About HIV/AIDS



WHAT IS HIV?

HIV stands for human immunodeficiency virus. It is the virus that causes AIDS. A member of a group of viruses called retroviruses, HIV infects human cells and uses the energy and nutrients provided by those cells to grow and reproduce.

WHAT IS AIDS?

AIDS stands for acquired immunodeficiency syndrome. It is a disease in which the body's immune system breaks down and is unable to fight off infections, known as "opportunistic infections," and other illnesses that take advantage of a weakened immune system.

CONTENTS

What is HIV?
HIV stands for human immunodeficiency virus. It is the virus that causes AIDS. A member of a group of viruses called retroviruses, HIV infects human cells and uses the energy and nutrients provided by those cells to grow and reproduce.
What is AIDS?
AIDS stands for acquired immunodeficiency syndrome. It is a disease in which the body’s immune system breaks down and is unable to fight off infections, known as "opportunistic infections," and other illnesses that take advantage of a weakened immune system.
When a person is infected with HIV, the virus enters the body and lives and multiplies primarily in the white blood cells. These are immune cells that normally protect us from disease. The hallmark of HIV infection is the progressive loss of a specific type of immune cell called T-helper, or CD4, cells. As the virus grows, it damages or kills these and other cells, weakening the immune system and leaving the person vulnerable to various opportunistic infections and other illnesses ranging from pneumonia to cancer. A person can receive a clinical diagnosis of AIDS, as defined by the U.S. Centers for Disease Control and Prevention (CDC), if he or she has tested positive for HIV and meets one or both of these conditions:
  • The presence of one or more AIDS-related infections or illnesses;
  • A CD4 count that has reached or fallen below 200 cells per cubic millimeter of blood. Also called the T-cell count, the CD4 count ranges from 450 to 1200 in healthy individuals.
How quickly do people infected with HIV develop AIDS?
In some people, the T-cell decline and opportunistic infections that signal AIDS develop soon after infection with HIV. But most people do not develop symptoms for 10 to 12 years, and a few remain symptom-free for much longer. As with most diseases, early medical care can help prolong a person’s life.
How many people are affected by HIV/AIDS?
The Joint United Nations Programme on HIV/AIDS (UNAIDS) estimates that there are now 33 million people living with HIV/AIDS worldwide. Most of them do not know they carry HIV and may be spreading the virus to others. In the U.S., approximately 1.1 million people are living with HIV/AIDS; about 56,300 Americans became newly infected with HIV in 2006. And the CDC estimates that one-fifth of all people with HIV in the U.S. do not know they are carrying the virus.
Since the beginning of the epidemic, AIDS has killed more than 25 million people worldwide, including more than 583,000 Americans. AIDS ranks with malaria and tuberculosis as one of the top three deadliest infectious diseases among adults and is the fourth leading cause of death worldwide. More than 15 million children have been orphaned by HIV.
How is HIV transmitted?
A person who has HIV carries the virus in certain body fluids, including blood, semen, vaginal secretions, and breast milk. The virus can be transmitted only if such HIV-infected fluids enter the bloodstream of another person. This kind of direct entry can occur (1) through the linings of the vagina, rectum, mouth, and the opening at the tip of the penis; (2) through intravenous injection with a syringe; or (3) through a break in the skin, such as a cut or sore. Usually, HIV is transmitted through:
  • Unprotected sexual intercourse (either vaginal or anal) with someone who has HIV. Women are at greater risk of HIV infection through vaginal sex than men, although the virus can also be transmitted from women to men. Anal sex (whether male-male or male-female) poses a high risk mainly to the receptive partner, because the lining of the anus and rectum is extremely thin and is filled with small blood vessels that can be easily injured during intercourse.
  • Sharing needles or syringes with someone who is HIV infected. Laboratory studies show that infectious HIV can survive in used syringes for a month or more. That’s why people who inject drugs should never reuse or share syringes, water, or drug preparation equipment. This includes needles or syringes used to inject illegal drugs such as heroin, as well as steroids. Other types of needles, such as those used for body piercing and tattoos, can also carry HIV.
  • Infection during pregnancy, childbirth, or breast-feeding (mother-to-infant transmission). Any woman who is pregnant or considering becoming pregnant and thinks she may have been exposed to HIV—even if the exposure occurred years ago—should seek testing and counseling. In the U.S., mother-to-infant transmission has dropped to just a few cases each year because pregnant women are routinely tested for HIV. Those who test positive can get drugs to prevent HIV from being passed on to a fetus or infant, and they are counseled not to breast-feed.
  • Unprotected oral sex with someone who has HIV. There are far fewer cases of HIV transmission attributed to oral sex than to either vaginal or anal intercourse, but oral-genital contact poses a clear risk of HIV infection, particularly when ejaculation occurs in the mouth. This risk goes up when either partner has cuts or sores, such as those caused by sexually transmitted infections (STIs), recent tooth-brushing, or canker sores, which can allow the virus to enter the bloodstream.
How is HIV not transmitted?
HIV is not an easy virus to pass from one person to another. It is not transmitted through food or air (for instance, by coughing or sneezing). There has never been a case where a person was infected by a household member, relative, co-worker, or friend through casual or everyday contact such as sharing eating utensils or bathroom facilities, or through hugging or kissing. (Most scientists agree that while HIV transmission through deep or prolonged "French" kissing may be possible, it would be extremely unlikely.) Here in the U.S., screening the blood supply for HIV has virtually eliminated the risk of infection through blood transfusions (and you cannot get HIV from giving blood at a blood bank or other established blood collection center). Sweat, tears, vomit, feces, and urine do contain HIV, but have not been reported to transmit the disease (apart from two cases involving transmission from fecal matter via cut skin). Mosquitoes, fleas, and other insects do not transmit HIV.
How can I reduce my risk of becoming infected with HIV through sexual contact?
If you are sexually active, protect yourself against HIV by practicing safer sex. Whenever you have sex, use a condom or "dental dam" (a square of latex recommended for use during oral-genital and oral-anal sex). When used properly and consistently, condoms are extremely effective. But remember:
  • Use only latex condoms (or dental dams). Lambskin products provide little protection against HIV.
