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HIV virus, disease
Did you mean: AIDS (in medicine), human immunodeficiency virus (medical term), HIV (abbreviation) Dictionary Home > Library > Words > Dictionary HIV (āch'ī-vē') n. A retrovirus that causes AIDS by infecting helper T cells of the immune system. The most common serotype, HIV-1, is distributed worldwide, while HIV-2 is primarily confined to West Africa. [H(UMAN) I(MMUNODEFICIENCY) V(IRUS).]

Genetics Encyclopedia

Home > Library > Health > Genetics Encyclopedia HIV HIV, the human immunodeficiency virus, is the virus that causes AIDS, a debilitating and deadly disease of the human immune system. HIV is one of the world's most serious health problems: at the end of 2001, more than 40 million people worldwide were infected with HIV and living with the virus or AIDS. The World Health Organization estimates that about 20 million people have died from AIDS since the infection was first described in 1981. Nearly 500,000 of those deaths have occurred in the United States. Although there is no cure for the disease, therapies exist that reduce

the symptoms of AIDS and can extend the life spans of HIV-infected individuals. Researchers are also pursuing protective vaccines, but a reliable vaccine might still require years to develop.
Hiv and Aids

HIV infects certain cells and tissues of the human immune system and takes them out of commission, rendering a person susceptible to a variety of infections and cancers. These infections are caused by so-called opportunistic agents, pathogens that take advantage of the compromised immune system but that would be unable to cause infection in people with a healthy immune system. Rare cancers such as Kaposi's sarcoma also take hold in HIV-infected individuals. The collection of diseases that arise because of HIV infection is called acquired immune deficiency syndrome, or AIDS. HIV is classified as a lentivirus ("lenti" means "slow") because the virus takes a long time to produce symptoms in an infected individual.
Hiv Life Cycle: Entering Cells

Like a typical virus, HIV infects a cell and appropriates the host's cellular components and machinery to make many copies of itself. The new viruses then break out of the cell and infect other cells. HIV stores its genetic information on an RNA molecule rather than a DNA chromosome. This is a distinguishing characteristic of retroviruses, which are viruses that must first convert their RNA genomes into DNA before they can reproduce. Each HIV virion (viral particle) is a small sphere composed of several layers. The external layer is a membrane coat, or envelope, obtained from the host cell in which the particle was made. Underneath this membrane lies a shell made from proteins, called a nucleocapsid. Inside the protein shell are two copies of the virion's RNA genome and three kinds of proteins, which are used by the virion to establish itself once inside the cell that it infects. Two proteins, called gp120 and gp41, enable the virion to recognize the type of cell to enter. These proteins project from the HIV membrane coat. Gp120 binds to two specific proteins found on the target cell's surface (these target-cell proteins are called receptors). The first receptor, CD4, is found on immune system cells known as CD4 T cells, and also sometimes on two cell types known as macrophages and dendritic cells. The immune system uses CD4 T cells in the initial step in making antibodies against infectious agents. After binding to CD4, the HIV protein called gp120 binds with a second cell membrane protein, commonly referred to as the co-receptor. The co-receptor can be one of many different proteins, depending on the cell type. The two most common are CXCR4, which is normally found on CD4 T cells, and CCR5, a receptor found on CD4 T cells as well as on certain macrophages and dendritic cells. In the absence of HIV, CXCR4 and CCR5 allow these immune system cells to respond to chemical signals, but when HIV infects the cells, the HIV commandeers their usage. In some cases, individuals have a mutation in their co-receptor that prevents HIV from entering their cells. Once gp120 has bound to both the CD4 receptor and co-receptor, the gp41 protein fuses HIV's membrane envelope with the cellular membrane, injecting the virus into

