scholarly journals Dengue epidemic in the state of Rio de Janeiro, Brazil, 1990–1: co-circulation of dengue 1 and dengue 2 serotypes

1993 ◽  
Vol 111 (1) ◽  
pp. 163-170 ◽  
Author(s):  
R. M. R. Nogueira ◽  
M. P. Miagostovich ◽  
E. Lampe ◽  
R. W. Souza ◽  
S. M. O. Zagne ◽  
...  

SummaryDuring 1990 and 1991, dengue fever was detected in the State of Rio de Janeiro, Brazil. It occurred in two epidemic waves; one, from January to August 1990, caused predominantly by dengue virus type 1 (DEN-1) the other from October 1990 to May 1991 caused by type 2 virus (DEN-2). Dengue was confirmed by virus isolation and/or IgM capture enzyme-linked immunosorbent assay (MAC-ELISA) in 2109/5964 (35·4%) of the cases. DEN-2 virus was isolated from 180 patients. HAI tests indicated that of these previous infection with DEN-1 had occurred in 130 (72%). The epidemic was classified as dengue fever, but severe and even fatal cases occurred in association with secondary infection.

1993 ◽  
Vol 35 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Marize P. Miagostovich ◽  
Rita M.R. Nogueira ◽  
Silvia M.B. Cavalcanti ◽  
Keyla B.F. Marzochi ◽  
Hermann G. Schatzmayr

Laboratorial studies were carried out on 3178 patients with signs and symptoms suggestive of dengue infection from April 1986 to December 1987 in the State of Rio de Janeiro, Brazil. The epidemic had two peaks following the first virus isolation and affected the inhabitants of 17 counties. Both sex and all age groups were affected. Dengue virus type 1 was isolated from 1039 sera and the number of confirmed cases was increased to 1874 (59%) by MAC-ELISA. Isolation rate confirmed cases reached 80% in the specimens obtained until the 4th day after the onset of disease and viraemia ranged from 10 3.0 to 10(8.5) TCID50/ml.


1974 ◽  
Vol 73 (2) ◽  
pp. 263-270 ◽  
Author(s):  
T. Maguire ◽  
J. A. R. Miles ◽  
F. N. Macnamara ◽  
P. J. Wilkinson ◽  
F. J. Austin ◽  
...  

SUMMARYA dengue epidemic due to type 2 virus involving some 3,400 cases began in Fiji early in 1971, had a peak during May, June and July, and cases have continued to occur with a low incidence during 1972 and 1973. Many of the notified cases showed classical dengue fever symptoms and there were no confirmed cases of haemorrhagic fever. A serological survey indicated that there had been at least 20,000 subclinical infections. It is probable that the virus was introduced to Fiji either through the port of Lautoka or Nadi international airport in February 1971. The normal travel patterns of residents must have spread the virus to all the more accessible localities but, with the exception of Rotuma, it caused infections only in areas where Aedes aegypti was available as a vector. There was no evidence that pre-existing dengue type 1 serum antibody gave any protection during this epidemic.


2014 ◽  
Vol 60 (1) ◽  
pp. 35-39 ◽  
Author(s):  
Eleonora Altman ◽  
Blair A. Harrison ◽  
Vandana Chandan ◽  
Robert Slinger

Lipopolysaccharide (LPS) of Helicobacter pylori exhibits several unique structures, such as Lewis (Le) antigens, α-1,6-glucan, and dd-heptan. To investigate the relationship between LPS structure and resistance to clarithromycin, 41 Canadian isolates of H. pylori were characterized by whole-cell ELISA (enzyme-linked immunosorbent assay), sugar analysis, immunoblotting, and indirect immunofluorescence. The expression of type 2 Lewis X and (or) Lewis Y antigens was detected in 22 of 23 (95.7%) clarithromycin-resistant and in 14 of 18 (77.7%) clarithromycin-susceptible H. pylori strains (P < 0.05), and 8 isolates co-expressed type 1 and type 2 Le antigens (8/41, 19.5%). A significantly higher frequency of α-1,6-glucan (P < 0.01) was detected in clarithromycin-resistant strains than in clarithromycin-susceptible strains (19/23 (82.6%) versus 11/18 (61.1%)). Sugar analysis of selected α-1,6-glucan-positive H. pylori strains confirmed that they frequently contained elevated amounts of dd-heptose. Clarithromycin-resistant isolates were also characterized by low expression levels or absence of CagA (17/23, 73.9%). Indirect immunofluorescence studies carried out on selected H. pylori strains with rabbit immune sera specific for α-1,6-glucan confirmed broad recognition of α-1,6-glucan epitope. The binding was not affected by LPS glycotype of H. pylori isolates examined nor by their CagA status or resistance to clarithromycin. These findings suggest α-1,6-glucan as a potential vaccine target, especially in an era of increasing clarithromycin resistance in H. pylori.


1995 ◽  
Vol 37 (6) ◽  
pp. 517-521 ◽  
Author(s):  
Rivaldo Venâncio da Cunha ◽  
Márcio Dias ◽  
Rita M. R. Nogueira ◽  
Nelson Chagas ◽  
Marize P. Miagostovich ◽  
...  