  • Use only water-based lubricants. Latex condoms are virtually useless when combined with oil- or petroleum-based lubricants such as Vaseline or hand lotion. (People with latex allergies can use polyethylene condoms with oil-based lubricants).
  • Use protection each and every time you have sex.
  • If necessary, consult a nurse, doctor, or health educator for guidance on the proper use of latex barriers.
Are there other ways to avoid getting HIV through sex?
The male condom is the only widely available barrier against sexual transmission of HIV. Female condoms are fairly unpopular in the U.S. and still relatively expensive, but they are gaining acceptance in some developing countries. Efforts are also under way to develop topical creams or gels called "microbicides," which could be applied prior to sexual intercourse to kill HIV and prevent other STIs that facilitate HIV infection.
Is there a link between HIV and other sexually transmitted infections?
Having a sexually transmitted infection (STI) can increase your risk of acquiring and transmitting HIV. This is true whether you have open sores or breaks in the skin (as with syphilis, herpes, and chancroid) or not (as with chlamydia and gonorrhea). Where there are breaks in the skin, HIV can enter and exit the bloodstream more easily. But even when there are no breaks in the skin, STIs can cause biological changes, such as swelling of tissue, which may make HIV transmission more likely. Studies show that HIV-positive individuals who are infected with another STI are three to five times more likely to contract or transmit the virus through sexual contact.
How can I avoid acquiring HIV from a contaminated syringe?
If you are injecting drugs of any type, including steroids, do not share syringes or other injection equipment with anyone else. (Disinfecting previously used needles and syringes with bleach can reduce the risk of HIV transmission.) If you are planning to have any part of your body pierced or to get a tattoo, be sure to see a qualified professional who uses sterile equipment. Detailed HIV prevention information for drug users who continue to inject is available from the CDC’s National Prevention Information Network at 1-800-458-5231 or online at www.cdc.gov/idu.
Are some people at greater risk of HIV infection than others?
HIV does not discriminate. It is not who you are but what you do that determines whether you can become infected with HIV. In the U.S., roughly half of all new HIV infections are related directly or indirectly to injection drug use, i.e., using HIV-contaminated needles or having sexual contact with an HIV-infected drug user. With 56,300 Americans contracting HIV in 2006, there are clearly many people who are still engaging in high-risk behaviors, and infection rates remain alarmingly high among young people, women, African Americans, and Hispanics. The fastest rising infection rates are now found among men who have sex with men, who comprised 53 percent of those newly infected with HIV in 2006; a third of those men were under 30 years of age.
Are women especially vulnerable to HIV?
Women are at least twice as likely to contract HIV through vaginal sex with infected males than vice versa. This biological vulnerability is worsened by social and cultural factors that often undermine women’s ability to avoid sex with partners who are HIV-infected or to insist on condom use. In the U.S., the proportion of HIV/AIDS cases among women more than tripled, from 8 percent in 1985 to 26 percent in 2005. African-American and Hispanic women represent less than one-quarter of U.S. women, but account for 80 percent of new infections among American women each year. In 2005, HIV/AIDS was the fourth leading cause of death for African-American men aged 25-44, and the third for African-American women.
Are young people at significant risk of HIV infection?
Many of the 1.1 million people now living with HIV in the U.S. became infected when they were teenagers. The CDC’s 2007 statistics show that about 48 percent of American high school students had been sexually active. Young people aged 13–29 accounted for 34 percent of HIV infections in 2006. Many young people also use drugs and alcohol, which can increase the likelihood that they will engage in high-risk sexual behavior.
Are there treatments for HIV/AIDS?
For many years, there were no effective treatments for AIDS. Today, a number of drugs are available to treat HIV infection. Some others are designed to treat the opportunistic infections and illnesses that affect people with AIDS.
The former group of drugs prevents HIV itself from reproducing and destroying the body’s immune system:
  • Nucleoside/nucleotide reverse transcriptase inhibitors are incorporated into the virus’s DNA and prevent reverse transcriptase from adding nucleotides to form functional viral DNA. They include abacavir, didanosine (ddl), emtricitabine (FTC), lamivudine (3TC), stavudine (d4T), tenofovir, and zidovudine (AZT);
  • Non-nucleoside reverse transcriptase inhibitors attach themselves to reverse transcriptase to prevent HIV from converting RNA into DNA, thus preventing the cell from producing new virus. "Non-nukes" include delavirdine, efavirinz, etravirine, and nevirapine;
  • Protease inhibitors attack the HIV enzyme protease and include amprenavir, atazanavir, darunavir, fosamprenavir, indinavir, lopinavir, nelfinavir, ritonavir, and tipranavir;
  • An entry inhibitor prevents HIV from entering healthy CD4 cells by targeting the CCR5 protein. Maraviroc is the only FDA-approved entry inhibitor;
  • A fusion inhibitor stops the virus from entering cells by targeting the gp41 protein on HIV’s surface. Enfuvirtide is the only FDA-approved fusion inhibitor; and
  • An integrase inhibitor blocks the action of an enzyme produced by HIV that allows it to integrate into the DNA. It is effective against HIV that has become resistant to other antiretroviral drugs. Raltegravir is the only FDA-approved integrase inhibitor.
HIV patients take these drugs in combination—a regimen known as highly active antiretroviral therapy (HAART). When taken as directed, anti-HIV treatment can reduce the amount of HIV in the bloodstream to very low levels and often enables the body’s immune cells to rebound to normal levels.
In addition to antiretroviral therapy, several drugs can be taken to help prevent a number of opportunistic infections including Pneumocystis carinii pneumonia, toxoplasmosis, cryptococcus, and cytomegalovirus infection. Once opportunistic infections occur, the same drugs can be used at higher doses to treat these infections, and chemotherapy drugs are available to treat the cancers that commonly occur in AIDS.