Other proteins include those that make up the protein shell. however. These cells are responsible for recognizing foreign invaders to a person's body and initiating antibody production to ward off the infection. most of the RNA molecules remain in the nucleus long enough to get processed. and replicase. some of whose functions are not well understood. the resting place for CD4 T cells. However. These RNA molecules are then processed in the nucleus to become templates for several of the HIV proteins. and the life cycle halts. Tat encourages the cellular machinery to copy HIV's proviral DNA into RNA molecules. waiting for the T cell to become activated by the immune system. the reverse transcriptase.the target cell. Once in the cytoplasm. then drawing in two unprocessed RNA molecules and filling up the remaining space with integrase. The new virions bud from the host-cell membrane. These RNA molecules. the protein that trims. and dendritic cells. Along with the normal cellular protein products. where they are being reproduced. more Rev is made. the T cells start producing many proteins. Rev. into the host cell's cytoplasm. At this point. Early in HIV reproduction. As time passes. The viral integrase then helps insert the DNA copies into the cell's chromosome. HIV destroys the T cells slowly. becomes increasingly full of HIV. One of the proteins in the chain is the protease. people are susceptible to a variety of diseases. The reverse transcriptase copies the RNA strands into DNA. The mature virus particles are now ready to infect other cells. become templates to make different HIV proteins. a T cell carrying an HIV provirus also produces HIV proteins. a viral integrase. . the viral protein shell opens up and releases the viral proteins—a reverse transcriptase. which have undergone little or no processing. The first HIV proteins made are called Tat and Rev. appropriating some of that membrane to form an outer coat in the process. with only a few RNA molecules from which to make protein. Hiv Life Cycle: Reproduction When the immune system recruits T cells to fight an infection. in all the time before an HIV-infected individual shows any symptoms. and viral particles are also released into the bloodstream. After the newly created proteins are processed to the right size. and integrase. sometimes taking a decade to destroy a person's immunity. they form new virions by first assembling into a shell. The newer proteins are made in long chains that require trimming before they become functional. the virus has been reproducing rapidly. protease. on the other hand. Hiv's Immune-System Impairment Mechanism One of the most disastrous effects of HIV infection is the loss of the immune system's CD4 T cells. a small quantity of Rev is made. and a protease—along with the viral RNA strands. The lymph tissue. Therefore. the virus is called a provirus. and Tat continues to instigate RNA production. macrophages. The provirus may remain dormant in the cell's chromosome for months or years. Without them. A higher amount of Rev protein increases the speed with which RNA molecules are ejected from the nucleus. ushers the HIV's RNA molecules from the nucleus.

In addition. it kills them indirectly by causing the cells to "commit suicide" by inducing apoptosis. without therapeutic intervention. Drugs called protease inhibitors prevent the viral protease from trimming down the large proteins . Thus. patients can acquire cancers such as B-cell lymphoma. the immune system must generate new antibodies to fight the infection. Known as "highly active antiretroviral therapy" (HAART). a healthy person counts more than 1. It kills them directly by reproducing within them. The chickenpox virus may come out of dormancy. or it kills them indirectly by triggering other immune cells to recognize the infected T cell and kill it as part of the immune system's normal function. then breaking them upon exit. Unfortunately. Targeting Life-Cycle Points Drugs meant to knock out HIV target the activities of two HIV proteins. An obscure form of pneumonia. Meanwhile. an HIV infection is a dramatic balance between a replicating. they are either actively killed or induced to commit suicide. the immune system can no longer ward off the daily bombardment of pathogens that all human organisms experience. is also common in AIDS patients. With each new protein. As infected T cells die. People infected with HIV who are treated by HAART are now living longer. eventually loses the battle. however. HIV presents its proteins to the immune system. As with any infectious agent. ever changing virus and the replenishing stores of T cells that are fighting it. however.) Anti-Hiv Drug Therapy Drugs that interfere with viral replication can slow down HIV disease. Common infectious agents thus overwhelm the system. Since 1995.000. is hampered by the fact that HIV mutates rapidly. This antibody production. the immune system.HIV's main target is the population of CD4 T cells within a host's body. manifesting itself as the painful disease known as shingles. These include unusual fungal infections such as thrush. HAART requires drugs of both types. HIV kills them in one of three ways. which is a cancer of the immune system. AIDS doctors report at least twenty-six different opportunistic diseases specific to HIV infection. Once the CD4 T cells are depleted. Doctors generally consider patients with fewer than 200 CD4 T cells per cubic milliliter of blood as having AIDS. doctors have found that rotating patients through three different drugs in very high doses significantly improves the health of AIDS patients. this therapeutic approach also reduces the amount of HIV circulating in the bloodstream to nearly undetectable levels. the HIV virus is not completely hidden from the immune system. the reverse transcriptase and the protease. Early trials relied on the administration of one drug at a time. and HIV patients become susceptible to a variety of "opportunistic" diseases that take advantage of the body's reduced ability to fight them off. in time HIV mutated enough to render the drugs ineffective. changing the proteins it displays to the immune system. (In contrast. which develops antibodies against it. called pneumocystis pneumonia. healthier lives than ever before. the immune system generates more to take their place. As new T cells become infected. While patients' health improved and their T cell count rose.

