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Dengue fever emerged in Bangladesh in 2000. We tested 225 serum samples from febrile patients and 184 blood donors in 1996 and 1997 for dengue antibodies; 55 (24.4% ) febrile patients had dengue antibodies ( 65.5% with secondary infection pattern), compared with one (0.54%) donor (p <0.001), suggesting that dengue transmission was ongoing well before 1996.
In April-May 2001 an outbreak of dengue fever occurred in two suburbs in Townsville, north Queensland. This was the first outbreak in the Townsville region since a very large outbreak in 1992-1993. Notification delays resulted in late detection of the outbreak. Once recognised, control measures were implemented and rapid control was achieved. Dengue serotype 2 was the causative virus and 9 cases of dengue fever were documented. The approach to management of dengue fever outbreaks and vector control strategies have been improved and refined in the years since the 1992-1993 outbreak. These measures, in addition to favourable weather conditions, were likely to have contributed to the successful containment of this outbreak.
In 2002 three separate outbreaks of dengue were detected in north Queensland, including the first documented outbreak of dengue 4 in Australia. Molecular analyses identified Thailand and Indonesia as the likely origin of two of the outbreaks. Investigations during 2002 also included a suspected dengue outbreak in the Torres Strait which proved to be a false alarm, and a number of imported cases of dengue in north Queensland.
The isolation of dengue 4 virus from adult Aedes aegypti, reared from eggs collected in nature, is reported for the first time. From the locality where the isolate was made, 25 pools consisting of 1,848 Ae. aegypti reared from eggs were processed. In this study, 10 different localities were sampled and a total of 10,957 Ae. aegypti adults, collected as eggs or larvae in nature, were processed for virus isolation. From a total of 158 mosquito pools tested, one recovery of dengue 4 virus was made. The isolation of dengue 4 virus from this field-collected material gives further evidence that transovarial transmission of dengue viruses occurs in nature.
The first known transmission of dengue 3 virus in Africa was documented by virus isolation during an epidemic of dengue-like illness in Pemba, Mozambique, in late 1984 and early 1985. Dengue 3 virus was the only serotype isolated. Most patients appeared to be experiencing secondary flavivirus infections, but whether this was the result of previous dengue, yellow fever, or other flavivirus infection is not known. Two cases of hemorrhagic disease with shock and death were associated with the epidemic.
A set of sense and anti-sense oligomeric DNA primers, degenerate in the third "wobble" base position of codons so as to match all known dengue virus sequences, was evaluated as universal primers in a polymerase chain reaction (PCR) assay for the rapid diagnosis of dengue virus infections. Virus-specific complementary DNA (cDNA) was prepared by reverse transcription (RT) of total RNA extracted from serum. Amplified cDNA was identified by nucleic acid hybridization with four serotype-specific, oligomeric DNA probes. Using sera from patients admitted with dengue fever, RT/PCR followed by nucleic acid hybridization using radiolabeled probes was 68% sensitive (50/74; 95% confidence interval [CI] = 57-78%) and 100% specific. Chemiluminescent detection of hybridized products was 62% sensitive (26/42; 95% CI = 46-75%). Using specimens from which a virus isolate had been obtained, RT/PCR followed by nucleic acid hybridization with radiolabeled probes was 80% sensitive (40/50; 95% CI = 69-91%) and 100% specific. The results suggest that RT/PCR using degenerate primers is a sensitive and specific method for the detection of dengue viruses in clinical specimens.
In 1981, an epidemic of dengue hemorrhagic fever (DHF) caused by dengue-2 virus occurred in Cuba. This was the first DHF epidemic reported in the Western Hemisphere. In this study, we have analyzed four dengue-2 Cuban strains for two short genomic fragments: one on the envelope (E) glycoprotein and one at the E/nonstructural protein-1 (NS1) gene junction. The E segment of these 1981 Cuban isolates were more closely related to older dengue-2 virus strains such as New Guinea C 1944, Thailand 1964, Sri Lanka 1968, and Burma 1976 than to more recent isolates of this virus from Jamaica and Vietnam. More than 9% of the divergence with strains isolated from Jamaica and Vietnam was observed at the E/NS1 gene junction. One nucleotide change was observed between the first strain isolated during the epidemic and the rest of the Cuban strains. This mutation induced a nonconserved amino acid change from phenylalanine to leucine at position 43 that was not observed in any of the other strains with which it was compared.
