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At least 19 recordsLinked to original sources
PubMed2005

Variation in interferon sensitivity and induction among strains of eastern equine encephalitis virus.

Eastern equine encephalitis virus (EEEV) causes human encephalitis in North America (NA), but in South America (SA) it has rarely been associated with human disease, suggesting that SA strains are less virulent. To evaluate the hypothesis that this virulence difference is due to a greater ability of NA strains to evade innate immunity, we compared replication of NA and SA strains in Vero cells pretreated with interferon (IFN). Human IFN-alpha, -beta, and -gamma generally exhibited less effect on replication of NA than SA strains, supporting this hypothesis. In the murine model, no consistent difference in IFN induction was observed between NA and SA strains. After infection with most EEEV strains, higher viremia levels and shorter survival times were observed in mice deficient in IFN-alpha/beta receptors than in wild-type mice, suggesting that IFN-alpha/beta is important in controlling replication. In contrast, IFN-gamma receptor-deficient mice infected with NA and SA strains had similar viremia levels and mortality rates to those of wild-type mice, suggesting that IFN-gamma does not play a major role in murine protection. Mice pretreated with poly(I-C), a nonspecific IFN inducer, exhibited dose-dependent protection against fatal eastern equine encephalitis, further evidence that IFN is important in controlling disease. Overall, our in vivo results did not support the hypothesis that NA strains are more virulent in humans due to their greater ability to counteract the IFN response. However, further studies using a better model of human disease are needed to confirm the results of differential human IFN sensitivity obtained in our in vitro experiments.

Animals↗
PubMed1995

Differential reactivity of immune sera from human vaccinees with field strains of eastern equine encephalitis virus.

Eastern equine encephalitis (EEE) virus is a mosquito-borne alphavirus that can produce a severe and often fatal acute encephalitis in humans, with significant neurologic sequelae in survivors. Due to the serious nature of the disease, an investigational inactivated EEE vaccine (PE-6) is available to individuals at risk for infection. Both serologic and recent molecular analyses of EEE viruses have demonstrated marked differences between the two antigenic varieties of EEE virus, designated North American (NA) and South American (SA). In view of these findings, we have examined the reactivity of sera from three individuals immunized with the EEE vaccine, derived from an NA isolate, with field strains of EEE virus. Anti-EEE serum antibodies from vaccinees reacted strongly in Western blot assays with both of the envelope (E1 and E2) glycoproteins of each NA strain examined, while reactivities with the glycoproteins of SA strains were substantially weaker and variable and dependent upon both the immune response of the vaccinee and the virus isolate assayed. Most striking was the modest to virtual lack of reactivity with the E2 protein of SA strains. Antigenic differences among the glycoproteins of EEE viruses were not as pronounced in immunoprecipitation analysis. Most significantly, although human immune sera displayed high neutralizing titers against each of the NA isolates examined, only negligible neutralizing titers were obtained against SA isolates. These data suggest that immunized individuals would mount an effective antibody response against infection with NA strains of EEE virus, but that further investigation is clearly warranted to fully assess the protective capability of the vaccine against infection with SA strains.

Antibodies, Viral↗
PubMed2006

A dynamic transmission model of eastern equine encephalitis virus.

Eastern equine encephalitis virus (EEEV) is one of several arthropod-borne viruses (arboviruses) endemic to the United States. Interactions between arthropod (mosquito) vectors and avian amplification host populations play a significant role in the dynamics of arboviral transmission. Recent data have suggested the hypothesis that an increased rate of successful feeding on young-of-the-year (YOY) birds might play a role in the dynamics of EEEV transmission. To test this hypothesis, we developed a model to explore the effect of the interactions of the vectors and avian host populations on EEEV transmission. Sensitivity analyses conducted using this model revealed eleven parameters that were capable of disproportionately affecting the predicted level of EEEV infection in the vertebrate reservoir and vector populations. Of these, four parameters were related to the interaction of the vector with young-of-the-year birds. Furthermore, adult birds could not substitute for young-of-the-year in initiating and maintaining a predicted enzootic outbreak of EEEV. Taken together, the model predicted that young-of-the-year birds play a key role in establishing and maintaining enzootic outbreaks of EEEV.

Journal Article↗
PubMed2005

Noncytopathic replication of Venezuelan equine encephalitis virus and eastern equine encephalitis virus replicons in Mammalian cells.

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.

Amino Acid Sequence↗
PubMed1987

Infection of a poikilothermic cell line (XL-2) with eastern equine encephalitis and western equine encephalitis viruses.