the AZT caps the growing DNA molecule and halts DNA production.made late during infection.. by sharing hypodermic needles or by accidental needle sticks).. the reverse transcriptase and the integrase. New York: PrenticeHall. Multidrug "cocktails" can delay onset. leaving the host unprotected against infection. Like other viruses. Without those proteins. 2001. et al. HIV needs a host cell to multiply.g. HIV attacks and gradually destroys the immune system." In Immunobiology: The Immune System in Health and Disease. A rapid mutation rate helps it foil both the immune system and treatment attempts. 1999. The virus first multiplies in lymph nodes near the site of infection. Gerald. and avoidance of needle sharing have reduced infection rates in some areas. Stine.S. Acquired Immune Deficiency Syndrome: Biological. People. the proteins that reproduce HIV's genetic information. Randy. In addition. Reverse transcriptase inhibitors include azidothymidine (AZT). 1997. or breast milk. 3rd ed. Shilts. 2000. marking the onset of AIDS. Once it spreads through the body. Drugs that inhibit the reverse transcriptase prevent it from copying the RNA into DNA. —Mary Beckman Britannica Concise Encyclopedia Home > Library > Reference > Britannica Concise Encyclopedia HIV Retrovirus associated with AIDS. whose structure resembles the DNA nucleotide thymine. For more information on HIV. When reverse transcriptase builds DNA with AZT instead of thymine. . A pregnant woman can pass the virus to her fetus across the placenta. semen and female genital secretions. Social and Legal Issues. New York: St. Department of Health and Human Services. "Failures of Host Defense Mechanisms. These drugs work early in the life cycle of HIV. It cannot be spread through casual contact but instead is contracted mainly through exposure to blood and blood products (e. Bibliography Janeway. are not functional. and the AIDS Epidemic. Martin's Press. usually about 10 years later. No vaccine or cure exists. but missing doses can lead to drug resistance. due to AZT's slight difference in structure from the thymine that DNA production requires. visit Britannica. symptoms appear. Abstinence from sex. And the Band Played On: Politics.com. 4th ed. ———. use of condoms or other means to prevent sexual transmission of the disease. It attacks helper T cells and can infect other cells. Washington DC: National Institute of Allergy and Infectious Diseases and U. Medical. HIV Infection and AIDS: An Overview. Charles A. the viral shell cannot be assembled. New York: Current Biology Publications.

Scientists surmise that it jumped from an animal population. There are two types of HIV: HIV-1 and HIV-2. before it succumbs and permits the well-known signs of AIDS to develop. Wikipedia Home > Library > Reference > Wikipedia HIV Human immunodeficiency virus . The first case documented in humans dates from 1959.Columbia Encyclopedia Home > Library > Reference > Columbia Encyclopedia HIV (Human Immunodeficiency Virus). has a slower course than HIV-1. probably African monkeys or chimpanzees. producing billions of CD4 cells daily. either of two closely related retroviruses that invade T-helper lymphocytes and are responsible for AIDS. HIV-2. the virus that causes AIDS. The resultant viral DNA inserts itself into a cell's DNA and is reproduced along with the cell and its daughters. seen more often in western Africa. HIV-1 is responsible for the vast majority of AIDS in the United States. an enzyme called reverse transcriptase allows it to act as the template for its own RNA to DNA transcription. The virus was isolated by Luc Montagnier of France's Pasteur Institute in 1983. CD4. In many cases. There are many strains of both types and the virus mutates rapidly. Health Dictionary Home > Library > Health > Health Dictionary HIV (aych-eye-VEE) An abbreviation for human immunodeficiency virus. was agreed upon. a person's immune system will fight off the invasion of HIV for many years. Receptors on these cells appear to enable the viral RNA to enter the cell. always trying to keep up with the HIV's mutations. once the RNA is inside the cell. or T-helper lymphocytes) that would ordinarily fight off such a viral infection. It went through several name changes before the official name. The exact origin of the virus in humans is unclear. As with all retroviruses. HIV is especially lethal because it attacks the very immune system cells (variously called T4. a trait that has made it especially difficult for researchers to find an effective treatment or vaccine. to humans via a bite or meat. human immunodeficiency virus.

or through breast milk. and transmission from an infected mother to her baby at birth. HIV is present as both free virus particles and virus within infected immune cells. or AIDS-associated retrovirus (ARV). a condition in humans in which the immune system begins to fail. contaminated needles. preejaculate. Previous names for the virus include human T-lymphotropic virus-III (HTLV-III). vaginal fluid. leading to life-threatening opportunistic infections. semen. lymphadenopathy-associated virus (LAV). The four major routes of transmission are unprotected sexual intercourse. or breast milk. [1][2] Infection with HIV occurs by the transfer of blood. .Stylized rendering of a cross section of the human immunodeficiency virus Virus classification Group: Group VI (ssRNA-RT) Family: Retroviridae Genus: Lentivirus Species Human immunodeficiency virus 1 Human immunodeficiency virus 2 • • International Statistical Classification of Diseases and Related Health Problems Codes Classification & external resources ICD-10 B20-B24 ICD-9 042-044 Human immunodeficiency virus (HIV) is a retrovirus that can lead to acquired immunodeficiency syndrome (AIDS). Within these bodily fluids.