A seroepidemiologic survey was carried out in schoolchildren from public schools of the Niterói municipality, state of Rio de Janeiro, Brazil, after a period of sequential epidemics by dengue virus type 1 and 2 (DEN-1 and DEN-2). 450 blood samples were obtained by fingertip puncture and collected on filter paper discs. The hemagglutination inhibition (HAI) test was carried out using DEN-1 and DEN-2 antigens. HAI titres were demonstrated in 66% (297/450) of the sera and the geometric means of the titres were 1/182 and 1/71 for DEN-1 and DEN-2, respectively. Secondary infections were observed in 61% (181/297) of positive cases. Among these, 75% (135/181) were under fifteen years old. No dengue haemorrhagic fever (DHF) was reported in these children. Asymptomatic or oligosymptomatic infections were detected in 56% of the studied population. The absolute and relative frequencies of positive tests by age group and sex did not evidence statistically significant difference. The number of individuals infected probably produced a immunologic barrier responsible for the non occurrence of dengue epidemic in the latter years.


2020 ◽  
Author(s):  
Paul Pickering ◽  
Leon Hugo ◽  
Gregor J Devine ◽  
John G Aaskov ◽  
wenjun Liu

Abstract Background: Humans are the primary hosts of dengue viruses (DENV). However, sylvatic cycles of transmission can occur among non-human primates and human encroachment into forested regions can be a source of emergence of new strains such as the highly divergent and sylvatic strain of DENV2, QML22, recovered from a dengue fever patient returning to Australia from Borneo. The objective of the present study was to evaluate the vector competence of Australian Aedes aegypti mosquitoes for this virus. Methods: Four- to five-day-old mosquitoes from two strains of Ae. aegypti from Queensland, Australia, were fed a meal of sheep blood containing 108 50% cell culture infectious dose per ml (CCID50/ml) of either QML22 or an epidemic strain of DENV serotype 2 (QML16) isolated from a dengue fever patient in Australia in 2015. Mosquitoes were maintained at 28 °C, 75% relative humidity and sampled 7, 10 and 14 days post-infection (dpi). Live virions in mosquito bodies (abdomen/thorax), legs and wings and saliva expectorates from individual mosquitoes were quantified using a cell culture enzyme-linked immunosorbent assay (CCELISA) to determine infection, dissemination and transmission rates. Results: The infection and dissemination rates of the sylvatic DENV2 strain, QML22, were significantly lower than that for QML16. While the titres of virus in the bodies of mosquitoes infected with either of these viruses were similar, titres in legs and wings were significantly lower in mosquitoes infected with QML22 at most time points although they reached similar levels by 14 dpi. QML16 was detected in 16% (n = 25) and 28% (n = 25) of saliva expectorates at 10 and 14 dpi, respectively. In contrast, no virus was detected in the saliva expectorates of QML22 infected mosquitoes. Conclusions: Australia urban/peri-urban Ae. aegypti species are susceptible to infection by the sylvatic and highly divergent DENV 2 QML22 but replication of QML22 is attenuated relative to the contemporary strain, QML16. A salivary gland infection or escape barrier may be acting to prevent infection of saliva and would prevent onward transmission of this highly divergent virus in Australia.


2016 ◽  
Vol 3 (4) ◽  
Author(s):  
Ivano de Filippis ◽  
Priscila Conrado Guerra Nunes ◽  
Claudia Ferreira de Andrade ◽  
Bianca de Santis Gonçalves ◽  
Eliane Saraiva de Araújo ◽  
...  

2004 ◽  
Vol 78 (23) ◽  
pp. 12919-12928 ◽  
Author(s):  
Ana P. Goncalvez ◽  
Robert H. Purcell ◽  
Ching-Juh Lai

ABSTRACT The epitope determinants of chimpanzee Fab antibody 1A5, which have been shown to be broadly reactive to flaviviruses and efficient for cross-neutralization of dengue virus type 1 and type 2 (DENV-1 and DENV-2), were studied by analysis of DENV-2 antigenic variants. Sequence analysis showed that one antigenic variant contained a Gly-to-Val substitution at position 106 within the flavivirus-conserved fusion peptide loop of the envelope protein (E), and another variant contained a His-to-Gln substitution at position 317 in E. Substitution of Gly106Val in DENV-2 E reduced the binding affinity of Fab 1A5 by approximately 80-fold, whereas substitution of His317Gln had little or no effect on antibody binding compared to the parental virus. Treatment of DENV-2 with β-mercaptoethanol abolished binding of Fab 1A5, indicating that disulfide bridges were required for the structural integrity of the Fab 1A5 epitope. Binding of Fab 1A5 to DENV-2 was competed by an oligopeptide containing the fusion peptide sequence as shown by competition enzyme-linked immunosorbent assay. Both DENV-2 antigenic variants were shown to be attenuated, or at least similar to the parental virus, when evaluated for growth in cultured cells or for neurovirulence in mice. Fab 1A5 inhibited low pH-induced membrane fusion of mosquito C6/36 cells infected with DENV-1 or DENV-2, as detected by reduced syncytium formation. Both substitutions in DENV-2 E lowered the pH threshold for membrane fusion, as measured in a fusion-from-within assay. In the three-dimensional structure of E, Gly106 in domain II and His317 in domain III of the opposite E monomer were spatially close. From the locations of these amino acids, Fab 1A5 appears to recognize a novel epitope that has not been mapped before with a flavivirus monoclonal antibody.


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