Researchers are continuing to develop new drugs that act at critical steps in the virus’s life cycle. Efforts are under way to identify new targets for anti-HIV medications and to discover ways of restoring the ability of damaged immune systems to defend against HIV and the many illnesses that affect people with HIV. Ultimately, advances in rebuilding the immune systems of HIV patients will benefit people with a number of serious illnesses, including cancer, Alzheimer’s disease, multiple sclerosis, and immune deficiencies associated with aging and premature birth.
Is there a cure for AIDS?
There is still no cure for AIDS. And while new drugs are helping some people who have HIV live longer, healthier lives, there are many problems associated with them:
  • Anti-HIV drugs are highly toxic and can cause serious side effects, including heart damage, kidney failure, and osteoporosis. Many (perhaps even most) patients cannot tolerate long-term treatment with HAART.
  • HIV mutates quickly. Even among those who do well on HAART, roughly half of patients experience treatment failure within a year or two, often because the virus develops resistance to existing drugs. In fact, as many as 10 to 20 percent of newly infected Americans are acquiring viral strains that may already be resistant to current drugs.
  • Because treatment regimens are unpleasant and complex, many patients miss doses of their medication. Failure to take anti-HIV drugs on schedule and in the prescribed dosage encourages the development of new drug-resistant viral strains.
  • Even when patients respond well to treatment, HAART does not eradicate HIV. The virus continues to replicate at low levels and often remains hidden in "reservoirs" in the body, such as in the lymph nodes and brain.
In the U.S., the number of AIDS-related deaths has decreased dramatically because of widely available, potent treatments. But more than 95 percent of all people with HIV/AIDS live in the developing world, and many have little or no access to treatment.
Is there a vaccine to prevent HIV infection?
Despite continued intensive research, experts believe it will be at least a decade before we have a safe, effective, and affordable AIDS vaccine. And even after a vaccine is developed, it will take many years before the millions of people at risk of HIV infection worldwide can be immunized. Until then, other HIV prevention methods, such as practicing safer sex and using sterile syringes, will remain critical.
Can you tell whether someone has HIV or AIDS?
You cannot tell by looking at someone whether he or she is infected with HIV or has AIDS. An infected person can appear completely healthy. But anyone infected with HIV can infect other people, even if they have no symptoms.
How can I know if I’m infected?
Immediately after infection, some people may develop mild, temporary flu-like symptoms or persistently swollen glands. Even if you look and feel healthy, you may be infected. The only way to know your HIV status for sure is to be tested for HIV antibodies—proteins the body produces in an effort to fight off infection. This usually requires a blood sample. If a person’s blood has HIV antibodies that means the person is infected.
Should I get tested?
If you think you might have been exposed to HIV, you should get tested as soon as possible. Here’s why:
  • Even in the early stages of infection, you can take concrete steps to protect your long-term health. Regular check-ups with a doctor who has experience with HIV/AIDS will enable you (and your family members or loved ones) to make the best decisions about whether and when to begin anti-HIV treatment, without waiting until you get sick.
  • Taking an active approach to managing HIV may give you many more years of healthy life than you would otherwise have.
  • If you are HIV positive, you will be able to take the precautions necessary to protect others from becoming infected.
  • If you are HIV positive and pregnant, you can take medications and other precautions to significantly reduce the risk of infecting your infant, including not breast-feeding.
How can I get tested?
Most people are tested by private physicians, at local health department facilities, or in hospitals. In addition, many states offer anonymous HIV testing. It is important to seek testing at a place that also provides counseling about HIV and AIDS. Counselors can answer questions about high-risk behavior and suggest ways you can protect yourself and others in the future. They can also help you understand the meaning of the test results and refer you to local AIDS-related resources.
Though less readily available, there is also a viral load test that can reveal the presence of HIV in the blood within three to five days of initial exposure, as well as highly accurate saliva tests that are nearly equivalent to blood tests in determining HIV antibody status. In many clinics you can now get a test called OraQuick, which gives a preliminary result in 20 minutes. You can also purchase a kit that allows you to collect your own blood sample, send it to a lab for testing, and receive the results anonymously. Only the Home Access brand kit is approved by the Food and Drug Administration. It can be found at most drugstores.
Keep in mind that while most blood tests are able to detect HIV infection within four weeks of initial exposure, it can sometimes take as long as three to six months for HIV antibodies to reach detectable levels. The CDC currently recommends testing six months after the last possible exposure to HIV.
The CDC’s National AIDS Hotline can answer questions about HIV testing and refer you to testing sites in your area. Operators are available toll-free, 24 hours a day, seven days a week, at:
  • 1-800-CDC-INFO (800-232-4636)
  • 101-515-8000 (TTY/deaf access)
How can I help fight HIV/AIDS?
