• Dengue Virus

Dengue IgG Microwell Serum ELISA Catalog# DEN-G (Export Only)

Dengue fever, caused by any of the four serotypes of dengue virus, is endemic in Southeast Asia as well as South and Central America. Repeat infection with a second type of dengue virus is thought to cause dengue hemorrhagic fever in about 10 percent of infected people. Dengue antibodies do not confer immunity beyond 3-6 weeks to a second dengue type. Epidemiological factors, clinical findings (including fever, tachycardia, thrombocytopenia, etc.), exposure in endemic regions, and other laboratory results should be considered in diagnosing acute disease. Acute disease diagnosis will also include a positive laboratory confirmation in many cases. Infection with dengue virus can result in a wide disease spectrum, from a mild fever to life-threatening dengue hemorrhagic fever and dengue shock syndrome.1 Symptoms of classical dengue fever, following a 5-8 day incubation period, include rash, severe headache, nausea, vomiting, chills, malaise, macular rash and may include lymphadenopathy. Hemorrhagic dengue fever involves increased blood vessel permeability which can lead to shock and death in about 10% of reported cases. Dengue fever can only be treated by supportive care and is prevented by mosquito control. In primary infections, circulating IgM antibody to the viral coat proteins is detected 5-6 days after the onset of illness, and gradually decreases within 1-2 months of onset. IgG antibody to dengue virus is detected approximately 14 days after onset in primary infections, and by day 2 in secondary infections. In secondary infections, IgM antibody may reappear but gradually diminishes, while IgG antibody persists, often at high titer. These patterns of dengue antibody development permit serological differentiation of primary and secondary infections. Characteristically, acute patients with primary infections have a higher IgM:IgG ratio than are found in secondary infections. Patients with secondary infections generally have higher IgG levels. Acute or recent infections are identified by a rise in antibody titer as well as high IgM levels. The Flaviviridae family includes the four serotypes of dengue virus as well as the yellow fever and Japanese encephalitis viruses. There is substantial cross reactivity among flaviviruses, due to the presence of common antigenic determinants. The four dengue serotypes cross react among themselves, but there are also unique determinants for each serotype. Although infection with a given serotype confers durable protection against that serotype, dengue virus serotypes are not cross-protective, and reinfection with a second serotype has been linked to development of the more severe hemorrhagic form of dengue referred to as dengue hemorrhagic fever. Determination of the infecting serotype may be important in gauging the potential severity of a dengue outbreak.1 The most straightforward diagnosis of a recent infection is achieved by detection of the virus in patient's blood, either by isolating the virus in susceptible cell cultures or mosquitoes, or by identifying viral RNA with hybridization6 or PCR8 techniques. However, these methods are laborious and require specialized laboratory facilities. In addition, the level of circulating virus wanes as the antibody level rises, and these procedures are successful only when done within about 5 days of onset of illness. Serological methods to detect dengue antibodies have been the most commonly used diagnostic procedures. The ELISA microwell method for the detection of IgM antibodies is currently the most useful procedure for providing a specific serological diagnosis of dengue infection. This method is reported to be as sensitive as the Hemagglutination Inhibition (HI) method.7 The IgM ELISA method is generally replacing other techniques for IgM determination because of its sensitivity, potential for automation and ability to accommodate large numbers of samples. For the determination of IgM antibody by the ELISA method, it has been recommended that measures be taken to eliminate IgG antibodies from current or previous flavivirus infections, since IgG antibodies may be present in excess and depress the sensitivity for the detection of IgM.