the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on December 1. macrophages and dendritic cells. with no noticeable symptoms. In 2005 alone. When CD4+ T cell numbers decline below a critical level. of which more than 570. making it one of the most destructive pandemics in recorded history. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly. killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. If untreated. enveloped RNA viruses. HIV infection in humans is now pandemic. positive-sense. Origin and discovery See AIDS origin. retarding economic growth and increasing poverty.[4] According to current estimates.4–3. Upon entry of the target cell. As of January 2006. increases the life expectancy of people infected with HIV.[5] Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection. direct viral killing of infected cells. where available. . cell-mediated immunity is lost. resulting in a minimum estimate of 18 million orphans.[6] HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells).3 million lives.6% of the world's living population is infected with HIV.000 were children. increased rates of apoptosis in infected cells. It is hoped that current and future treatments may allow HIV-infected individuals to achieve a life expectancy approaching that of the general public (see Treatment). 1981.[9] Lentiviruses have many common morphologies and biological properties. Classification HIV was classified as a member of the genus Lentivirus.[7] Treatment with anti-retrovirals. and a large number of virus particles are liberated that can then infect other cells. which are characteristically responsible for long-duration illnesses with a long incubation period. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase so that the genome can be transcribed. and thirdly. or the virus becomes active and replicates. the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. AIDS claimed an estimated 2.Screening of blood products for HIV in the developed world has largely eliminated transmission through blood transfusions or infected blood products in these countries. and the body becomes progressively more susceptible to opportunistic infections.[10] Lentiviruses are transmitted as single-stranded. HIV is set to infect 90 million people in Africa. Many species are infected by lentiviruses. two pathways are possible: either the virus becomes latent and the infected cell continues to function. It is estimated that about 0. secondly. eventually most HIV-infected individuals develop AIDS (Acquired Immunodeficiency Syndrome) and die.[3] A third of these deaths are occurring in subSaharan Africa.[8] part of the family of Retroviridae. however about one in ten remains healthy for many years. Once the virus has infected the cell. but routine access to antiretroviral medication is not available in all countries.

such as the reuse of needles in Third World countries. It is also of concern for persons receiving medical care in regions where there is prevalent substandard hygiene in the use of injection equipment. Transmission For more details on this topic. hemophiliacs and recipients of blood transfusions (though most transfusions are checked for HIV in the developed world) and blood products.[11] [12] HIV-1 is the virus that was initially discovered and termed LAV.5[19] * assuming no condom use Since the beginning of the pandemic. oral.500[16] Needle-sharing injection drug use 67[17] * Receptive anal intercourse 50[18][19] Percutaneous needle stick 30[20] * Receptive penile-vaginal intercourse 10[18][19][21] * Insertive anal intercourse 6. Sexual transmission can occur when infected sexual secretions of one partner come into contact with the genital. three main transmission routes for HIV have been identified: • • Sexual route.[13] HIV-1 is more virulent.5[18][19] * Insertive penile-vaginal intercourse 5[18][19] Receptive fellatio* 1[19] * Insertive fellatio 0. HIV-2 may have originated from the Sooty Mangabey (Cercocebus atys). The majority of HIV infections are acquired through unprotected sexual relations. Blood or blood product route. This transmission route can account for infections in intravenous drug users. an Old World monkey of Guinea-Bissau. or rectal mucous membranes of another. see AIDS transmission and prevention Estimated per act risk for acquisition of HIV-1 by exposure route[14] Estimated infections Exposure Route per 10. It is easily transmitted and is the cause of the majority of HIV infections globally.000[15] Childbirth 2.000 exposures to an infected source Blood Transfusion 9.Two species of HIV infect humans: HIV-1 and HIV-2. Health care workers . HIV can also be spread through the sharing of needles. HIV-1 is thought to have originated in southern Cameroon after jumping from wild chimpanzees (Pan troglodytes troglodytes) to humans during the twentieth century. Gabon.[13] Early history See AIDS origin#History of known cases and spread for early cases of HIV / AIDS. HIV2 is less transmittable and is largely confined to West Africa. and Cameroon.

and scarification procedures can also be at risk of infection. and 48% respectively. when used alone or with vaginal contraceptives like a diaphragm.[28] South African medical experts are concerned that the repeated use of unsterilized blades in the ritual (not medical) circumcision of adolescent boys may be spreading HIV. and doctors. it should not be considered a barrier to infection. but there are no recorded cases of infection by these secretions and the potential risk of transmission is negligible. a panel of experts convened by WHO and the UNAIDS Secretariat has "recommended that male circumcision now be recognized as an additional important intervention to reduce the risk of heterosexually acquired HIV infection in men.• such as nurses. As a result. actually increases the male to female transmission rate due to inflammation of the vagina. although this occurs more rarely. Spermicide. in which uncircumcised men were randomly assigned to be medically circumcised in sterile conditions and given counseling and other men were not circumcised.[16] Breast feeding also presents a risk of infection for the baby. Mother-to-child transmission (MTCT). People who give and receive tattoos."[27] Research is clarifying whether there is a historical relationship between rates of male circumcision and rates of HIV in differing social and cultural contexts. this can be reduced to 1%.[22] The use of physical barriers such as the latex condom is widely advocated to reduce the sexual transmission of HIV. tears and urine of infected individuals. 53%. HIV-2 is transmitted much less frequently by the MTCT and sexual route than HIV-1.[29] Structure and genome Main article: HIV structure and genome Diagram of HIV . laboratory workers. HIV has been found at low concentrations in the saliva. The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. where drug treatment and Cesarian section are available. Critics point out that any correlation between circumcision and HIV is likely to come from cultural factors (which govern not only whether someone is circumcised. the transmission rate between the mother and child is 25%.[23] Trials. have also been infected. In the absence of treatment.[24] Kenya[25] and Uganda[26] showing reductions in HIV transmission for heterosexual sex of 60%. piercings.[16] However. have been conducted in South Africa. but also their sexual practices and beliefs).