Everyone can play a role in confronting the HIV/AIDS epidemic. Here are just a few suggestions for how you can make a difference:

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From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Dengue fever (disambiguation). Dengue fever Classification and external resources The typical rash seen in dengue fever ICD-10 A90. ICD-9 061 DiseasesDB 3564 MedlinePlus 001374 eMedicine med/528 MeSH C02.782.417.214 Dengue fever (UK: /ˈdɛŋɡeɪ/, US: /ˈdɛŋɡiː/), also known as breakbone fever, is an infectious tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic morbilliform skin rash. In a small proportion of cases the disease develops to the life-threatening dengue hemorrhagic fever (bleeding, low levels of blood platelets and blood plasma leakage) and dengue shock syndrome (circulatory failure). Dengue is transmitted by several species of mosquito within the Aedes genus, principally A. aegypti. The virus has four different types; infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type is believed to increase the risk of severe complications. As there is no vaccine, prevention is sought by reducing the habitat and the number of mosquitoes and limiting exposure to bites. Treatment of acute dengue is supportive, using either oral or intravenous rehydration for mild or moderate disease, and intravenous fluids and blood transfusion for more severe cases. The incidence of dengue fever has increased dramatically over the last 50 years, with around 50–100 million people infected yearly. Dengue is currently endemic in more than 110 countries. Early descriptions of the condition date from 1779, and its viral cause and the transmission were elucidated in the early 20th century. Dengue has become a worldwide problem since the Second World War. Contents [hide] 1 Signs and symptoms 1.1 Clinical course 1.2 Associated problems 2 Cause 2.1 Virology 2.2 Transmission 2.3 Predisposition 3 Mechanism 3.1 Viral reproduction 3.2 Severe disease 4 Diagnosis 4.1 General 4.2 Classification 4.3 Virology and serology 5 Prevention 6 Management 7 Epidemiology 8 History 8.1 Etymology 8.2 Discovery 9 Research 10 Notes 11 References 12 External links Signs and symptoms Schematic depiction of the symptoms of dengue fever People infected with dengue virus are commonly asymptomatic or only have mild symptoms such as an uncomplicated fever.[1][2] Others have more severe illness, and in a small proportion it is life-threatening.[1] The incubation period (time between exposure and onset of symptoms) ranges from 3–14 days, but most often it is 4–7 days.[3] This means that travellers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home.[4] Children often experience symptoms similar to those of the common cold and gastroenteritis (vomiting and diarrhea),[5] but are more susceptible to the severe complications.[4] Clinical course The characteristic symptoms of dengue are: a sudden-onset fever, headache (typically behind the eyes), muscle and joint pains, and a rash. The alternative name for dengue, "break-bone fever", comes from the associated muscle and joints pains.[1][6] The course of infection is divided into three phases: febrile, critical, and recovery.[7] The febrile phase involves high fevers, frequently over 40 °C (104 °F) and is associated with generalized pain and a headache; this usually lasts two to seven days.[6][7] Flushed skin and some small red spots called petechiae, which are caused by broken capillaries, may occur at this point,[7] as may some mild bleeding from mucous membranes of the mouth and nose.[4][6] The critical phase, if it occurs, follows the resolution of the high fever and typically lasts one to two days.[7] During this phase there may be significant fluid accumulation in the chest and abdominal cavity due to increased capillary permeability and leakage. This leads to depletion of fluid from the circulation and decreased blood supply to vital organs.[7] During this phase, organ dysfunction and severe bleeding (typically from the gastrointestinal tract) may occur.[4][7] Shock and hemorrhage occur in less than 5% of all cases of dengue,[4] however those who have previously been infected with other serotypes of dengue virus ("secondary infection") have an increased risk.[4][8] The recovery phase occurs next, with resorption of the leaked fluid into the bloodstream.[7] This usually lasts two to three days.[4] The improvement is often striking, but there may be severe itching and a slow heart rate.[4][7] It is during this stage that a fluid overload state may occur, which if it affects the brain may reduce the level of consciousness or cause seizures.[4] Associated problems Dengue may occasionally affect several other body systems.[7] This may be either in isolation or along with the classic dengue symptoms.[5] A decreased level of consciousness occurs in 0.5–6% of severe cases. This may be caused by infection of the brain by the virus or indirectly due to impairment of vital organs, for example, the liver.[5][9] Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain-Barré syndrome.[5] Infection of the heart and acute liver failure are among the rarer complications of dengue.[4][7] Cause Virology Main article: Dengue virus A TEM micrograph showing dengue virus virions (the cluster of dark dots near the center) Dengue fever virus (DENV) is an RNA virus of the family Flaviviridae; genus Flavivirus. Other members of the same family include yellow fever virus, West Nile virus, St. Louis encephalitis virus, Japanese encephalitis virus, tick-borne encephalitis virus, Kyasanur forest disease virus, and Omsk hemorrhagic fever virus.[9] Most are transmitted by arthropods (mosquitoes or ticks), and are therefore also referred to as arboviruses (arthropod-borne viruses).[9] The dengue virus genome (genetic material) contains about 11,000 nucleotide bases, which code for the three different types of protein molecules that form the virus particle (C, prM and E) and seven other types of protein molecules (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) that are only found in infected host cells and are required for replication of the virus.[8][10] There are four strains of the virus, which are called serotypes, and these are referred to as DENV-1, DENV-2, DENV-3 and DENV-4.[2] All four serotypes can cause the full spectrum of disease.[8] Infection with one serotype is believed to produce lifelong immunity to that serotype but only short term protection against the others.[2][6] The severe complications on secondary infection seem to occur particularly if someone previously exposed to serotype DENV-1 then contracts serotype DENV-2 or serotype DENV-3, or if someone previously exposed to type DENV-3 then acquires DENV-2.[10] Transmission The mosquito Aedes aegypti feeding off a human host Dengue virus is primarily transmitted by Aedes mosquitoes, particularly A. aegypti.