Disordered expression of inhibitory receptors on the NK1-type natural killer (NK) leukaemic cells from patients with hypersensitivity to mosquito bites.
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Recent studies have revealed the existence of a distinct type of NK cell leukaemia of the juvenile type, which presents with hypersensitivity to mosquito bites (HMB) as an essential clinical manifestation and is infected with clonal Epstein-Barr virus (EBV). This disorder is thus called HMB-EBV-NK disease and has been reported in Orientals, mostly from Japan. We investigated the profile of cytokine production and the expression of both types of NK inhibitory receptors, i.e. CD94 lectin-like dimers and killer-cell immunoglobulin-like receptors, in NK leukaemic cells from three patients with HMB-EBV-NK disease. It was found that freshly isolated NK leukaemic cells expressed mRNA for interferon-gamma (IFN-gamma) and additionally produced IL-10 upon stimulation with IL-2, indicating that the NK cells were of NK1 type. More than 98% of NK cells from the patients bore CD94 at a higher level than did normal NK cells, whereas p70 or NKAT2, belonging to immunoglobulin-like receptor, was not expressed in those NK cells. Freshly isolated leukaemic NK cells transcribed mRNA for CD94-associated molecule NKG2C at an abnormally high level, and upon stimulation with IL-2 and/or IL-12 they expressed NKG2A as well. The disordered expression of these inhibitory receptors not only provides some insights into the pathogenesis of HMB-EBV-NK disease but also can be used as phenotypic markers for the diagnosis of this type of NK cell leukaemia. (+info)
Probable locally acquired mosquito-transmitted Plasmodium vivax infection--Suffolk County, New York, 1999.
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In the United States, malaria transmission was eliminated in the 1940s, and malaria eradication was certified in 1970 (1). Since then, 60 small localized outbreaks of probable mosquito-transmitted malaria have been reported to CDC (2-6). Before 1995, the number of imported malaria cases reported to the Suffolk County (New York) Department of Health Services ranged from zero to eight per year. Since 1995, seven to 17 cases per year have been reported. In all of these cases, a history of residing in or traveling to an area with endemic malaria outside the United States was confirmed. This report describes the investigation of two cases of Plasmodium vivax malaria that occurred in Suffolk County in August 1999; the patients had no history of travel outside of the United States. (+info)
Etiology of interepidemic periods of mosquito-borne disease.
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Dengue viruses and malaria protozoa are of increasing global concern in public health. The diseases caused by these pathogens often show regular seasonal patterns in incidence because of the sensitivity of their mosquito vectors to climate. Between years in endemic areas, however, there can be further significant variation in case numbers for which public health systems are generally unprepared. There is an acute need for reliable predictions of within-year and between-year epidemic events. The prerequisite for developing any system of early warning is a detailed understanding of the factors involved in epidemic genesis. In this report we discuss the potential causes of the interepidemic periods in dengue hemorrhagic fever in Bangkok and of Plasmodium falciparum malaria in a highland area of western Kenya. The alternative causes are distinguished by a retrospective analysis of two unique and contemporaneous 33-year time series of epidemiological and associated meteorological data recorded at these two sites. We conclude that intrinsic population dynamics offer the most parsimonious explanation for the observed interepidemic periods of disease in these locations. (+info)
West Nile virus activity--New York and New Jersey, 2000.
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In late August 1999, an outbreak of encephalitis caused by West Nile virus (WNV) was detected in New York City and subsequently identified in neighboring counties (1). In response, an extensive mosquito-control and risk-reduction campaign was initiated, including aerial and ground applications of mosquito adulticides throughout the affected areas. No human WNV infections were found in New York City with an onset date after the campaign was completed. Cases continued to occur among humans in surrounding counties that did not undertake mosquito-control efforts until later, suggesting that the campaign may have reduced human risk. In May 2000, CDC issued guidelines to direct national surveillance, prevention, and control efforts (2) and provided funds to support these efforts in 19 state and local health departments where WNV transmission had occurred or where transmission would probably occur based on known bird migration patterns. This report presents the findings of surveillance activities. (+info)
Update: West Nile virus activity--Northeastern United States, January-August 7, 2000.
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Surveillance programs initiated in response to the 1999 West Nile virus (WNV) outbreak have detected increased transmission in the northeastern United States (1). Seventeen states along the Atlantic and gulf coasts, New York City (NYC), and Washington, D.C., have conducted WNV surveillance and are reporting to CDC (1). Surveillance for WNV infection includes monitoring of mosquitoes, sentinel chicken flocks, wild birds, and potentially susceptible mammals (e.g., horses and humans) (2). This report summarizes findings of this surveillance system through August 7, 2000. (+info)
Determinants in the envelope E protein and viral RNA helicase NS3 that influence the induction of apoptosis in response to infection with dengue type 1 virus.
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One mechanism by which dengue (DEN) virus may cause cell death is apoptosis. In this study, we investigated whether the genetic determinants responsible for acquisition by DEN type 1 (DEN-1) virus of mouse neurovirulence interfere with the induction of apoptosis. Neurovirulent variant FGA/NA d1d was generated during the adaptation of the human isolate of DEN-1 virus strain FGA/89 to grow in newborn mouse brains and mosquito cells in vitro [Despres, P. Frenkiel, M. -P. Ceccaldi, P.-E. Duarte Dos Santos, C. and Deubel, V. (1998) J. Virol., 72: 823-829]. Genetic determinants possibly responsible for mouse neurovirulence were studied by sequencing the entire genomes of both DEN-1 viruses. Three amino acid differences in the envelope E protein and one in the nonstructural NS3 protein were found. The cytotoxicity of the mouse-neurovirulent DEN-1 variant was studied in different target cells in vitro and compared with the parental strain. FGA/NA d1d was more pathogenic for mouse neuroblastoma cells and attenuated for human hepatoma cells. Changes in virus replicative functions and virus assembly may account, in a large part, for the differences in the induction of apoptosis. Our data suggest that identified amino acid substitutions in the envelope E protein and viral RNA helicase NS3 may influence DEN-1 virus pathogenicity by altering viral growth. (+info)
The global spread of malaria in a future, warmer world.
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The frequent warnings that global climate change will allow falciparum malaria to spread into northern latitudes, including Europe and large parts of the United States, are based on biological transmission models driven principally by temperature. These models were assessed for their value in predicting present, and therefore future, malaria distribution. In an alternative statistical approach, the recorded present-day global distribution of falciparum malaria was used to establish the current multivariate climatic constraints. These results were applied to future climate scenarios to predict future distributions, which showed remarkably few changes, even under the most extreme scenarios. (+info)
Estimation of the sporozoite rate of malaria vectors using the polymerase chain reaction and a mathematical model.
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We developed a sensitive polymerase chain reaction (PCR) method for the detection of Plasmodium falciparum DNA from mosquitoes collected in the field. Plasmodium falciparum was detected from 15.2% of 1-parous mosquitoes, Anopheles farauti, in the Solomon Islands through use of the PCR method. A novel mathematical model was developed to estimate the sporozoite rate based on the malaria-positive rate of 1-parous mosquitoes. Using this model, the sporozoite rate of Anopheles farauti in the Solomon Islands was calculated to be 0.09%. This method enables estimation of the sporozoite rate based on a relatively small number (100-200) of mosquitoes compared with the number needed for the ELISA method. (+info)