Dengue fever is a tropical mosquito disease caused by dengue virus. Symptoms usually begin three to fourteen days after infection. These may include high fever, headache, vomiting, muscle and joint pain, and a typical skin rash. Recovery generally takes two to seven days. In a small proportion of cases, the disease develops dengue hemorrhagic fever that is life-threatening, resulting in bleeding, low blood platelet levels and leakage of blood plasma, or into dengue shock syndrome , where harmful low blood pressure occurs.
Dengue is spread by some species of Aedes mosquitoes, especially A. aegypti . The virus has five different types; infections with one type usually provide lifelong immunity for that type, but only short-term immunity to the other. Subsequent infections of different types increase the risk of severe complications. A number of tests are available to confirm the diagnosis including detecting antibodies against the virus or RNA.
Vaccines for dengue have been approved and commercially available in a number of countries. Other prevention methods are to reduce mosquito habitat and limit bite exposure. This can be done by removing or covering puddles and wearing clothes that cover most of the body. Acute dengue treatment is supportive and involves administering oral or intravenous fluids for mild or moderate disease. For more severe cases, blood transfusions may be needed. About half a million people need to be admitted to the hospital a year. Paracetamol (acetaminophen) is recommended as a substitute for nonsteroidal anti-inflammatory drugs (NSAIDs) for fever reduction and pain relief in dengue because of an increased risk of bleeding from NSAID use.
Dengue has been a global problem since World War Two and is common in more than 110 countries. Every year between 50 and 528 million people are infected and about 10,000 to 20,000 people die. The earliest explanation of the date of the outbreak of 1779. The cause and spread of the virus was understood early in the 20th century. In addition to eliminating mosquitoes, work is underway for drugs targeted directly to the virus. These are classified as neglected tropical diseases.
Video Dengue fever
Signs and symptoms
Usually, people infected with dengue virus show no symptoms (80%) or have only mild symptoms such as uncomplicated fever. Others have more severe disease (5%), and in small proportions it is life-threatening. The incubation period (time between exposure and onset of symptoms) ranges from 3 to 14 days, but most often is 4 to 7 days. Therefore, travelers returning from endemic areas are unlikely to have dengue fever if fever or other symptoms start more than 14 days after arriving home. Children often experience the same symptoms as common colds and gastroenteritis (vomiting and diarrhea) and have a greater risk of complications, although early symptoms are generally mild but include high fever.
Clinical course
Typical symptoms of dengue fever are sudden onset fever, headache (usually located behind the eyes), muscle and joint pain, and rash. The alternative name for dengue, "breakbone fever", comes from muscle and associated joint pain. Travel infection is divided into three phases: febril, critical, and recovery.
The fever phase involves high fever, potentially over 40 ° C (104 ° F), and is associated with general pain and headaches; this usually lasts two to seven days. Nausea and vomiting can also occur. The rash occurs in 50-80% of those who experience symptoms on the first or second day of symptoms such as reddened skin, or later in the course of the disease (days 4-7), such as a measles-like rash. Rashes described as "white islands in the red ocean" have also been observed. Some petechiae (small red spots that are not lost when the skin is pressed, caused by a damaged capillary) may appear at this point, such as some minor bleeding from the mucous membranes of the mouth and nose. The fever itself is biphasic or a classic saddleback in nature, broken and then returned for a day or two.
In some people, the disease progresses to a critical phase when the fever improves. During this period, there is a plasma leak from the blood vessels, usually lasting one to two days. This can cause fluid accumulation in the chest and abdominal cavity as well as the thinning of fluid from the circulation and decreased blood supply to vital organs. There may also be organ dysfunction and severe bleeding, usually from the gastrointestinal tract. Shock (dengue shock syndrome) and bleeding (dengue hemorrhagic fever) occur in less than 5% of all dengue cases, but those previously infected with other serotypes of dengue virus ("secondary infection") are at increased risk. This critical phase, although rare, occurs relatively more commonly in children and young adults.