[2] These mosquitoes usually live between the latitudes of 35° North and 35° South below an elevation of 1,000 metres (3,300 ft).[2] They bite primarily during the day.[11] Other mosquito species—Aedes albopictus, A. polynesiensis and several A. scutellaris—may also transmit the disease.[2] Humans are the primary host of the virus,[2][9] but it may also circulate in nonhuman primates.[12] An infection may be acquired via a single bite.[13] A mosquito that takes a blood meal from a person infected with dengue fever becomes itself infected with the virus in the cells lining its gut. About 8–10 days later, the virus spreads to other tissues including the mosquito's salivary glands and is subsequently released into its saliva. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Aedes aegypti prefers to lay its eggs in artificial water containers and tends to live in close proximity to humans, and prefers to feed off people rather than other vertebrates.[14] Dengue may also be transmitted via infected blood products and through organ donation.[15][16] In countries such as Singapore, where dengue is endemic, the risk is estimated to be between 1.6 and 6 per 10,000 transfusions.[17] Vertical transmission (from mother to child) during pregnancy or at birth has been observed.[13] Other person-to-person modes of transmission have been reported, but are very unusual.[6] Predisposition Severe disease is more common in babies and young children, and in contrast to many other infections it is more common in children that are relatively well nourished.[4] Women are more at risk than men.[10] Dengue may be life-threatening in people with chronic diseases such as diabetes and asthma.[10] It is thought that polymorphisms (normal variations) in particular genes may increase the risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin,[1] CTLA4, TGFβ,[8] DC-SIGN, and particular forms of human leukocyte antigen.[10] A common genetic abnormality in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk.[18] Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection.[10] Mechanism When a mosquito carrying DENV bites a person, the virus enters the skin together with the mosquito's saliva. It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signalling proteins (such as interferon) that are responsible for many of the symptoms, such as the fever, the flu-like symptoms and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow) can be affected, and fluid from the bloodstream leaks through the wall of small blood vessels into body cavities. As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction of the bone marrow leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue.[18] Viral reproduction After entering the skin, DENV binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens).[18] The virus enters the cells through binding between viral proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins called DC-SIGN, mannose receptor and CLEC5A.[8] DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main one.[10] The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is replicated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins, and the viral RNA is copied. Immature virus particles are transported to the Golgi apparatus, the part of the cell where the some of the proteins receive necessary sugar chains (glycoproteins). The now mature new viruses bud on the surface of the infected cell and are released by exocytosis. They are then able enter other white blood cells (such as monocytes and macrophages).[8] The initial reaction of infected cells is to produce the interferon, a cytokine that raises a number of defenses against viral infection through the innate immune system by augmenting the production of a large group of proteins (mediated by the JAK-STAT pathway). Some serotypes of DENV appear to have mechanisms to slow down this process. Interferon also activates the adaptive immune system, which leads to the generation of antibodies against the virus as well as T cells that directly attack any cell infected with the virus.[8] Various antibodies are generated; some bind closely to the viral proteins and target them for phagocytosis (ingestion by specialized cells) and destruction, but some bind the virus less well and appear instead to deliver the virus into a part of the phagocytes where it is not destroyed but is able to replicate further.[8] Severe disease Further information: Antibody-dependent enhancement It is not entirely clear why secondary infection with a different strain of DENV places people at risk of dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is that of antibody-dependent enhancement (ADE). The exact mechanism behind ADE is unclear. It may be caused by poor binding of non-neutralizing antibodies and delivery into the wrong compartment of white blood cells that have ingested the virus for destruction.[8][10] There is a suspicion that ADE is not the only mechanism underlying severe dengue-related complications,[1] and various lines of research have implied a role for T cells and soluble factors (such as cytokines and the complement system).[18] Severe disease is marked by two problems: dysfunction of endothelium (the cells that line blood vessels) and disordered blood clotting.[5] Endothelial dysfunction leads to the leakage of fluid from the blood vessels into the chest and abdominal cavities, while coagulation disorder is responsible for the bleeding complications. Higher levels of virus in the blood and involvement of other organs (such as the bone marrow and the liver) are associated with more severe disease. Cells in the affected organs die, leading to the release of cytokines and activation of both coagulation and fibrinolysis (the opposing systems of blood clotting and clot degradation). These alterations together lead to both endothelial dysfunction and coagulation disorder.[18] Diagnosis General Warning signs[19] Abdominal pain Ongoing vomiting Liver enlargement Mucosal bleeding High hematocrit with low platelets Lethargy The diagnosis of dengue is typically made clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas.[1] Early disease can however be difficult to differentiate from other viral infections.[4] A probable diagnosis is based on the findings of fever plus two of the following: nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning sign (see table) in someone who lives in an endemic area.[19] Warning signs typically occur before the onset of severe dengue.[7] The tourniquet test, which is particularly useful in settings where no laboratory investigations are readily available, involves the application of a blood pressure cuff for five minutes, followed by the counting of any petechial hemorrhages; a higher number makes a diagnosis of dengue more likely.