Specificity of the murine T helper cell immune response to various alphaviruses.
(42/76)
We investigated the specificity of the T helper (Th) cell immune response to three alphaviruses: Venezuelan equine encephalomyelitis (VEE), eastern equine encephalitis (EEE) and western equine encephalitis (WEE). Single cell suspensions were prepared from spleens of virus-primed C3H mice, and T lymphocyte populations were enriched by nylon wool chromatography. T cells were incubated in vitro with irradiated, syngeneic splenic stimulator cells previously exposed to purified virus. Cellular proliferation was measured by [3H]thymidine uptake 5 days post-stimulation. The predominant proliferating cell type secreted interleukin-2 and was of the Th cell phenotype Thy-1+, Lyt-1+,2-, L3T4+. Stimulation of VEE, EEE and WEE virus-primed Th cells with homologous and heterologous virus resulted primarily in a proliferative response specific for the immunizing virus. The corresponding antibody response, as measured by ELISA using purified virus as antigen, was also specific for the immunizing virus. The magnitude of the blastogenic response of VEE TC-83 virus-primed lymphocytes to a battery of VEE subtype viruses was remarkably similar to schemes of antigenic classification. The results indicate that the dominant Th cell epitopes on these alphaviruses represent regions largely virus-specific and lead to a virus-specific B cell response which does not change over time after primary inoculations of mice with VEE and WEE viruses and multiple inoculations of mice with EEE virus. (+info)
Impact of climate on western equine encephalitis in Manitoba, Minnesota and North Dakota, 1980-1983.
(43/76)
Information was collected on confirmed outbreaks of western equine encephalitis (WEE) in North America east of the Rockies for 1981 and 1983 (epidemic years) and 1980 and 1982 (non-epidemic years). The initial pattern of outbreaks in Manitoba, Minnesota and North Dakota was determined for each year. Backward (and in some instances forward) wind trajectories were computed for each day 4-15 days (incubation period) before the initial outbreaks of WEE in a given area of province or state. During these years the timing and location of WEE outbreaks in horses and man, seroconversion in chickens, the maximum Culex tarsalis counts at Winnipeg and first isolation of WEE virus from C. tarsalis could be correlated with trajectories of winds from states further south within acceptable intervals. It is suggested that C. tarsalis mosquitoes infected with WEE virus are carried on the wind from Texas on the Gulf of Mexico, where they continue to breed during the northern winter months, to northern Texas and Oklahoma in the spring. In May, June and July C. tarsalis are carried north on southerly winds from these states through Kansas and Nebraska to North Dakota, Minnesota, Wisconsin and Manitoba. Distances of 1250-1350 km are traversed in 18-24 h at heights up to 1.5 km with temperatures greater than or equal to 13 degrees C. Landing takes place where the warm southerly winds meet cold fronts associated with rain. Convergence leads to concentration of C. tarsalis and determines where outbreaks occur. It is possible that return of new generations of C. tarsalis to the south may occur later in the year. The development of an epidemic of WEE in the northern states and provinces would appear to depend on (i) suitable trajectories from the south in June and July with temperatures greater than or equal to 13 degrees C meeting cold fronts with rain, (ii) sufficient C. tarsalis infected with WEE virus at source, carried on the wind and locally, (iii) C. tarsalis biting horses and man, (iv) maintenance of local mosquito populations in August and (v) susceptible hosts (birds) at source and susceptible hosts (horses and man) locally. Possible methods of prediction involving determination of trajectories, identification of C. tarsalis blood meals, measuring seroconversion in calves are discussed in addition to the methods already in use. (+info)
Complex-specific immunoglobulin M antibody patterns in humans infected with alphaviruses.
(44/76)
Sera from humans with serologically confirmed eastern equine encephalitis, western equine encephalitis, Pogosta (Ockelbo), Mayaro, Ross River, and chikungunya virus infections were tested by immunoglobulin M (IgM) antibody capture enzyme immunoassay. Diagnostically useful IgM antibody titers were detected, and selected sera with high IgM antibody titers were tested for IgM antibody with nine heterologous alphaviruses. The results provide evidence for the complex specificity of IgM antibody and indicate the usefulness of this test in both individual cases and epidemic situations. (+info)
Specificity of immunoglobulin M and G antibody responses in humans infected with eastern and western equine encephalitis viruses: application to rapid serodiagnosis.