The first confirmed outbreak of dengue fever in Peru occurred during 1990 in Iquitos, a city of approximately 300,000 residents in the Amazon region. Because of the apparent establishment of endemic transmission of this mosquito-borne viral disease following the outbreak, epidemiologic studies were initiated in 1992. Blood specimens and data on demographic, environmental, and medical history factors were collected from volunteers in an urban sector of Iquitos, in a rural area on the outskirts of Iquitos, and in three nearby jungle communities. A follow-up blood specimen was obtained approximately one year later from a sample of subjects. Sera were tested for dengue IgG antibody by an enzyme-linked immunosorbent assay, and specificity was verified using a plaque-reduction neutralization test. Dengue antibody prevalence was 66% in the urban population, 26% in the rural population, and 32-67% in the three jungle areas. A significant association was found between age and antibody prevalence, with a steady increase in prevalence from 18% among subjects less than five years of age to greater than 90% for subjects more than 50 years old. Increased antibody prevalence also was associated with urban and jungle residence and with a piped source of household drinking water. Seroconversions were documented in four of five surveyed communities. These results indicate that dengue virus transmission continues in and around Iquitos and suggest that transmission also occurred prior to the 1990 epidemic.
Cocirculation of two genetic subtypes of dengue serotype 2 viruses was first observed in the 1980 epidemic season in Thailand. To further delineate the evolutionary history and the contribution of these subtypes to subsequent epidemics, we determined the envelope glycoprotein gene sequence of 20 dengue serotype 2 viruses isolated from infected patients during 1987 and compared them with those derived from earlier years. Subtype IIIa strains represented the majority (18 of 19) of dengue type 2 viruses derived from Bangkok metropolitan area, whereas all three strains from a province in the northeastern region belonged to subtype IIIb, indicating uneven local distribution of dengue subtypes within the same year. Three types of sequence variation were identified in both subtypes: substitutions that were unique to individual strains; substitutions that were shared among all subtype IIIa or IIIb viruses of both the 1980 and 1987 epidemics; and those that were shared only among all subtypes IIIa or IIlb viruses of the 1987 epidemic, but were absent from the corresponding subtypes of 1980. While the first and second types of substitution were indicative of the most recent random mutations and previous mutations that had been fixed in virus populations, respectively, the third type suggested possible occurrence of a genetic bottleneck and subsequent expansion of one or a limited number of subtype IIIa strains in Bangkok between 1980 and 1987. Immunoblot analysis of intracellular NS1 antigen with anti-NS1 monoclonal antibodies also revealed antigenic heterogeneity of the NS1 protein that correlated with the subdivision based on envelope protein variation.
Differences in larval habitats cause variation in the size of Aedes aegypti (L.) adults. We suspected that such size variation was related to the ease with which the mosquitoes could be infected with dengue virus. Using a rearing procedure that produced three distinct size classes of mosquitoes, we determined the percentage of mosquitoes that developed disseminated dengue-2 infection following oral feeding with a suspension containing 3.3 x 10(7) plaque-forming units/ml. Mosquitoes were reared from eggs deposited by females captured in either of two villages in Chachoengsao Province or in Bangkok, Thailand. More of the larger mosquitoes (10.7%) were infected than the medium (5.6%) or small (5.7%) mosquitoes. Mosquitoes from Bangkok were less easily infected (5.0%) than mosquitoes from either of the two villages (8.5% and 10.7%). These results suggest that quantitative risk assessment of dengue transmission may be very difficult unless inoculation rate is measured directly. Also, control procedures that reduce density of larvae in individual containers may exacerbate dengue transmission by creating larger mosquitoes that are more easily infected.
We evaluated laboratory methods to confirm a clinical diagnosis of dengue. Acute sera were collected from personnel (n = 414) supporting the United Nations Mission in Haiti and presenting with febrile illness consistent with dengue fever or no apparent underlying cause. Dengue virus was recovered from 161 of 379 acute sera by inoculation into C6/36 cell culture. While 93 of 414 acute sera had detectable IgM antibodies, the IgM capture ELISA (MAC ELISA) had a sensitivity of only 13% compared with the virus isolation gold standard. If presumptive dengue fever cases were identified by both virus isolation and the presence of IgM, virus isolation and the MAC ELISA had clinical sensitivities of 69% and 40%, respectively. This study suggests that a combination of laboratory methods that target virus or subviral components as well as anti-viral IgM antibodies may be necessary for sensitive laboratory diagnosis with acute sera.
A biotin-streptavidin system was adapted to an IgM-capture ELISA for detection of dengue antibodies in human sera. To develop this assay, high titers of antibodies to flavivirus were purified by ion-exchange chromatography (DEAE-cellulose) and labeled with biotin. Heavy chain-specific goat anti-human IgM was first bound to the wells of a polystyrene microtiter plate, followed by binding of IgM in test specimens, and the use of tetravalent dengue antigens (dengue 1-4), biotin-labeled anti-flavivirus IgG, and streptavidin-peroxidase conjugate. The sensitivity and specificity of the IgM-capture biotin-streptavidin ELISA (IgM-BS-ELISA) in acute sera were 83.3% of patients with dengue infection and 95.3% of nondengue-infected cases, respectively. The positive predictive value was 92.4% and the negative predictive value was 89.2%. The efficiency of test was 90.4%. In convalescent sera, the sensitivity and specificity of IgM-BS-ELISA were 100% and 92.6%, respectively. The predictive values of positive and negative results were 90.3% and 100%, respectively. The efficiency of test was 95.6%. The agreement rate of IgM-BS-ELISA and standard hemagglutination inhibition test was good: kappa (kappa) values were 0.79 for acute sera and 0.91 for convalescent sera. The correlation between two methods was quite good, with correlation coefficients (r) of 0.76 for acute sera and 0.85 for convalescent sera (P < 0.001). The results indicate that the IgM-BS-ELISA is highly sensitive, specific, simple to perform, and rapid.