Recovery phase occurs next, with resorption of leaking fluid into the bloodstream. This usually lasts two to three days. This increase is often noticeable, and can be accompanied by severe itching and a slow heartbeat. Other rashes may occur either with maculopapular or vasculitic appearance, followed by exfoliation. During this stage, the state of excess fluid may occur; if it affects the brain, it can cause a decrease in the level of consciousness or seizures. Feelings of fatigue can last for weeks in adults.
Related matter
Dengue can sometimes affect some other body systems, either in isolation or along with classic dengue fever symptoms. Decreased levels of consciousness occur in 0.5-6% of severe cases, caused by inflammation of the brain by the virus or indirectly as a result of damage to vital organs, for example, the liver.
Other neurological disorders have been reported in the dengue context, such as transverse myelitis and Guillain-Barrà © Å © syndrome. Cardiac infection and acute liver failure are one of the rare complications.
A pregnant woman who develops dengue may have a higher risk of miscarriage as well as low birth weight and premature birth.
Maps Dengue fever
Cause
Virology
Dengue Fever Virus (DENV) is an RNA virus of the Flaviviridae family ; genus Flavivirus . Other members of the same genus include yellow fever virus, West Nile virus, St. Louis encephalitis, Japanese encephalitis virus, tick-borne encephalitis virus, the Kyasanur forest disease virus, and the Omsk dengue virus. Most are transmitted by arthropods (mosquitoes or lice), and are therefore also referred to as arbovirus (thi thropod- bo rne viruses).
The dengue virus genome (genetic material) contains about 11,000 nucleotide bases, which encode three types of protein molecules (C, prM and E) that form viral particles and seven other non-structural protein molecules (NS1, NS2a, NS2b). , NS3, NS4a, NS4b, NS5) found in infected stem cells only and required for viral replication. There are five virus strains, called serotypes, in which the first four are referred to as DENV-1, DENV-2, DENV-3 and DENV-4. The fifth type was announced in 2013. The difference between serotypes is based on their antigenicity.
Transmission
Dengue virus is mainly transmitted by mosquitoes Aedes , especially A. aegypti . These mosquitoes usually live between latitudes 35 Â ° North and 35 Â ° South below 1,000 meters (3,300 feet) altitude. They usually bite during the morning and evening, but they can bite and spread the infection at any time of the day. Other species that transmit the disease include A. albopictus , A. polynesiensis and A. scutellaris . Humans are the main host of the virus, but also circulate in nonhuman primates. Infection can be obtained through one bite. A female mosquito that takes blood food from a person infected with dengue fever, during a period of fever 2 to 10 days, becomes itself infected with a virus in the cells that line the stomach. About 8-10 days later, the virus spreads to other tissues including the mosquito's salivary glands and then released into its saliva. Viruses appear to have no adverse effects on mosquitoes, which remain infected for life. Aedes aegypti is primarily involved, preferring to put its eggs in an artificial water container, to live near humans, and to feed people rather than other vertebrates.
Dengue can also be transmitted through infected blood products and through organ donation. In countries such as Singapore, where dengue is endemic, the risk is estimated between 1.6 and 6 per 10,000 transfusions. Vertical transmission (from mother to child) during pregnancy or at birth has been reported. Other person-to-person transmission modes have also been reported, but very unusual. The genetic variation in the dengue virus is a particular region, indicating that formation into new territory is relatively rare, although dengue has appeared in new areas in recent decades.
Predisposition
Severe disease is more common in infants and children, and unlike many other infections, the disease is more common in relatively well-nourished children. Other risk factors for severe illness include female gender, high body mass index, and viral load. While each serotype can cause a full spectrum of illnesses, viral strains are a risk factor. Infection with one serotype is considered to produce lifelong immunity for that species, but only short-term protection against the other three. The risk of severe illness due to secondary infection increases if a person has previously been exposed to serotype serotype DENV-1 serotonype DENV-2 or DENV-3, or if someone previously exposed to DENV-3 acquires DENV-2. Dengue can be life-threatening in people with chronic diseases like diabetes and asthma.