(45/76)
Paired sera from 20 humans with eastern equine encephalitis (EEE) virus infections and from 17 humans with western equine encephalitis (WEE) virus infections, all with previously demonstrated fourfold or greater rises or falls in hemagglutination-inhibiting, complement-fixing, or neutralizing antibody titers, were tested for immunoglobulin M (IgM) and IgG antibodies by an enzyme immunoassay. All individuals with EEE and 14 of 17 individuals with WEE had IgM antibody, some as early as 1 day after onset. Two of the three persons with WEE who did not develop IgM antibody died. IgM antibody declined but persisted for at least 3 months after the onset of illness in one individual each with EEE and WEE. IgG antibody was not detected until the middle of week 2 after onset. The sensitivity of the IgM antibody capture enzyme immunoassay described and the specificity, as shown by the absence of heterologous alphavirus reactivity, indicate that this is the test of choice for the rapid diagnosis of human infections caused by EEE and WEE viruses. (+info)
Relevance of detection of immunoglobulin M antibody response in birds used for arbovirus surveillance.
(46/76)
Young chickens were inoculated with 5,000 PFU of eastern equine encephalitis (EEE) virus and bled at intervals thereafter for determinations of hemagglutination-inhibiting (HI), neutralizing (N), immunoglobulin M (IgM), and IgG antibodies. HI, N, and IgM antibodies were first detected 4 days after infection, and IgG was detected 7 days after infection. All four antibodies persisted through day 90 after infection. HI, N, and IgM antibody titers remained elevated and were not cross-reactive with the related alphavirus western equine encephalitis (WEE) virus. IgG antibody titers also remained high, but heterologous reactivity to WEE virus increased with time after infection. Serum samples from sentinel chickens and wild birds infected in nature with EEE, WEE, or St. Louis encephalitis virus and submitted to this laboratory from state and local health departments were tested for IgM antibody by using anti-chicken IgM for capture and for IgG antibodies to the EEE and WEE viruses. There was essentially complete correlation between HI, N, and either IgM (indicating recent infections) or IgG (indicating more remote infections) antibody. We conclude that the IgM antibody capture enzyme immunoassay can be used as a specific and sensitive assay to replace the routinely used HI test for detecting antibody in sentinel chickens and in young, wild birds used for arbovirus surveillance. The test is rapid and relatively inexpensive and can be performed in essentially all adequately supplied laboratories. (+info)
Western equine encephalitis virus is a recombinant virus.
(47/76)
The alphaviruses are a group of 26 mosquito-borne viruses that cause a variety of human diseases. Many of the New World alphaviruses cause encephalitis, whereas the Old World viruses more typically cause fever, rash, and arthralgia. The genome is a single-stranded nonsegmented RNA molecule of + polarity; it is about 11,700 nucleotides in length. Several alphavirus genomes have been sequenced in whole or in part, and these sequences demonstrate that alpha-viruses have descended from a common ancestor by divergent evolution. We have now obtained the sequence of the 3'-terminal 4288 nucleotides of the RNA of the New World Alphavirus western equine encephalitis virus (WEEV). Comparisons of the nucleotide and amino acid sequences of WEEV with those of other alphaviruses clearly show that WEEV is recombinant. The sequences of the capsid protein and of the (untranslated) 3'-terminal 80 nucleotides of WEEV are closely related to the corresponding sequences of the New World Alphavirus eastern equine encephalitis virus (EEEV), whereas the sequences of glycoproteins E2 and E1 of WEEV are more closely related to those of an Old World virus, Sindbis virus. Thus, WEEV appears to have arisen by recombination between an EEEV-like virus and a Sindbis-like virus to give rise to a new virus with the encephalogenic properties of EEEV but the antigenic specificity of Sindbis virus. There has been speculation that recombination might play an important role in the evolution of RNA viruses. The current finding that a widespread and successful RNA virus is recombinant provides support for such an hypothesis. (+info)
Sensitive enzyme immunoassay for detecting immunoglobulin M antibodies to Sindbis virus and further evidence that Pogosta disease is caused by a western equine encephalitis complex virus.
(48/76)
An antibody capture enzyme immunoassay (EIA) was adapted for the detection of immunoglobulin M (IgM) antibody to Sindbis (SIN) virus. Sera from humans with a febrile illness characterized by rash and arthralgia in eastern Finland (Pogosta [POG] disease) and Sweden (Ockelbo disease) and from humans with western equine encephalitis (WEE) virus infection in the United States were tested for IgM antibodies by EIA. Seroconversions were documented in patients with POG disease and with WEE virus infections by using SIN virus as antigen and rabbit anti-SIN virus immunoglobulin; this confirms previous observations that POG disease is caused by a virus closely related to SIN virus and that IgM antibodies to WEE complex alphaviruses are not type specific. This IgM EIA provided a sensitive diagnostic and research tool applicable to epidemiologic problems posed by POG disease. (+info)