[7] It may be difficult to distinguish dengue fever and chikungunya, a similar viral infection that shares many symptoms and occurs in similar parts of the world to dengue.[6] Often, investigations are performed to exclude other conditions that cause similar symptoms, such as malaria, leptospirosis, typhoid fever, and meningococcal disease.[4] The earliest change detectable on laboratory investigations is a low white blood cell count, which may then be followed by low platelets and metabolic acidosis.[4] In severe disease, plasma leakage may result in hemoconcentration (as indicated by a rising hematocrit) and hypoalbuminemia.[4] Pleural effusions or ascites may be detected by physical examination when large,[4] but the demonstration of fluid on ultrasound may assist in the early identification of dengue shock syndrome.[1][4] The use of ultrasound is limited by lack of availability in many settings.[1] Classification The World Health Organization's 2009 classification divides dengue fever into two groups: uncomplicated and severe.[1][19] This replaces the 1997 WHO classification, which needed to be simplified as it had been found to be too restrictive, but the older classification is still widely used.[19] The 1997 classification divided dengue into undifferentiated fever, dengue fever, and dengue hemorrhagic fever.[4][20] Dengue hemorrhagic fever was subdivided further into four grades (grade I–IV). Grade I is the presence only of easy bruising or a positive "tourniquet test" (see below) in someone with fever, grade II is the presence of spontaneous bleeding into the skin and elsewhere, grade III is the clinical evidence of shock, and grade IV is shock so severe that blood pressure and pulse cannot be detected.[20] Grades III and IV are referred to as "dengue shock syndrome".[19][20] Virology and serology Dengue fever may also be diagnosed by microbiological laboratory testing.[19] This can be done by virus isolation in cell cultures, nucleic acid detection by PCR, viral antigen detection or specific antibodies (serology).[10][21] Virus isolation and nucleic acid detection are more accurate than antigen detection, but these tests are not widely available due to their greater cost.[21] All tests may be negative in the early stages of the disease.[4][10] Apart from serology, laboratory tests are only of diagnostic value during the acute phase of the illness. Tests for dengue virus-specific antibodies, types IgG and IgM, can be useful in confirming a diagnosis in the later stages of the infection. Both IgG and IgM are produced after 5–7 days. The highest levels (titres) of IgM are detected following a primary infection, but IgM is also produced in secondary and tertiary infections. The IgM becomes undetectable 30–90 days after a primary infection, but earlier following re-infections. IgG, by contrast, remains detectable for over 60 years and, in the absence of symptoms, is a useful indicator of past infection. After a primary infection the IgG reaches peak levels in the blood after 14–21 days. In subsequent re-infections, levels peak earlier and the titres are usually higher. Both IgG and IgM provide protective immunity to the infecting serotype of the virus. In the laboratory test the IgG and the IgM antibodies can cross-react with other flaviviruses, such as yellow fever virus, which can make the interpretation of the serology difficult.[6][10][22] The detection of IgG alone is not considered diagnostic unless blood samples are collected 14 days apart and a greater than fourfold increase in levels of specific IgG is detected. In a person with symptoms, the detection of IgM is considered diagnostic.[22] Prevention A 1920s photograph of efforts to disperse standing water and thus decrease mosquito populations There are currently no approved vaccines for the dengue virus.[1] Prevention thus depends on control of and protection from the bites of the mosquito that transmits it.[11][23] The World Health Organization recommends an Integrated Vector Control program consisting of five elements: (1) Advocacy, social mobilization and legislation to ensure that public health bodies and communities are strengthened, (2) collaboration between the health and other sectors (public and private), (3) an integrated approach to disease control to maximize use of resources, (4) evidence-based decision making to ensure any interventions are targeted appropriately and (5) capacity-building to ensure an adequate response to the local situation.[11] The primary method of controlling A. aegypti is by eliminating its habitats.[11] This may be done by emptying containers of water or by adding insecticides or biological control agents to these areas.[11] Reducing open collections of water through environmental modification is the preferred method of control, given the concerns of negative health effect from insecticides and greater logistical difficulties with control agents.[11] People may prevent mosquito bites by wearing clothing that fully covers the skin and/or the application of insect repellent (DEET being the most effective).[13] Management There are no specific treatments for the dengue fever virus.[1] Treatment depends on the symptoms, varying from oral rehydration therapy at home with close follow-up, to hospital admission with administration of intravenous fluids and/or blood transfusion.[24] A decision for hospital admission is typically based on the presence of the "warning signs" listed in the table above, especially in those with preexisting health conditions.[4] Intravenous hydration is usually only needed for one or two days.[24] The rate of fluid administration is titrated to a urinary output of 0.5–1 mL/kg/hr, stable vital signs and normalization of hematocrit.[4] Invasive medical procedures such as nasogastric intubation, intramuscular injections and arterial punctures are avoided, in view of the bleeding risk.[4] Acetaminophen may be used for fever and discomfort while NSAIDs such as ibuprofen and aspirin are avoided as they might aggravate the risk of bleeding.[24] Blood transfusion is initiated early in patients presenting with unstable vital signs in the face of a decreasing hematocrit, rather than waiting for the hemoglobin concentration to decrease to some predetermined "transfusion trigger" level.[25] Packed red blood cells or whole blood are recommended, while platelets and fresh frozen plasma are usually not.[25] During the recovery phase intravenous fluids are discontinued to prevent a state of fluid overload.[4] If fluid overload occurs and vital signs are stable, stopping further fluid may be all that is needed.[25] If a person is outside of the critical phase, a loop diuretic such as furosemide may be used to eliminate excess fluid from the circulation.[25] Epidemiology See also: Dengue fever outbreaks Dengue distribution in 2006. Red: Epidemic dengue and Ae. aegypti Aqua: Just Ae. aegypti. Most people with dengue recover without any ongoing problems.