Eastern Equine Encephalitis (EEE) was in Cuba before the 1940s; the virus has been isolated from horses, birds, and rodents during epizootic as well as interepizootic periods. The only isolation of Western Equine Encephalitis (WEE) virus was from a sick pigeon found in the vicinity of Havana University. Both viruses can cause human disease; the isolation of WEE virus from the centre of an urban area emphasises the need for the prompt isolation and rapid identification of these agents. The object of this work was to compare the sensitivity of a continuous cell line (XL-2) from the toad, Xenopus laevis, with primary chick embryo cell cultures (CEC) routinely used for isolation as well as assay of these viruses. Both cell systems were infected with EEE virus isolated from horse brain and WEE virus isolated from a sick pigeon. A clear cytopathic effect (CPE) consisting of rounding and detachment of cells was observed in both cell cultures infected with the two viruses. By 18 hours post-infection, there was partial destruction of the cell monolayer and by 24 hours the CPE was total. The infectious titre of EEE and WEE viruses in XL-2 and CEC were similar. Both viruses produced small plaques (0.5-1.0 mm diameter) in XL-2 cells. Studies on the sensitivity of the XL-2 cells for direct isolation of the two viruses from field samples and for the detection of Cuban flaviviruses by the immunofluorescence test are in progress.

Alphavirus↗
PubMedDate not supplied

High mortality of domestic turkeys associated with Highlands J virus and eastern equine encephalitis virus infections.

High mortality occurred in two flocks of commercial turkey hens placed in southern North Carolina in fall 1991. Daily mortality peaked at 3.19% in Flock 1 and 3.79% in Flock 2. Clinical signs included restlessness, somnolence, vocalization, and acute death. Gross lesions included atrophy of the bursa of Fabricius, thymus, and spleen, and watery intestinal contents. Microscopic changes included moderate to marked lymphocyte necrosis and depletion in the bursa, thymus, and spleen, widely scattered necrosis of pancreatic acinar cells, and mild villous atrophy and fusion in the jejunum and ileum with cuboidal to low columnar epithelial cells covering the villous tips. In Flock 1, at 27 days of age, reovirus and picornavirus particles were detected in the feces. One week later, togavirus-like particles were observed in fecal contents, and two of seven serum samples showed seroconversion to Highlands J virus. Eleven days later, five of six serum samples were positive for antibodies against Highlands J virus, with a fourfold increase in the geometric mean titer. In Flock 2, seroconversion to eastern equine encephalitis virus was observed in four of 10 serum samples 11 days after the onset of clinical signs. Based on the above observations, it is suspected that these alphaviruses were the cause of the clinical syndrome.

Alphavirus↗
PubMed2006

Molecular identification of blood-meal sources in Culiseta melanura and Culiseta morsitans from an endemic focus of eastern equine encephalitis virus in New York.

Eastern equine encephalitis (EEE) virus perpetuates in an enzootic cycle involving ornithophilic mosquito vectors, principally Culiseta melanura (Coquillett) and avian amplification hosts. To better understand the role of Cs. melanura and Culiseta morsitans (Theobald) in the epizootiology of EEE virus, we collected blood-fed mosquitoes between 31 May and 15 October 2004 at two sites associated with an EEE virus focus in central New York and identified the source of vertebrate blood by nucleotide sequencing of polymerase chain reaction (PCR) products of the cytochrome b gene. Analysis of 484 Cs. melanura and 122 Cs. morsitans revealed that 94.2% and 86.9%, respectively, acquired blood solely from avian hosts. Blood meals derived exclusively from mammals were detected in 0.8% of Cs. melanura and 1.6% of Cs. morsitans. Individual mosquitoes containing mixed-blood meals from both avian and mammalian hosts were also detected in 5.0% of Cs. melanura and 11.5% of Cs. morsitans. Wood thrush constituted the most common vertebrate host for Cs. melanura (23.6%) and Cs. morsitans (30.9%), followed by American robin, song sparrow, ovenbird, red-eyed vireo, and common yellowthroat. Mammalian-derived blood meals were identified as white-tailed deer, horse, domestic cat, and eastern pipistrelle bat. There were three isolations of EEE virus from Cs. melanura and one from Cs. morsitans. These results suggest that wood thrush and a few other passerine birds may play key roles in supporting EEE virus transmission in the northeast and possibly throughout the geographic range of EEE in North America. The frequency of mammalian feedings also suggests that Cs. melanura and Cs. morsitans may play a role in the transmission of EEE virus to equines, in addition to maintaining enzootic transmission among avian hosts. We report the first isolation of arboviruses from mosquito vectors concomitant with the identifications of their blood meal sources.