consists of a cap made of three molecules called glycoprotein (gp) 120.[31] env. p7 and enzymes needed for the development of the virion such as reverse transcriptase.[33] Of the nine genes that are encoded within the RNA genome. in turn.000 copies of the viral protein p24. HIV can infect a variety of immune cells such as CD4+ T cells. HIV-1 entry to macrophages and CD4+ T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells and also with chemokine coreceptors. especially gp120. around 60 times smaller than a red blood cell) and roughly spherical. surrounded by the viral envelope which is composed of two layers of fatty molecules called phospholipids taken from the membrane of a human cell when a newly formed virus particle buds from the cell.[31] Tropism The term viral tropism refers to which cell types HIV infects. codes for a protein called gp160 that is broken down by a viral enzyme to form gp120 and gp41. vif.HIV is different in structure from other retroviruses. macrophages. gag. vpr. three of these genes. pol. They appear to be the first cells infected by HIV and perhaps the source of HIV production when CD4+ cells become depleted in the patient. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle. have been considered as targets of future treatments or vaccines against HIV. and vpu (or vpx in the case of HIV-2).[31] This is. ribonuclease and integrase.[31] The protein encoded by nef.[32] Macrophage (M-tropic) strains of HIV-1.[31] This protein.[34] This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. tat. Indeed. and the vpu-encoded protein influences the release of new virus particles from infected cells. and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.[32] Both these surface proteins. or cause disease.[31] The single-stranded RNA is tightly bound to nucleocapsid proteins. and microglial cells. It is about 120 nm in diameter (120 billionths of a meter. appears necessary for the virus to replicate efficiently.[31] The ends of each strand of HIV RNA contain an RNA sequence called the long terminal repeat (LTR). rev. Macrophages and microglial cells are the cells infected by .[30] It is composed of two copies of positive single-stranded RNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2. produce new copies of virus (replicate). or non-syncitia-inducing strains (NSI) use the β-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T cells. contain information needed to make the structural proteins for new virus particles. Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell. known as Env. are regulatory genes for proteins that control the ability of HIV to infect cells. macrophages play a key role in several critical aspects of HIV infection. and env.[32] This glycoprotein complex enables the virus to attach to and fuse with target cells to initiate the infectious cycle. for instance. proteases. nef. Embedded in the viral envelope are proteins from the host cell and about 70 copies of a complex HIV protein that protrudes through the surface of the virus particle. The six remaining genes. for example.

However. for entry. and those that use both. immune system collapse. but one model is that spermatozoa may selectively carry R5 HIV as they possess both CCR3 and CCR5 but not CXCR4 on their surface[42] and that genital epithelial cells preferentially sequester X4 virus.HIV in the central nervous system. phenotype.[44] These variants then replicate more aggressively with heightened virulence that causes rapid T cell depletion. Sexual intercourse is the major mode of HIV transmission. reducing its ability to infect target cells. T-tropic isolates. However. as not all R5 viruses are able to use CCR5 on macrophages for a productive infection[34] and HIV can also infect a subtype of myeloid dendritic cells. CXCR4. a ligand for CXCR4. HIV that use only the CCR5 receptor are termed R5. In tonsils and adenoids of HIV-infected patients. and presumably the X4. The α-chemokine. there is often a co-receptor switch in late-stage disease and T-tropic variants appear that can infect a variety of T cells through CXCR4. during the course of infection. the use of coreceptor alone does not explain viral tropism.[38] One example of how this occurs is people with the CCR5-Δ32 mutation. a selection process leads to a predominant transmission of the R5 virus through this pathway.[34][35][36] Dual-tropic HIV-1 strains are thought to be transitional strains of the HIV-1 virus and thus are able to use both CCR5 and LESTR as co-receptors for viral entry. SDF-1. The virions can then infect numerous cellular targets and disseminate into the whole organism. Some people are resistant to certain strains of HIV. suppresses replication of T-tropic HIV-1 isolates. viral adaptation to the use of CXCR4 instead of CCR5 may be a key step in the progression to AIDS. those that only use CXCR4 are termed X4. A number of studies with subtype B-infected individuals have determined that between 40 and 50% of AIDS patients can harbour viruses of the SI.[39][40][41] How this selective process works is still under investigation. Both X4 and R5 HIV are present in the seminal fluid which is passed from partner to partner.[43] In patients infected with subtype B HIV-1. X4R5. macrophages fuse into multinucleated giant cells that produce huge amounts of virus. these people are resistant to infection with R5 virus as the mutation stops HIV from binding to this coreceptor.[46][47] Replication cycle .[37] which probably constitute a reservoir that maintains infection when CD4+ T cell numbers have declined to extremely low levels. or syncitia-inducing (SI) strains replicate in primary CD4+ T cells as well as in macrophages and use the α-chemokine receptor.[45] Thus. It does this by down-regulating the expression of CXCR4 on the surface of these cells. and opportunistic infections that mark the advent of AIDS.