[19] The mortality is 1–5% without treatment,[4] and less than 1% with adequate treatment.[19] Severe disease carries a mortality of 26%.[4] Dengue is believed to infect 50 to 100 million people worldwide a year with half a million life-threatening infections requiring hospitalization,[1] resulting in approximately 12,500–25,000 deaths.[5][26] The burden of disease from dengue is estimated to be similar to other childhood and tropical diseases, such as tuberculosis, at 1600 disability-adjusted life years per million population.[10] It is the most common viral disease transmitted by arthropods.[8] As a tropical disease it is deemed only second in importance to malaria.[4] It is endemic in more than 110 countries.[4] The World Health Organization counts dengue as one of sixteen neglected tropical diseases.[27] The incidence of dengue increased 30 fold between 1960 and 2010.[28] This increase is believed to be due to a combination of urbanization, population growth, increased international travel, and global warming.[1] The geographical distribution is around the equator with 70% of the total 2.5 billion people living in endemic areas from Asia and the Pacific.[28] In the United States, the rate of dengue infection among those who return from an endemic area with a fever is 2.9–8.0%,[13] and it is the second most common infection after malaria to be diagnosed in this group.[6] Until 2003, dengue was classified as a potential bioterrorism agent, but subsequent reports removed this classification as it was deemed too difficult to transfer and only caused hemorrhagic fever in a relatively small proportion of people.[29] History Etymology The origins of the word "dengue" are not clear, but one theory is that it is derived from the Swahili phrase Ka-dinga pepo, which describes the disease as being caused by an evil spirit.[30] The Swahili word dinga may possibly have its origin in the Spanish word dengue, meaning fastidious or careful, which would describe the gait of a person suffering the bone pain of dengue fever.[31] However, it is possible that the use of the Spanish word derived from the similar-sounding Swahili.[30] Slaves in the West Indies having contracted dengue were said to have the posture and gait of a dandy, and the disease was known as "dandy fever".[32][33] The term "break-bone fever" was first applied by physician and Founding Father Benjamin Rush, in a 1789 report of the 1780 epidemic in Philadelphia. In the report he uses primarily the more formal term "bilious remitting fever".[29][34] The term dengue fever came into general use only after 1828.[33] Other historical terms include "breakheart fever" and "la dengue".[33] Terms for severe disease include "infectious thrombocytopenic purpura" and "Philippine", "Thai", or "Singapore hemorrhagic fever".[33] Discovery The first record of a case of probable dengue fever is in a Chinese medical encyclopedia from the Jin Dynasty (265–420 AD) which referred to a "water poison" associated with flying insects.[30][35] There have been descriptions of epidemics in the 17th century, but the most plausible early reports of dengue epidemics are from 1779 and 1780, when an epidemic swept Asia, Africa and North America.[35] From that time until 1940, epidemics were infrequent.[35] In 1906, transmission by the Aedes mosquitoes was confirmed, and in 1907 dengue was the second disease (after yellow fever) that was shown to be caused by a virus.[36] Further investigations by John Burton Cleland and Joseph Franklin Siler completed the basic understanding of dengue transmission.[36] The marked rise of spread of dengue during and after the Second World War has been attributed to ecologic disruption. The same trends also led to the spread of different serotypes of the disease to different areas, and the emergence of dengue hemorrhagic fever, which was first reported in the Philippines in 1953. In the 1970s, it became a major cause of child mortality. Around the same time it emerged in the Pacific and the Americas.[35] Dengue hemorrhagic fever and dengue shock syndrome were first noted in Middle and Southern America in 1981, as DENV-2 was contracted by people who had previously been infected with DENV-1 several years earlier.[9] Research Current research efforts to prevent and treat dengue have included different means of vector control,[37] vaccine development, and antiviral drugs.[23] With regards to vector control, a number of novel methods have been used to reduce mosquito numbers with some success including the placement of the fish Poecilia reticulata or copepods in standing water to eat the mosquito larva.[37] There are ongoing programs working on a dengue vaccine to cover all four serotypes.[23] One of the concerns is that a vaccine may increase the risk of severe disease through antibody-dependent enhancement.[38] The ideal vaccine is safe, effective after one or two injections, covers all serotypes, does not contribute to ADE, is easily transported and stored, and is both affordable and cost-effective.[38] A number of vaccines are currently undergoing testing.[10][29][38] It is hoped that the first products will be commercially available by 2015.[23] Apart from attempts to control the spread of the Aedes mosquito and work to develop a vaccine against dengue, there are ongoing efforts to develop antiviral drugs that might be used to treat attacks of dengue fever and prevent severe complications.[39][40] Discovery of the structure of the viral proteins may aid the development of effective drugs.[40] There are several plausible targets. The first approach is inhibition of the viral RNA-dependent RNA polymerase (coded by NS5), which copies the viral genetic material, with nucleoside analogs. Secondly, it may be possible to develop specific inhibitors of the viral protease (coded by NS3), which splices viral proteins.[41] Finally, it may be possible to develop entry inhibitors, which stop the virus entering cells, or inhibitors of the 5' capping process, which is required for viral replication.[39] Notes ^ a b c d e f g h i j k l m Whitehorn J, Farrar J (2010). "Dengue". Br. Med. Bull. 95: 161–73. doi:10.1093/bmb/ldq019. PMID 20616106. ^ a b c d e f g WHO (2009), pp. 14–16 ^ Gubler (2010), p. 379 ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa Ranjit S, Kissoon N (July 2010). "Dengue hemorrhagic fever and shock syndromes". Pediatr. Crit. Care Med. 12 (1): 90–100. doi:10.1097/PCC.0b013e3181e911a7. PMID 20639791. ^ a b c d e f Varatharaj A (2010). "Encephalitis in the clinical spectrum of dengue infection". Neurol. India 58 (4): 585–91. doi:10.4103/0028-3886.68655. PMID 20739797. ^ a b c d e f g h Chen LH, Wilson ME (October 2010). "Dengue and chikungunya infections in travelers". Curr. Opin. Infect. Dis. 23 (5): 438–44. doi:10.1097/QCO.0b013e32833c1d16. PMID 20581669. ^ a b c d e f g h i j k l WHO (2009), pp. 25–27 ^ a b c d e f g h i j Rodenhuis-Zybert IA, Wilschut J, Smit JM (August 2010). "Dengue virus life cycle: viral and host factors modulating infectivity". Cell. Mol. Life Sci. 67 (16): 2773–86. doi:10.1007/s00018-010-0357-z. PMID 20372965. ^ a b c d e Gould EA, Solomon T (February 2008). "Pathogenic flaviviruses". The Lancet 371 (9611): 500–9. doi:10.1016/S0140-6736(08)60238-X. PMID 18262042. ^ a b c d e f g h i j k l m Guzman MG, Halstead SB, Artsob H, et al. (December 2010). "Dengue: a continuing global threat". Nat. Rev. Microbiol. 