Animals↗
PubMed2006

Five-year surveillance of West Nile and eastern equine encephalitis viruses in Southeastern Virginia.

To investigate the occurrence of West Nile virus (WNV) and Eastern equine encephalitis virus (EEE) in southeastern Virginia, the Bureau of Laboratories at the Norfolk Department of Public Health (NDPH) analyzed mosquito pools and the sera of sentinel chickens from the southeastern Virginia area each year from 2000 to 2004. Mosquito pool supernatants were screened for the presence of viral RNA by conventional reverse transcription polymerase chain reaction (RT-PCR) and Taqman RT-PCR with the i-Cycler. Mosquito pools were also tested for virus activity by Vero cell culture. The primary enzootic vector of WNV was Culex (Cx.) pipiens and that of EEE was Culiseta (Cs.) melanura. During the five-year surveillance period, the peak minimum infection rates (MIRs) of WNV and EEE in these mosquito species were 2.7 (2002) and 0.9 (2001), respectively. In 2003, the MIRs in Cs. melanura for WNV and EEE were 0.24 and 0.56, respectively; and the MIR for WNV in Cx. pipiens was 0.64. In 2004, Cs. melanura was less active in the WNV transmission cycle (MIR = 0.07) than was Cx. pipiens (MIR = 1.8), and Cs. melanura was the only vector for EEE (MIR = 0.37). The trend was for EEE activity to peak in July; WNV activity peaked in August. Sentinel-chicken sera were tested for IgM antibodies, and peak IgM seroconversions to these arboviruses were recorded in August 2003 for WNV and in July 2003 for EEE. In 2004, the highest IgM seroconversions to EEE occurred later in August. The overall trend of arbovirus activity was greater in 2003 than in 2004.

Animals↗
PubMed1996

Transmission patterns of St. Louis encephalitis and eastern equine encephalitis viruses in Florida: 1978-1993.

Sentinel chickens were maintained at field sites in 40 Florida counties for varying periods between 1978 and 1993. For each county, the total number of St. Louis encephalitis virus (SLE) or eastern equine encephalitis (EEE) virus seroconversions were divided by the number of chickens exposed to calculate a mean annual seroconversion rate. These rates were used to evaluate the annual and geographical distributions of these viruses within Florida. For SLE, the rates in counties that reported human SLE cases during a widespread epidemic in 1990 were compared with adjusted mean annual seroconversion rates calculated by excluding the epidemic year seroconversion data. In general, actual rates were higher than adjusted rates in counties where human SLE cases were reported in 1990. Similar calculations were made for EEE virus that was unusually abundant in northern Florida during the spring and summer of 1991. In general, EEE virus was distributed in the panhandle and northern regions and SLE virus in the central and southern regions of the state. However, this distribution was not exclusive, and during years of high transmission, either virus can extend beyond its normal range. The annual distribution of SLE and EEE viruses was sporadic, ranging from years with little detectable activity to years with widespread, high-level transmission.

Animals↗
PubMed2002

Simultaneous detection of three mosquito-borne encephalitis viruses (eastern equine, La Crosse, and St. Louis) with a single-tube multiplex reverse transcriptase polymerase chain reaction assay.

Three mosquito-borne human encephalitis viruses (eastern equine encephalitis virus [EEE], St. Louis encephalitis virus [SLE], and La Crosse encephalitis virus [LAC]) are sympatric in the southeastern United States. However, little is known concerning the temporal and spatial pattern of the distribution of these viruses in this area. As part of surveillance activities to detect the transmission of these 3 viruses in the Tennessee Valley area, we developed a single-tube multiplex reverse transcriptase polymerase chain reaction (RT-PCR) assay capable of detecting these 3 mosquito-borne viruses in a single reaction. Three viruses were differentiated by size of amplified products. Sensitivities of the multiplex RT-PCR assay for SLE, EEE, and LAC were 1-3 log median tissue culture infective doses per pool, roughly comparable to the reported sensitivity of PCR detection assays for the individual viruses, and 1 log more sensitive than antigen-capture assays for SLE and EEE. The sensitivity of the multiplex PCR was not changed significantly when carried out in the presence of extracts prepared from 50 uninfected mosquitoes. The cost of the assay is estimated at $2.98 per test, similar to the cost of other RT-PCR-based assays for viruses. However, adaptation of the RT-PCR to a multiplex format adds less than $0.01 to the per-unit cost of an RT-PCR assay targeting a single virus species. Analysis of these data suggests that the single-tube multiplex RT-PCR assay represents a sensitive, specific, cost-effective, and rapid method for monitoring activities of the 3 endemic mosquito-borne human encephalitis viruses in mosquito populations in the southeastern United States.