Polymorphism (normal variation) in certain genes has been associated with an increased risk of severe dengue complications. Examples include a protein-coding gene known as TNF, mannan-binding lectins, CTLA4, TGF, DC-SIGN, PLCE1, and certain forms of human leukocyte antigen from HLA-B gene variation. A common genetic disorder, especially in Africans, known as lack of glucose-6-phosphate dehydrogenase, appears to increase the risk. Polymorphisms in genes for vitamin D and Fc receptors? R appears to offer protection against severe disease in secondary dengue infection.
Mechanism
When a dengue virus-carrying mosquito bites a person, the virus enters the skin along with the saliva of a mosquito. It binds and enters the white blood cells, and reproduces inside the cell as they move throughout the body. White blood cells respond by producing a number of signaling proteins, such as cytokines and interferons, which are responsible for many symptoms, such as fever, flu-like symptoms, and severe pain. In severe infections, viral production in the body is greatly increased, and more organs (such as liver and bone marrow) may be affected. The fluid from the bloodstream leaks through the walls of the small blood vessels into the body cavity due to capillary permeability. As a result, less blood circulates in the blood vessels, and blood pressure becomes so low that it can not supply enough blood to the vital organs. Furthermore, bone marrow dysfunction due to infection of stromal cells causes a reduction in platelet count, which is necessary for effective blood clotting; this increases the risk of bleeding, the main complication of other dengue fever.
Virus replication
Once inside the skin, dengue virus binds Langerhans cells (populations of dendritic cells in the skin that identify pathogens). The virus enters the cell by binding between viral proteins and membrane proteins in Langerhans cells, especially the C-type lectin called DC-SIGN, mannose receptor and CLEC5A. DC-SIGN, a non-specific receptor for foreign material in dendritic cells, appears to be a major entry point. Dendritic cells move to the nearest lymph nodes. Meanwhile, the viral genome is translated in membrane-bound vesicles in the cellular endoplasmic reticulum, in which cell protein synthesis tools produce new viral proteins that mimic viral RNA and begin to form viral particles. The immature viral particles are transported to the Golgi apparatus, the part of the cell where some proteins accept the required sugar chain (glycoprotein). New viruses are now released by exocytosis. They can then enter other white blood cells, such as monocytes and macrophages.
The initial reaction of infected cells is to produce interferon, a cytokine that increases the number of defenses against viral infections through the innate immune system by enlarging the production of a large group of proteins mediated by the JAK-STAT pathway. Some of the dengue virus serotypes seem to have mechanisms to slow down this process. Interferon also activates the adaptive immune system, leading to the formation of antibodies against viruses and T cells that directly attack virus-infected cells. Various antibodies are produced; some bind closely to viral proteins and target them to phagocytosis (consumption by specialized cells and destruction), but some bind viruses poorly and instead appear to transmit the virus into phagocytes where it is not destroyed but able to replicate further.
Severe illness
It is not entirely clear why secondary infections with different dengue virus strains place people at risk for dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is the increase in antibody-dependent (ADE). The exact mechanism behind ADE is unclear. This may be caused by poor binding of non-neutral antibodies and delivery into the wrong white blood cell compartment that has swallowed the virus for destruction. There is a suspicion that ADE is not the only mechanism underlying serious complications associated with dengue, and various research lines have implied the role of T cells and soluble factors such as cytokines and complement systems.
Severe disease is characterized by capillary permeability problems (fluid and protein removal usually contained in the blood) and blood clotting disorders. This change appears to be related to the state of irregular endothelial glycocalyx, which acts as a molecular filter of the blood component. Leaky capillaries (and critical phase) are thought to be caused by immune system responses. Other interesting processes include infected cells that become necrotic - which affects coagulation and fibrinolysis (the opposite system of blood clotting and clot degradation) - and low platelets in the blood, are also factors in normal clotting.