are injected into the cell. exposing the chemokine binding domains of gp120 and allowing them to interact with the target chemokine receptor.[48][49] Repeat sequences in gp41. allowing fusion of the membranes and subsequent entry of the viral capsid.[48][49] The gp160 spike contains binding domains for both CD4 and chemokine receptors. The HIV replication cycle Entry to the cell HIV enters macrophages and CD4+ T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell. the HIV RNA and various enzymes.[48][49] Once HIV has bound to the target cell.Schematic representation of the key structural features of HIV-1 entry into T cells.[48] . This loop structure brings the virus and cell membranes close together. which allows the N-terminal fusion peptide gp41 to penetrate the cell membrane.[48][49] The first step in fusion involves the highaffinity attachment of the CD4 binding domains of gp120 to CD4. HR1 and HR2 then interact.[48][49] This allows for a more stable two-pronged attachment. causing the collapse of the extracellular portion of gp41 into a hairpin. the envelope complex undergoes a structural change. Once gp120 is bound with the CD4 protein. including reverse transcriptase. discussed above) and both CD4 and a chemokine receptor (generally either CCR5 or CXCR4 but others are known to interact) on the cell surface. integrase. The two bottom images show alternate models for entry into cells.[48][49] The interactions of the trimeric envelope complex (gp160 spike. ribonuclease and protease.

This may mean that HIV-1 is better able to .[51] This process of reverse transcription is extremely errorprone and it is during this step that mutations may occur. The integration of the viral DNA into the host cell's genome is carried out by another viral enzyme called integrase. HIV-1 will bind to any appropriate RNA whereas HIV-2 will preferentially bind to the mRNA which was used to create the Gag protein itself. HIV-1 and HIV-2 appear to package their RNA differently. in the latent stage of HIV infection. The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA intermediate (vDNA). the integrated provirus is copied to mRNA which is then spliced into smaller pieces.[50] Replication and transcription Once the viral capsid enters the cell. the most important of which is NF-κB (NF kappa B). As Rev accumulates it gradually starts to inhibit mRNA splicing. These small pieces produce the regulatory proteins Tat (which encourages new virus production) and Rev. blue) to mediate export of unspliced and singly spliced mRNA from the nucleus to the cytoplasm. it binds to the Gag protein and is packaged into new virus particles. the structural proteins Gag and Env are produced from the full-length mRNA.[51] This integrated viral DNA may then lie dormant. an enzyme called reverse transcriptase liberates the single-stranded (+)RNA from the attached viral proteins and copies it into a complementary DNA. certain cellular transcription factors need to be present. They are currently thought to play an important role by transmitting HIV to T cells once the virus has been captured in the mucosa by DCs. [51] To actively produce the virus.[53] At this stage. In this replication process. but another route using mannose-specific C-type lectin receptors such as DC-SIGN can also be used. The full-length RNA is actually the virus genome.[52] This means that those cells most likely to be killed by HIV are in fact those currently fighting infection. Rev-mediated HIV mRNA transport. which is upregulated when T cells become activated. Such mutations may cause drug resistance. This vDNA is then transported into the cell nucleus. Rev (red) binds the Rev response element (RRE.[50] DCs are one of the first cells encountered by the virus during sexual transmission.HIV can infect dendritic cells (DCs) by this CD4-CCR5 route.

