNA transcripts and amplified once in these cells to yield a titer of 6.3 log10 PFU/ml. The ChimeriVax-D2 was not neurovirulent for 4-week-old outbred mice inoculated intracerebrally. This virus was evaluated in rhesus monkeys for its safety (induction of Viremia) and protective efficacy (induction of anti-dengue-2 neutralizing antibodies and protection against challenge). In one experiment, groups of non-YF-immune monkeys received graded doses of ChimeriVax-D2; a control group received only the vaccine diluents. All monkeys (except the control group) developed a brief Viremia and showed no signs of illness. Sixty-two days postimmunization, animals were challenged with 5.0 log10 focus forming units (FFU) of a wild-type dengue-2 virus. No Viremia (<1.7 log10 FFU/ml) was detected in any vaccinated group, whereas all animals in the placebo control group developed Viremia. All vaccinated monkeys developed neutralizing antibodies in a dose-dependent response. In another experiment, Viremia and production of neutralizing antibodies were determined in YF-immune monkeys that received either ChimeriVax-D2 or a wild-type dengue-2 virus. Low Viremia was detected in ChimeriVax-D2-inoculated monkeys, whereas all dengue-2-immunized animals became viremic. All of these animals were protected against challenge with a wild-type dengue-2 virus, whereas all YF-immune monkeys and nonimmune controls became viremic upon challenge. Genetic stability of ChimeriVax-D2 was assessed by continuous in vitro passage in VeroPM cells. The titer of ChimeriVax-D2, the attenuated phenotype for 4-week-old mice, and the sequence of the inserted prME genes were unchanged after 18 passages in Vero cells. The high replication efficiency, attenuation phenotype in mice and monkeys, immunogenicity and protective efficacy, and genomic stability of ChimeriVax-D2 justify it as a novel vaccine candidate to be evaluated in humans.
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recombinant chimaeric live attenuated vaccine chimerivax incorporating the envelope genes of japanese encephalitis sa14 14 2 virus and the capsid and nonstructural genes of yellow fever 17d virus is safe immunogenic and protective in non human primat
Vaccine, 1999Co-Authors: Thomas P Monath, Zhenxi Zhang, Kenneth F Soike, Juan Pablo Arroyo, Inessa S Levenbook, Simon Delagrave, Gwendolyn A Myers, Alan D T Barrett, Robert E Shope, Marion S RatterreeAbstract:Abstract Yellow fever 17D virus, a safe and effective live, attenuated vaccine, was used as a vector for genes encoding the protective antigenic determinants of a heterologous member of the genus Flavivirus , Japanese encephalitis (JE) virus, the leading cause of acute viral central nervous system infection and death throughout Asia. The viral envelope (prM and E) genes of a full-length cDNA clone of YF 17D virus were replaced with the corresponding genes of JE SA14-14-2, a strain licensed as a live, attenuated vaccine in China. Full-length RNA transcripts of the YF/JE chimaera were used to transfect Vero cells. The progeny virus (named `ChimeriVax™-JE'), was used to define safety after intracerebral (IC) inoculation of rhesus monkeys. Monkeys ( N =3) inoculated with a high dose (6.6 log 10 pfu) developed a brief Viremia, showed no signs of illness, developed high titers of anti-JE neutralizing antibody, and had minimal brain and spinal cord lesion scores according to criteria specified in the WHO monkey neurovirulence test. A control group of 3 monkeys that received a lower dose (4.2 log 10 pfu) of commercial YF 17D vaccine had slightly higher lesion scores. To develop a lethal monkey model of JE for vaccine protection tests, we inoculated groups of monkeys IC or intranasally (IN) with a JE virus strain found to be highly neurovirulent and neuroinvasive for mice. Monkeys inoculated IC, but not IN, developed severe encephalitis after an incubation period of 8–13 days. The ChimeriVax™-JE virus was passed in a cell line acceptable for human use (diploid fetal rhesus lung) and 4.3 or 5.3 log 10 pfu were inoculated into groups of 3 monkeys by the subcutaneous route. All 6 animals developed brief Viremias (peak titer 10 pfu/ml) and subsequently had anti-JE but no yellow fever neutralizing antibodies. On day 64, the monkeys were challenged IC with 5.5 log 10 pfu of virulent JE virus. The immunized animals had no detectable Viremia post-challenge, whereas 4 unimmunized controls became viremic. Only 1 of 6 (17%) vaccinated monkeys but 4 of 4 (100%) unvaccinated controls developed encephalitis. Histopathological examination 30 days after challenge confirmed that the protected, immunized animals had no or minimal evidence of encephalitis. These data demonstrated the ability of the ChimeriVax™-JE to induce a rapid humoral immune response and to protect against a very severe, direct intracerebral virus challenge. Target areas of neuronal damage and inflammation in monkeys infected IC with wild-type JE, the chimaeric virus and YF 17D were similar, indicating that the histopathological scoring system used for the WHO yellow fever monkey neurovirulence test will be applicable to control testing of chimaeric seed viruses and vaccines.