8 (12 Suppl): S7–S16. doi:10.1038/nrmicro2460. PMID 21079655. ^ a b c d e f WHO (2009), pp. 59–60 ^ "Vector-Borne Viral Infections". World Health Organization. Retrieved 17 January 2011. ^ a b c d Center for Disease Control and Prevention. "Chapter 5 – Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF)". 2010 Yellow Book. Retrieved 2010-12-23. ^ Gubler (2010), pp. 377–78 ^ Wilder-Smith A, Chen LH, Massad E, Wilson ME (January 2009). "Threat of dengue to blood safety in dengue-endemic countries". Emerg. Infect. Dis. 15 (1): 8–11. doi:10.3201/eid1501.071097. PMC 2660677. PMID 19116042. ^ Stramer SL, Hollinger FB, Katz LM, et al. (August 2009). "Emerging infectious disease agents and their potential threat to transfusion safety". Transfusion 49 Suppl 2: 1S–29S. doi:10.1111/j.1537-2995.2009.02279.x. PMID 19686562. ^ Teo D, Ng LC, Lam S (April 2009). "Is dengue a threat to the blood supply?". Transfus Med 19 (2): 66–77. doi:10.1111/j.1365-3148.2009.00916.x. PMC 2713854. PMID 19392949. ^ a b c d e Martina BE, Koraka P, Osterhaus AD (October 2009). "Dengue virus pathogenesis: an integrated view". Clin. Microbiol. Rev. 22 (4): 564–81. doi:10.1128/CMR.00035-09. PMC 2772360. PMID 19822889. ^ a b c d e f g h WHO (2009), pp. 10–11 ^ a b c WHO (1997). "Chapter 2: clinical diagnosis". Dengue haemorrhagic fever: diagnosis, treatment, prevention and control (2nd ed.). Geneva: World Health Organization.. pp. 12–23. ISBN 9241545003. ^ a b WHO (2009), pp. 90–95 ^ a b Gubler (2010), p. 380 ^ a b c d WHO (2009), p. 137 ^ a b c WHO (2009), pp. 32–37 ^ a b c d WHO (2009), pp. 40–43 ^ WHO media centre (March 2009). "Dengue and dengue haemorrhagic fever". World Health Organization. Retrieved 2010-12-27. ^ Neglected Tropical Diseases. "Diseases covered by NTD Department". World Health Organization. Retrieved 2010-12-27. ^ a b WHO (2009), p. 3 ^ a b c Barrett AD, Stanberry LR (2009). Vaccines for biodefense and emerging and neglected diseases. San Diego: Academic. pp. 287–323. ISBN 0-12-369408-6. ^ a b c Anonymous (2006). "Etymologia: dengue". Emerg. Infec. Dis. 12 (6): 893. ^ Harper D (2001). "Etymology: dengue". Online Etymology Dictionary. Retrieved 2008-10-05. ^ Anonymous (1998-06-15). "Definition of Dandy fever". MedicineNet.com. Retrieved 2010-12-25. ^ a b c d Halstead SB (2008). Dengue (Tropical Medicine: Science and Practice). River Edge, N.J: Imperial College Press. pp. 1–10. ISBN 1-84816-228-6. ^ Rush AB (1789). "An account of the bilious remitting fever, as it appeared in Philadelphia in the summer and autumn of the year 1780". Medical enquiries and observations. Philadelphia, Pa.: Prichard and Hall. pp. 104–117. ^ a b c d Gubler DJ (July 1998). "Dengue and dengue hemorrhagic fever". Clin. Microbiol. Rev. 11 (3): 480–96. PMC 88892. PMID 9665979. ^ a b Henchal EA, Putnak JR (October 1990). "The dengue viruses". Clin. Microbiol. Rev. 3 (4): 376–96. PMC 358169. PMID 2224837. ^ a b WHO (2009), p. 71 ^ a b c Webster DP, Farrar J, Rowland-Jones S (November 2009). "Progress towards a dengue vaccine". Lancet Infect Dis 9 (11): 678–87. doi:10.1016/S1473-3099(09)70254-3. PMID 19850226. ^ a b Sampath A, Padmanabhan R (January 2009). "Molecular targets for flavivirus drug discovery". Antiviral Res. 81 (1): 6–15. doi:10.1016/j.antiviral.2008.08.004. PMC 2647018. PMID 18796313. ^ a b Noble CG, Chen YL, Dong H, et al. (March 2010). "Strategies for development of Dengue virus inhibitors". Antiviral Res. 85 (3): 450–62. doi:10.1016/j.antiviral.2009.12.011. PMID 20060421. ^ Tomlinson SM, Malmstrom RD, Watowich SJ (June 2009). "New approaches to structure-based discovery of dengue protease inhibitors". Infectious Disorders Drug Targets 9 (3): 327–43. PMID 19519486. References Gubler DJ (2010). "Dengue viruses". In Mahy BWJ, Van Regenmortel MHV. Desk Encyclopedia of Human and Medical Virology. Boston: Academic Press. ISBN 0-12-375147-0. WHO (2009). Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. World Health Organization. ISBN 9241547871. External links Find more about Dengue fever on Wikipedia's sister projects: Definitions from Wiktionary Images and media from Commons Learning resources from Wikiversity News stories from Wikinews Quotations from Wikiquote Source texts from Wikisource Textbooks from Wikibooks Dengue fever at the Open Directory Project "Dengue". WHO. Retrieved 2010-12-24. "Dengue". US Centers for Disease Control and Prevention. Retrieved 2010-12-24. "Dengue fever". UK Health Protection Agency. Retrieved 2010-12-24. [hide]v · d · eZoonotic viral diseases (A80–B34, 042–079) Arthropod/ (arbovirus) Mosquito Bunyaviridae Arbovirus encephalitis: La Crosse encephalitis (LCV) · California encephalitis (CEV) Viral hemorrhagic fever: Rift Valley fever (RVFV) Flaviviridae Arbovirus encephalitis: Japanese encephalitis (JEV) · Australian encephalitis (MVEV, KUNV) · St. Louis encephalitis (SLEV) · West Nile fever (WNV) Viral hemorrhagic fever: Dengue fever (DV) other: Yellow fever (YFV) · Zika fever Togaviridae Arbovirus encephalitis: Eastern equine encephalomyelitis (EEEV) · Western equine encephalomyelitis (WEEV) · Venezuelan equine encephalomyelitis (VEEV) other: Chikungunya (CV) · O'Nyong-nyong fever (OV) · Ross River fever (RRV) Tick Bunyaviridae Viral hemorrhagic fever: Crimean-Congo hemorrhagic fever (CCHFV) Flaviviridae Arbovirus encephalitis: Tick-borne encephalitis (TBEV) · Powassan encephalitis (PV) · Deer tick virus encephalitis (DTV) Viral hemorrhagic fever: Omsk hemorrhagic fever (OHFV) · Kyasanur forest disease (KFDV/Alkhurma virus)) · Langat virus (LGTV) Reoviridae Colorado tick fever (CTFV) Mammal Rodent (Robovirus) Arenaviridae Viral hemorrhagic fever: Lassa fever (LV) · Venezuelan hemorrhagic fever (Guanarito virus) · Argentine hemorrhagic fever (Junin virus) · Bolivian hemorrhagic fever (Machupo virus) · Lujo virus Bunyaviridae Puumala virus · Andes virus · Sin Nombre virus · Hantavirus (HV) Bat Filoviridae VHF: Ebola hemorrhagic fever · Marburg hemorrhagic fever Rhabdoviridae Australian bat lyssavirus · Mokola virus · Duvenhage virus · Lagos bat virus · Chandipura virus(sandfly) Bornaviridae Menangle · Henipavirus · Borna disease (Borna disease virus) Multiple Rhabdoviridae Rabies (RV) M: VIR virs(prot)/clss cutn/syst (hppv/hiva, infl/zost/zoon)/epon drugJ(dnaa, rnaa, rtva, vacc) Retrieved from "http://en.wikipedia.org/wiki/Dengue_fever"

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