Diagnosis
Diagnosis of dengue is usually done clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas. However, early disease can be difficult to distinguish from other viral infections. Possible diagnoses are based on febrile findings plus the following two things: nausea and vomiting, rashes, general pain, low white blood cell count, positive tourniquet test, or warning sign (see table) for someone living in endemics. area. Warning signs usually occur before the onset of dengue fever is severe. The tourniquet test, which is particularly useful in settings where no laboratory examination is available, involves the application of a blood pressure cuff between the diastolic and systolic pressure for five minutes, followed by the counting of petechial bleeding; higher numbers make the diagnosis of dengue more likely with disconnection to more than 10 to 20 per 1 inch 2 (6.25 cm 2 ).
Diagnosis should be considered for anyone who has a fever within two weeks of being in the tropics or subtropics. It is difficult to distinguish dengue and chikungunya dengue fever, the same viral infection that shares many of the symptoms and occurs in the same parts of the world as dengue fever. Often, investigations are carried out to exclude other conditions that cause similar symptoms, such as malaria, leptospirosis, viral hemorrhagic fever, typhoid fever, meningococcal disease, measles, and influenza. Fever Zika also has symptoms similar to dengue.
The earliest changes detected in laboratory tests are low white blood cell counts, followed by low platelets and metabolic acidosis. High levels of aminotransferase (AST and ALT) of the liver are commonly associated with low platelets and white blood cells. In severe disease, plasma leak causes hemoconcentration (as shown by increased hematocrit) and hypoalbuminemia. Pleural effusion or ascites can be detected by physical examination when large, but fluid demonstrations on ultrasound may be helpful in early identification of dengue shock syndrome. The use of ultrasound is limited by the lack of availability in many settings. Dengue shock syndrome is present when pulse pressure drops to <= Ã, 20 mm Hg along with peripheral vascular collapse. Peripheral vascular damage is defined in children by delayed capillary refilling, rapid heartbeat, or cold extremities. While warning signs are an important aspect for early detection of potential serious diseases, evidence for certain clinical or laboratory markers is weak.
Classification
The World Health Organization 2009 classification divides dengue into two groups: not complicated and heavy. This replaces the WHO classification of 1997, which needs to be simplified as being considered too restrictive, although the old classification is still widely used including by the World Health Organization Regional Office for Southeast Asia in 2011. Severe dengue is defined as being associated with severe bleeding, severe organ dysfunction , or heavy plasma leakage while all other cases are not complicated. The 1997 classification divides dengue fever into undifferentiated fever, dengue fever, and dengue hemorrhagic fever. Dengue hemorrhagic fever is subdivided into class I-IV. Grade I is the presence of just an easy bruise or a positive tourniquet test in a person with fever, grade II is spontaneous bleeding to the skin and elsewhere, grade III is clinical evidence of shock, and grade IV is so severe that blood pressure and pulse can not be detected. Class III and IV are referred to as "dengue shock syndrome".
Laboratory test
The diagnosis of dengue can be confirmed by microbiological laboratory testing. This can be done by isolating the virus in cell culture, detection of nucleic acids by PCR, detection of viral antigens (such as for NS1) or specific antibodies (serology). Virus isolation and nucleic acid detection are more accurate than antigen detection, but these tests are not widely available because of their greater cost. Detection of NS1 during the fever phase of primary infection may be greater than 90% sensitive but only 60-80% in subsequent infections. All tests may be negative in the early stages of the disease. Detection of PCR and antigen viruses is more accurate in the first seven days. In 2012 PCR tests are introduced that can be run on equipment used to diagnose influenza; this will likely increase access to PCR-based diagnosis.