the genome of progeny virions may be composed of RNA strands from two different strains. The phylogenetic tree of the SIV and HIV (click on image for a detailed description).[54] This cleavage step can be inhibited by protease inhibitors. Assembly and release The final step of the viral cycle. begins at the plasma membrane of the host cell. These are transported to the plasma membrane of the host cell where gp41 anchors the gp120 to the membrane of the infected cell. The Env polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi complex where it is cleaved by protease and processed into the two HIV envelope glycoproteins gp41 and gp120. the more infections are present.mutate (HIV-1 infection progresses to AIDS faster than HIV-2 infection and is responsible for the majority of global infections). When simultaneous infection occurs. The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell. HIV proteases cleave the polyproteins into individual functional HIV proteins and enzymes. This hybrid virion then . During maturation. The mature virus is then able to infect another cell. Map showing HIV-1 subtype prevalence. Maturation either occurs in the forming bud or in the immature virion after it buds from the host cell.[55] This variability is compounded when a single cell is simultaneously infected by two or more different strains of HIV. The bigger the pie chart. Genetic variability HIV differs from many other viruses as it has very high genetic variability. assembly of new HIV-1 virons.[55] This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day. coupled with a high mutation rate of approximately 3 x 10-5 per nucleotide base per cycle of replication and recombinogenic properties of reverse transcriptase. with the generation of 109 to 1010 virions every day. This diversity is a result of its fast replication cycle. The various structural components then assemble to produce a mature HIV virion.

African green monkeys and sooty mangabeys. Coinfection with distinct subtypes gives rise to circulating recombinant forms (CRFs). and disease progression is unknown.[55] The closely related simian immunodeficiency virus (SIV) exhibits a somewhat different behavior: in its natural hosts.[63] The genetic sequence of HIV-2 is only partially homologous to HIV-1 and more closely resembles that of SIV than HIV-1. these heterologous hosts also develop simian AIDS.[61] The most prevalent are subtypes B (found mainly in North America and Europe). N.2% were of CRF_AE.[60] Group M is the most prevalent and is subdivided into eight subtypes (or clades). AIDS Symptoms and Complications and WHO Disease Staging System for HIV Infection and Disease . Three groups of HIV-1 have been identified on the basis of differences in env: M. the reverse transcriptase. 5. few laboratories focus on the other subtypes. based on the whole genome. and C (found mainly in Africa and Asia). but evokes only a mild immune response. by jumping back and forth between the two different RNA templates.[56] does not cause the development of simian AIDS. A and D (found mainly in Africa). and O. and the remaining 5. As this happens. 3. if any.7% were of subtype A/CRF02_AG. The clinical course of infection For more details on this topic. these subtypes form branches in the phylogenetic tree representing the lineage of the M group of HIV-1.infects a new cell where it undergoes replication. infection of heterologous hosts (rhesus or cynomologus macaques) with SIV results in the generation of genetic diversity that is on the same order as HIV in infected humans.[58] By contrast. between genetic diversification. In 2000.[62] Most HIV-1 research is focused on subtype B.3% were of subtype D. see AIDS Diagnosis. immune response. 47. the last year in which an analysis of global subtype prevalence was made.3% were of subtype B. will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes. 26.[57] and does not undergo the extensive mutation and recombination typical of HIV. which are geographically distinct. 12.[59] The relationship.[55] This recombination is most obvious when it occurs between subtypes.2% of infections worldwide were of subtype C.3% were composed of other subtypes and CRFs. the retrovirus is present in high levels in the blood.

or acute infection. Infected individuals may experience all. Even if patients go to their doctors or a hospital. though it does not eliminate the virus. and may also include. it is often not recognized as a sign of HIV infection. nausea and vomiting. However. This acute viremia is associated in virtually all patients with the activation of CD8+ T cells.[64] This response is accompanied by a marked drop in the numbers of circulating CD4+ T cells. headache. Symptoms have an average duration of 28 days and usually last at least a week although duration of symptoms may vary. The initial infection with HIV generally occurs after transfer of body fluids from an infected person to an uninfected one. the primary. they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. as the CD4+ T cell counts rebound to around 800 cells per mL (the normal value is 1200 cells per mL ). or none of these symptoms. rash. and neurological symptoms. myalgia. which kill HIV-infected cells. lymphadenopathy. The CD8+ T cell response is thought to be important in controlling virus levels. The stage of infection can be determined by measuring the patient's CD4+ T cell count. Consequently. or seroconversion. is a period of rapid viral replication that immediately follows the individual's exposure to HIV leading to an abundance of virus in the peripheral blood with levels of HIV commonly approaching several million viruses per mL. and subsequently with antibody production. The first stage of infection. thrush. which peak and then decline. the most common symptoms of which may include fever.A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection. CD4+ T cell count (cells per µL) HIV RNA copies per mL of plasma Infection with HIV-1 is associated with a progressive decrease of the CD4+ T cell count and an increase in viral load. these primary symptoms are not used to diagnose HIV infection as they do not develop in all cases and because many are caused by other more common diseases. recognizing the syndrome can be important because the patient is much more infectious during this period. weight loss. mouth and esophagal sores. but less commonly.[65] During this period (usually 2-4 weeks post-exposure) most individuals (80 to 90%) develop an influenza or mononucleosis-like illness called acute HIV infection. pharyngitis. [67] . enlarged liver/spleen. some.[66] Because of the nonspecific nature of these illnesses. and the level of HIV in the blood. A good CD8+ T cell response has been linked to slower disease progression and a better prognosis. any particular individual's disease course may vary considerably. malaise.

