Who invented dengue fever

Because A. Even though this species is dependent on human habitations and buildings, breeding sites can be occult, difficult-to-find and are often overlooked. Two new vector control approaches are being tested in the field currently. One, developed by Oxitec, involves the release of genetically modified male A. When male engineered mosquitoes are released into the wild and mate with wild females, their offspring inherit the self-limiting trait and the larvae die before reaching adulthood, resulting in local population decline.

This approach has been used successfully in pilot field trials resulting in a reduction of the mosquito population and dengue virus transmission, and it has recently been approved for a pilot test in the Florida Keys, where the risk of Zika virus transmission is a concern.

The advantage of this approach is that the mosquitoes do all the work in finding breeding sites after their release. The disadvantage is that continuous release of modified male mosquitos is required to keep the population from rebounding. A second approach to vector control is the establishment of Wolbachia bacteria in the guts of the mosquitoes, which blocks infection by dengue, Zika and chikungunya viruses.

Although a broad range of insects carry Wolbachia , the bacteria are not infectious and cannot be transmitted to animals, including humans. It spreads into insect populations by altering the reproductive success of the insect that carries it. Wolbachia -infected female mosquitoes do not suffer adverse effects and produce normal numbers of offspring that carry Wolbachia , which, in turn, block infection by the target viruses.

Initially, this reproductive effect will be very small because there will be few Wolbachia -infected mosquitoes in the population, but over successive generations, the numbers of male and female mosquitoes infected with Wolbachia will increase. The advantage using Wolbachia bacteria is that once they are introduced into the mosquito population, they can be maintained without constant re-releases.

Again, the mosquitoes do the work of finding breeding sites. This approach is being tested currently in the field in several countries, including Australia, Brazil, Columbia, Indonesia and Vietnam. Vaccine development is complicated by the need to include all four dengue serotypes for simultaneous administration. There is concern regarding the risk for antibody-dependent enhancement ADE of infection that could result in more severe disease. ADE occurs after recovery from infection by one dengue virus, which elicits lifelong immunity against that particular virus serotype but confers only partial and transient protection against subsequent infection by any of the other three dengue viruses.

These cross-reactive antibodies do not neutralize the virus but facilitate virus attachment and entry into susceptible cells. A structural perspective of the flavivirus life cycle. Nature Reviews Microbiology 3, 13—22 Figure Detail. Once the virus has entered a host cell, the virus penetrates deeper into the cell while still inside the endosome.

How does the virus exit the endosome, and why? Researchers have learned that two conditions are needed for the dengue virus to exit the endosome:. These two conditions allow the virus envelope to fuse with the endosomal membrane, and that process releases the dengue nucleocapsid into the cytoplasm of the cell. Once it is released into the cell cytoplasm, how does the virus replicate itself? In the cytoplasm, the nucleocapsid opens to uncoat the viral genome.

This process releases the viral RNA into the cytoplasm. The viral RNA then hijacks the host cell's machinery to replicate itself.

The virus uses ribosomes on the host's rough endoplasmic reticulum ER to translate the viral RNA and produce the viral polypeptide. This polypeptide is then cut to form the ten dengue proteins. The newly synthesized viral RNA is enclosed in the C proteins, forming a nucleocapid.

This step adds the viral envelope and protective outer layer. The immature viruses travel through the Golgi apparatus complex, where the viruses mature and convert into their infectious form.

The mature dengue viruses are then released from the cell and can go on to infect other cells. Beasley, D. Hoffman London: Imperial College Press, : 29— Centers for Disease Control and Prevention.

Chakraborty, T. Dengue Fever and Other Hemorrhagic Viruses. New York: Chelsea House, Guzman M. Nature Reviews Microbiol ogy 8 , S7—S16 Halstead, S. Dengue hemorrhagic fever: Two infections and antibody dependent enhancement, a brief history and personal memoir.

Revista Cubana de Medicina Tropical 54 , — Kuhn, R. Structure of dengue virus: Implications for flavivirus organization, maturation, and fusion. Cell , — Li, L. The flavivirus precursor membrane-envelope protein complex: Structure and maturation. Science , — Lopez, S. How viruses hijack endocytic machinery. Nature Education 3 , 16 Lupi, O.

Mosquito-borne hemorrhagic fevers. He has subsequently pursued a career in private industry. A biopharmaceutical company that became Acambis Inc. Acambis later partnered with Sanofi Pasteur to conduct human clinical trials of the vaccine in Asia, Africa and Latin America.

Acambis was acquired by Sanofi in Recombinant dengue virus antigens Several studies have contributed in terms of developing new reagents or technology for diagnostic purposes Table VI. Assessment of public awareness on dengue virus infection Dengue is one of the major public health problems which can be controlled with active participation of the community. Conclusions Dengue disease continues to involve newer areas, newer populations and is increasing in magnitude, epidemic after epidemic.

Acknowledgment Authors thank Drs C. References 1. Whitehorn J, Farrar J. Br Med Bull. Dengue: Guidelines for diagnosis, treatment, prevention, and control in sub-Saharan Africa and 13 countries in South America.

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