This laboratory test is only a diagnostic value during the acute phase of the disease with the exception of serology. Tests for specific antibodies of dengue virus, type IgG and IgM, may be useful in confirming the diagnosis at the later stages of the infection. Both IgG and IgM are produced after 5-7 days. The highest level (titer) IgM is detected after primary infection, but IgM is also produced in reinfection. IgM becomes undetectable 30-90 days after primary infection, but earlier after re-infection. IgG, on the other hand, remains detectable for more than 60 years and, in the absence of symptoms, is a useful indicator of previous infections. After primary infection, IgG reaches peak levels in the blood after 14-21 days. In subsequent reinfection, the levels are faster and titer is usually higher. Both IgG and IgM provide protective immunity to infectious viral serotypes. In testing for IgG and IgM antibodies there may be cross reactivity with other flaviviruses that may produce false positives after recent infections or vaccinations with yellow fever virus or Japanese encephalitis. IgG detection alone was not considered diagnostic unless blood samples were collected 14 days apart and more than fourfold increase in specific IgG levels detected. In someone with symptoms, IgM detection is considered diagnostic.
Prevention
Prevention depends on the control and protection of the mosquito bites that transmit it. The World Health Organization recommends an Integrated Vector Control program consisting of five elements:
- Advocacy, social mobilization, and legislation to ensure that public and community health agencies are strengthened;
- Collaboration between the health sector and other sectors (public and private);
- Integrated approach to disease control to maximize resource use;
- Evidence-based decision-making to ensure every intervention is properly targeted; and
- Capacity building to ensure an adequate response to the local situation.
The main method of controlling A. aegypti is by removing its habitat. This is done by removing open water sources, or if this is not possible, by adding insecticides or biological control agents to this area. Common spraying with organophosphoric or pyrethroid insecticides, although sometimes done, is not considered effective. Reducing open water collection through environmental modification is the preferred control method, given the concerns of negative health effects of insecticides and greater logistical difficulties with control agents. People can prevent mosquito bites by wearing clothes that completely cover the skin, using mosquito nets while resting, and/or mosquito repellent applications (DEET being the most effective). However, this method does not seem to be effective enough, since the frequency of outbreaks appears to increase in some areas, perhaps because urbanization increases the habitat of aegypti . The range of diseases seems to be growing probably due to climate change.
Vaccines
By 2016, some effective dengue vaccines are becoming commercially available in the Philippines and Indonesia. It has also been approved for use by Mexico, Brazil, El Salvador, Costa Rica, Singapore, and Paraguay. In Indonesia it costs around US $ 207 for the recommended three doses.
The vaccine is produced by Sanofi and runs under the brand name Dengvaxia. It is based on a weak combination of yellow fever virus and each of the four dengue serotypes. Two vaccine studies found that 60% were effective and prevented more than 80 to 90% of severe cases. This is less than some people want. By 2017, manufacturers recommend that vaccines be used only on people who have previously had dengue infection because if there is no evidence it will aggravate subsequent infections.
There are ongoing programs that work on dengue vaccines to cover all four serotypes. Now there is a fifth serotype that needs to be taken into account. One concern is that the vaccine may increase the risk of severe illness through increased antibody-dependent (ADE). The ideal vaccine is safe, effective after one or two injections, covering all serotypes, not contributing to ADE, easily transportable and stored, and affordable and cost-effective.
Anti-dengue Day
International Anti-Dengue Day is observed annually on June 15th. This idea was first agreed in 2010 with the first event held in Jakarta, Indonesia in 2011. Further events are held in 2012 in Yangon, Myanmar and in 2013 in Vietnam. The goal is to raise public awareness of dengue, mobilize resources for prevention and control, and to demonstrate the Asian region's commitment to tackling the disease.
Management
There is no specific antiviral drug for dengue fever; However, maintaining proper fluid balance is important. Treatment depends on the symptoms. Those who drink, urinate, have no "warning signs" and other healthy can be treated at home with daily follow-up therapy and oral rehydration. Those who have other health problems, have "warning signs", or can not arrange follow-up regularly should be hospitalized. In those with severe dengue care should be provided in areas where there is access to the intensive care unit.