Animals↗
PubMedDate not supplied

Decreased egg production in turkeys experimentally infected with eastern equine encephalitis virus or Highlands J virus.

Turkey breeder hens were experimentally infected with strains of eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus previously isolated from turkey hens experiencing decreased egg production. Depression and inappetance were observed on day 1 postexposure (PE) in hens inoculated with either EEE virus or HJ virus, and egg production fell in each virus-inoculated group from approximately 75% to less than 20% within 2-3 days PE. Egg production remained depressed (less than 20%) for 15 days in EEE-virus-inoculated hens and for 7 days in HJ-virus-inoculated hens. EEE virus and HJ virus were recovered from various tissues on days 1-5 PE, and virus was detected in eggs laid on days 2-5 PE. The findings of this study confirm that EEE virus and HJ virus are potential causes of decreased egg production in turkey breeder hens.

Alphavirus Infections↗
PubMedDate not supplied

Experimental infection of young broiler chickens with eastern equine encephalitis virus and Highlands J virus.

Two-week-old broiler chickens were experimentally infected with either eastern equine encephalitis (EEE) virus or Highland J (HJ) virus. Mortality rates were 24/30 (80%) in EEE-virus-inoculated chickens and 2/30 (7%) in HJ-virus-inoculated chickens. Chickens inoculated with EEE virus exhibited severe depression and somnolence on days 1-6 postexposure (PE), with 17/30 birds dying during this period. After day 6 PE, EEE-virus-inoculated chickens exhibited abdominal distention, depression, and growth retardation, and an additional seven chickens died. Pathologic changes in EE-virus-inoculated chickens dying on days 1-6 PE consisted of multifocal necrosis in the heart and liver, as well as lymphoid depletion and necrosis in the thymus, spleen, and bursa of Fabricius. Ascites, pericardial effusion, and right ventricular dilatation of the heart were the predominant lesions in chickens dying after day 6 PE. No clinical signs were observed in sham-inoculated controls or in most HJ-virus-inoculated chickens. Ascites, pericardial effusion, and multifocal myocardial necrosis were observed in 2/30 HJ-virus-inoculated chickens that died or were euthanatized after development of clinical signs. These findings indicate that both EEE virus and HJ virus are pathogenic for young chickens.

Alphavirus↗
PubMed1975

Replication of eastern equine encephalitis viruses (New Jersey and Louisiana strains and the Ets-4 mutant) in rabbit kidney cells.

Virus yield, viral RNA synthesis, viral protein synthesis, cytopathology, and virus-induced shutoff of host protein synthesis were examined in rabbit kidney (RK) cells infected with eastern equine encephalitis (EEE) viruses. The New Jersey (NJ) strain replicated most rapidly, and exhibited a distinct patter in the synthesis of structural and non-structural viral proteins. The Louisiana (LA) strain and the Ets-4 mutant appeared to be similar in RK celles and chick embryo fibroblasts. Although the viral peptides comprising the viral RNA polymerase could not be conclusively identified, two non-structural proteins of molecular weights 105,000 and 85,000 were temporally associated with increasing rates of polymerase activity in NJ-infected RK cells and were found in increased amounts in Ets-4-infected cells compared to La-infected cells.

Animals↗
PubMedDate not supplied

Experimental transmission of eastern equine encephalitis virus and Highlands J virus via semen of infected tom turkeys.

Tom turkeys were experimentally inoculated with eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus; semen was examined for presence of virus and ability to transmit infection by artificial insemination. Mild depression and inappetence were observed in tom turkeys inoculated with either EEE virus or HJ virus. Toms were viremic on days 1-2 postinoculation (PI), and virus was shed in semen on days 1-5 PI. Semen collected from EEE-virus-inoculated or HJ-virus-inoculated toms on days 1-2 PI and inseminated into turkey breeder hens transmitted the infection. EEE virus was detected in one of 10 hens after insemination with semen from EEE-virus-inoculated toms, and HJ virus was detected in three of 10 hens after insemination with semen from HJ-virus-inoculated toms. These results indicate that semen is a potential vehicle for transmission of EEE virus and HJ virus.

Alphavirus Infections↗