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laboratory transmission of eastern equine encephalomyelitis virus to chickens by chicken mites acari dermanyssidae
Journal of Medical Entomology, 1993Co-Authors: Lance A Durden, Kenneth J Linthicum, Thomas P MonathAbstract:: Pools of adult female chicken mites, Dermanyssus gallinae (De Geer), were allowed to feed on chicks that had been inoculated with eastern equine encephalomyelitis (EEE) virus and that had a Viremia level of 10(6.2)-10(6.6) plaque-forming units per milliliter of blood. Virus remained detectable by plaque assay in samples of these mites for 30 d after the infectious blood meal. Virus was not recovered from any of 151 progeny of virus-exposed female mites. Mites that had fed on viremic chicks were allowed to feed on naive chicks 3, 7, 11, 15, or 30 d later. EEE virus was transmitted to chicks by these mites on days 3 (one transmission in four trials) and 7 (one transmission in four trials). Both transmissions were confirmed by the presence of virus in chick blood 24-72 h after mites had fed, and by plaque-reduction neutralization assays of 21-d convalescent chick sera against the original viral strain.
Georges Mourad - One of the best experts on this subject based on the ideXlab platform.
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monthly screening for bk Viremia is an effective strategy to prevent bk virus nephropathy in renal transplant recipients
Transplant Infectious Disease, 2011Co-Authors: C Almeras, Vincent Foulongne, Valerie Garrigue, Ilan Szwarc, Fernando Vetromile, Georges MouradAbstract:C. Almeras, F. Vetromile, V. Garrigue, I. Szwarc, V. Foulongne, G. Mourad. Monthly screening for BK Viremia is an effective strategy to prevent BK virus nephropathy in renal transplant recipients. Transpl Infect Dis 2011: 13: 101–108. All rights reserved Abstract: Background. BK polyomavirus virus (BKV) nephropathy (BKVN) is the most common viral infection that affects renal allografts. Because a specific antiviral therapy is lacking, BKVN may result in graft dysfunction and/or loss. We prospectively analyzed whether monthly nucleic acid testing (NAT) for BKV replication in blood and immediate reduction of immunosuppression (IS) could prevent BKVN. Methods. NAT was performed at monthly intervals for 6 months and then at 12 months in 119 de novo renal transplant recipients. In viremic patients (presumptive BKVN), a graft biopsy was systematically performed and IS was immediately reduced. Results. BKV Viremia occurred in 13 (10.9%) patients after a median time of 90 days (23–241); 77% of patients were viremic before month 4. After reduction of IS, viral load was undetectable in 11 patients, remained low in 1, and continued to increase in 1 patient who developed definitive BKVN despite reduction of IS, and finally returned to dialysis 6 months after transplantation. Conclusion. BKV infection is an early complication. Monthly NAT in blood during the first 6 months and immediate reduction of IS in viremic patients almost completely prevent definitive BKVN.
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does reduction in immunosuppression in viremic patients prevent bk virus nephropathy in de novo renal transplant recipients a prospective study
Transplantation, 2008Co-Authors: C Almeras, Vincent Foulongne, Valerie Garrigue, Ilan Szwarc, Fernando Vetromile, Michel Segondy, Georges MouradAbstract:Background. BK virus nephropathy (BKVN) is a severe complication of renal transplantation, resulting in graft loss in >50% of cases. Because patients with BKV Viremia are at high risk for developing BKVN, the aim of our study was to analyze whether early reduction of immunosuppression (IS) could prevent BKVN in viremic patients. Methods. BKV viruria was prospectively screened every 3 months by real-time polymerase chain reaction during the first year after transplantation in 123 consecutive renal transplant recipients. Plasma viral load was measured by polymerase chain reaction whenever viruria was positive; in viremic patients a graft biopsy was systematically performed and IS was reduced. Results. Viruria, Viremia, and BKVN occurred in 48.8%, 10.5%, and 2.4% of patients, respectively. In the 13 patients with positive Viremia, initial graft biopsy showed BKVN in two. After reduction of IS in patients without BKVN, Viremia disappeared in 8 of 11, decreased in 2 of 11, and increased in one patient who eventually developed BKVN. In contrast, Viremia remained positive in one patient with BKVN and disappeared in the second but renal function deteriorated in both of them. Initial viral load was higher in patients who developed BKVN. Conclusion. Reduction of IS is probably an effective therapeutic option to clear Viremia and prevent BKVN in viremic renal transplant patients.