Intravenous hydration, if necessary, is usually only necessary for one or two days. In children with shock due to dengue the rapid dose of 20 mL/kg makes sense. The level of fluid administration is then titrated to urine output 0.5-1 mL/kg/hour, stable vital signs and normalization of hematocrit. The smallest amount of fluid needed to achieve this is recommended.
Invasive medical procedures such as nasogastric intubation, intramuscular injections and arterial punctures are avoided, given the risk of bleeding. Paracetamol (acetaminophen) is used for fever and discomfort while NSAIDs such as ibuprofen and aspirin are avoided because they can exacerbate the risk of bleeding. Blood transfusion begins in early people who come with unstable vital signs in the face of a decrease in hematocrit, rather than waiting for the hemoglobin concentration to decrease to some predetermined level of "transfusion triggers". Red blood cells are packed or whole blood is recommended, while platelets and fresh frozen plasma are usually not. There is not enough evidence to determine whether corticosteroids have a positive or negative effect on dengue fever.
During the recovery phase the intravenous fluid is stopped to prevent excess fluid state. If excess fluid occurs and vital signs are stable, stopping further fluids may be all that is needed. If a person is beyond a critical phase, a loop diuretic such as furosemide can be used to remove excess fluid from the circulation.
Epidemiology
Most people with dengue fever recover without any ongoing problems. The mortality rate is 1-5%, and less than 1% with adequate care; but those who developed low blood pressure significantly may have a death rate of up to 26%. Common dengue in more than 110 countries. In 2013, it caused about 60 million symptomatic infections worldwide, with 18% hospitalization and about 13,600 deaths. The cost of Dengue cases worldwide is estimated at US $ 9 billion. During the decade of the 2000s, 12 countries in Southeast Asia were estimated to have about 3 million infections and 6,000 deaths annually. Reported in at least 22 countries in Africa; but it is possible in all of them with 20% of the population at risk. This makes it one of the most common vector diseases worldwide.
Infection is most commonly found in urban environments. In recent decades, the expansion of villages, towns and cities in areas where it is common, and increased mobility have increased the number of epidemics and viruses in circulation. Dengue fever, formerly restricted to Southeast Asia, has now spread to southern China, countries in the Pacific Ocean and America, and may pose a threat to Europe.
The rate of dengue increased 30-fold between 1960 and 2010. This increase is believed to be caused by a combination of urbanization, population growth, increased international travel, and global warming. Geographical distribution around the equator. Of the 2.5 billion people living in areas where generally 70% come from Asia and the Pacific. Dengue infection is second only to malaria as a cause of fever being diagnosed among travelers returning from developing countries. It is the most common viral disease transmitted by arthropods, and has a burden of disease that is estimated to be 1,600 years of life tailored to disability per million inhabitants. The World Health Organization calculates dengue as one of seventeen neglected tropical diseases.
Like most arboviruses, dengue viruses are preserved in nature in cycles involving blood vacuum vectors and preferred vertebrate hosts. The virus is preserved in the forests of Southeast Asia and Africa with transmissions from the female mosquito Aedes - species other than A. aegypti - to their offspring and lower the primates. In cities and towns, the virus is mainly transmitted by the highly domesticated A. aegypti . In rural areas, the virus is transmitted to humans by aegypti and other species of Aedes such as A. albopictus . Both species have a wide range in the second half of the 20th century. In all settings, infected primates or lower humans greatly increase the amount of dengue virus in circulation, in a process called amplification.
History
The first record of a possible case of dengue is in the Chinese medical encyclopaedia of the Jin Dynasty (265-420 AD) which refers to the "water poison" associated with flying insects. The main vector, A. aegypti , spread over Africa in the 15th to 19th centuries was partly due to increased secondary globalization of the slave trade. There is a description of the epidemic in the 17th century, but the most plausible early report of the dengue epidemic was from 1779 and 1780, when the epidemic struck Asia, Africa and North America. From then until 1940, epidemics were rare.