An epidemic of dengue type 2 infection occurred in North Queensland during 1992 and 1993. A random serosurvey of 1,000 residents of a population that experienced this epidemic only during 1993 was conducted to determine the proportion of the population at risk for secondary infection in the event of another epidemic with a different serotype. The ability of an ELISA to detect prior exposure to the dengue virus was compared with the hemagglutination inhibition assay. Dengue 2 virus plaque-reduction neutralization assays were performed to evaluate the specificity of the antibody response. Antibodies to dengue virus, or closely related flaviviruses, were detected in 61.9%. Seroprevalence increased with age and correlated well with known previous epidemics in the region. The sensitivity and specificity of the ELISA was 99.2% and 96.2%, respectively. An estimated 26% of the population was infected during the 1993 epidemic.
A commercial capture ELISA for specific IgM and IgG antibodies produced during dengue infection (PanBio Dengue Duo) showed excellent sensitivity (99%, n = 78) using sera collected at hospital discharge compared with established ELISA and hemagglutination inhibition (HAI) assays. Furthermore, the ELISA was able to diagnose 79% of the dengue cases using sera collected at hospital admission. The ELISA also showed high specificity (92%) in paired sera from patients without flavivirus infection (n = 26), although 45% of the patients with Japanese encephalitis (n = 20) showed elevation of IgG but not IgM. The IgG capture ELISA showed good correlation with the HAI assay (r = 0.83, P < 0.0001), and IgG levels could be used to distinguish between primary and secondary infection, with 100% of primary infections and 96% of secondary infections being correctly classified. This ELISA should prove useful in the clinical diagnosis of dengue infections.
During the dengue epidemic in northern Queensland in 1981 and 1982, type I dengue was serologically confirmed in 196 patients (mean age, 32.2 years) from the Cairns district. The most common symptoms were fever (99%), headache (92%), rash (91%), myalgia (93%), skin itching (75%) and arthralgia (60%). Haemorrhagic manifestations were noted in 14 patients. Most only showed skin petechiae. One patient also had bleeding from the gastrointestinal and urinary tracts. No cases of shock were recorded. Leucopenia was present in 57% of patients. A discussion on the relevance of these findings to dengue haemorrhagic fever/dengue shock syndrome is included. A serological survey after the epidemic suggests that approximately 7% of the population have antibodies to dengue as a result of the recent epidemic.
In Venezuela the problem of Dengue infection has become worst during the last decade, turning the country into an hyperendemic region where three of the four serotypes co-circulate. The Dengue has become a problem of Public Health, so the knowledge of the virus, its life cycle and characteristics, as well as the different aspects related with its biology are extremely important to fight the virus and for the develop of a vaccine. In a general way, the present work describes different aspects related to the molecular biology of the Dengue virus and its life cycle: the structure, composition, production of structural and non structural protein and its relation to the replication cycle of the virus. Some aspects related with the assembly and release of particles from infected cells are also discussed. With this a general view of the molecular biology of the Dengue virus and its replication in the host cell is shown.
Nitric oxide (NO) is a multifunctional molecule that is involved in citotoxic as well as citoprotective processes, it's synthesis is highly regulated by the cell because an alteration in NO production is associated with a variety of pathologies, such as Septic, Anaphylactic and Hemorrhagic Shock. The clinical feature of dengue virus infection has a spectrum that goes from mild, dengue fever, to a severe disease, dengue hemorrhagic fever/dengue shock. Here, some evidences are discussed that links NO with the pathology of the severe disease cause by dengue virus.
The plaque reduction neutralization assay was standardized to differentiate an infection caused by dengue from another infection produced by yellow fever. Serum samples from Cuban donors were used to this end. Information on previous vaccination against yellow fever was available. Samples from Costa Rican patients with a clinical picture of dengue and with no antecedents of vaccination against yellow fever were also utilized. The optimal plaque staining day was the fifth day and the smallest serum dilution capable of differentiating an infection resulting from dengue from another infection caused by yellow fever was of 1/5. According to the high specificity of the standardized technique, risk factor studies of dengue hemorrhagic fever could be made among individuals vaccinated against yellow fever, which is a present and important topic.