In 1906, transmissions by Aedes mosquitoes were confirmed, and in 1907 dengue fever was the second disease (after yellow fever) shown to be caused by a virus. Further investigations by John Burton Cleland and Joseph Franklin Siler complement the basic understanding of the transmission of dengue fever.
The spread of dengue during and after the Second World War has been linked to ecological disorders. The same trend also causes the spread of various serotypes of disease to new areas, and the emergence of dengue hemorrhagic fever. The severe form of the disease was first reported in the Philippines in 1953; in the 1970s, it has been a major cause of childhood death and has appeared in the Pacific and America. Dengue hemorrhagic fever and dengue shock syndrome were first recorded in Central and South America in 1981, when DENV-2 was contracted by people who had previously been infected with DENV-1 a few years earlier.
Etymology
The origin of the Spanish word dengue is uncertain, but may be derived from dinga in the Swahili Ka-dinga pepo phrase, which describes the disease as being caused by demons. Slaves in the West Indies contracted by dengue are said to have cool posture and road style, and the disease is known as "dandown fever".
The term "break-bone fever" was applied by doctors and founder of the United States, Benjamin Rush, in a 1789 report on the 1780 epidemic in Philadelphia. In the title of the report, he uses a more formal term, "gall fever". The term dengue came to the public only after 1828. Other historical terms include "breakheart fever" and "la dengue fever". The terms for severe illness include "infectious thrombocytopenic purpura" and "Philippines", "Thailand", or "dengue fever".
Society and culture
Dengue outbreaks increase the need for blood products while reducing the number of potential blood donors due to potential viral infections. A person who has dengue infection is usually not allowed to donate blood for at least the next six months.
Research
Research efforts to prevent and treat dengue include various ways of vector control, vaccine development, and antiviral drugs.
Vector
With regard to vector control, a number of new methods have been used to reduce the number of mosquitoes with some success including the placement of guppy ( Poecilia reticulata) or copepods in standing water to eat mosquito larvae. There are also trials with genetically modified men A. aegypti which after being released to a wild couple with females, and making their offspring unable to fly. Wolbachia
Efforts are underway to infect mosquito populations with bacteria from the genus Wolbachia , which makes mosquitoes partially resistant to dengue virus. While artificially induced infections with Wolbachia are effective, it is not clear whether naturally acquired infections are protective. Work is still ongoing until 2015 to determine the best type of Wolbachia to use.
Treatment
In addition to efforts to control the spread of Aedes mosquitoes, there are ongoing efforts to develop antiviral drugs that will be used to treat dengue attacks and prevent severe complications. The discovery of viral protein structures can help the development of effective drugs. There are some reasonable targets. The first approach is the inhibition of virus-dependent RNA polymerase RNA (encoded by NS5), which copies the viral genetic material, with a nucleoside analogue. Secondly, it is possible to develop a specific inhibitor of the viral protease (encoded by NS3), which unifies the viral proteins. Finally, it is possible to develop entry inhibitors, which stop the virus from entering cells, or inhibitors of 5? process capping, which is necessary for viral replication.
References
External links
- Demam berdarah di Curlie (berdasarkan DMOZ)
- "Dengue". WHO . Diperoleh 27 Juni 2011 .
- "Dengue". Pusat Pengendalian dan Pencegahan Penyakit AS . Diperoleh 27 Juni 2011 .
- "Demam Dengue". Lembaga Perlindungan Kesehatan Inggris . Diperoleh 27 Juni 2011 .
- "DengueMap". Pusat Pengendalian dan Pencegahan Penyakit AS/HealthMap . Diperoleh 27 Juni 2011 .
Source of the article : Wikipedia
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