and oral ulcerations. During this early phase of infection. otitis media. and there are other tumors and infections that are less prominent but still significant. During this time. and infections with a variety of opportunistic microbes appear. Epstein-Barr virus-induced B-cell lymphomas. cell-mediated immunity is lost.History and physical findings for primary HIV infection[67] sensitivity specificity Fever 88% 50% Malaise 73% 58% Myalgia 60% 74% Rash 58% 79% Headache 55% 56% Night sweats 50% 68% Sore throat 43% 51% Lymphadenopathy 38% 71% Arthralgia 28% 87% Nasal congestion 18% 62% A strong immune defense reduces the number of viral particles in the blood stream. Not all patients with AIDS get all these infections or tumors. where large amounts of virus become trapped in the follicular dendritic cells (FDC) network. infection with cytomegalovirus (another herpes virus) or Mycobacterium avium complex is more prominent. HIV is active within lymphoid organs. resistance is lost early on to oral Candida species and to Mycobacterium tuberculosis. Individuals who are in this phase are still infectious. most of which are normally controlled by robust CD4+ T cell-mediated immunity then start to affect the patient. The first symptoms often include moderate and unexplained weight loss. Typically. a tumor of endothelial cells that occurs when HIV proteins such as Tat interact with Human Herpesvirus-8. bronchitis.[70] Furthermore. In the final stages of AIDS.[68] The surrounding tissues that are rich in CD4+ T cells may also become infected. only . recurring respiratory tract infections (such as sinusitis.[70] For example. Clinical latency can vary between two weeks and 20 years. less than 1% of the sexually active urban population in Africa have been tested and this proportion is even lower in rural populations. CD4+ CD45RO+ T cells carry most of the proviral load. reactivation of latent herpes viruses may cause worsening recurrences of herpes simplex eruptions. HIV test Main article: HIV test Many HIV-positive people are unaware that they are infected with the virus. Later. pharyngitis). or Kaposi's sarcoma. and viral particles accumulate both in infected cells and as free virus. marking the start of the infection's clinical latency stage. Pneumonia caused by the fungus Pneumocystis jirovecii is common and often fatal.[69] When CD4+ T cell numbers decline below a critical level. which leads to an increased susceptibility to oral candidiasis (thrush) and tuberculosis. shingles. skin rashes. prostatitis. Common opportunistic infections and tumors.

However. which may be either an incomplete antibody response to HIV in an infected person. Only specimens that are repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are considered HIV-positive and indicative of HIV infection. Specimens with a reactive ELISA result are retested in duplicate.g. Abacavir . this assay is not widely used. viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations. In these situations.g. tested or receive their test results.[74] Current treatment for HIV infection consists of highly active antiretroviral therapy.a nucleoside analog reverse transcriptase inhibitors (NARTIs or NRTIs) The chemical structure of Abacavir There is currently no vaccine or cure for HIV or AIDS.[73] Although IFA can be used to confirm infection in these ambiguous cases. a few tested specimens might provide inconclusive results because of a low quantity specimen.[72] If the result of either duplicate test is reactive. Although much less commonly available. a second specimen is collected and tested for HIV infection.5% of pregnant women attending urban health facilities are counselled. or nonspecific reactions in an uninfected person. an immunofluorescence assay (IFA)).[70] Again. The only known method of prevention is avoiding exposure to the virus. Treatment See also AIDS Treatment and Antiretroviral drug.0. this proportion is even lower in rural health facilities. Generally. the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e. an antiretroviral treatment. a second specimen should be collected more than a month later and retested for persons with indeterminate Western blot results. or HAART.[71] HIV-1 testing consists of initial screening with an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1.. Specimens with a nonreactive result from the initial ELISA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred.[70] Since donors may therefore be unaware of their infection.[75] This has been highly beneficial to .[72] In addition. Specimens that are repeatedly ELISAreactive occasionally provide an indeterminate Western blot result. less commonly. Western blot or.. known as post-exposure prophylaxis is believed to reduce the risk of infection if begun directly after exposure. nucleic acid testing (e. donor blood and blood products used in medicine and medical research are routinely screened for HIV.

Typically.[77] In developed countries where HAART is available. often HAART resistant.1 years from the time of infection if treatment was started when the CD4 count was 350/µL. meal restrictions or other issues along with side effects that create intentional non-adherence also contribute to this problem. Because AIDS progression in children is more rapid and less predictable than in adults. In the absence of HAART. HAART sometimes achieves far less than optimal results. dyslipidaemia. and high levels of HIV-1. or "classes. whether due to pill number. They then decide when to recommend starting treatment. dosing frequency. it would take more than a lifetime for HIV infection to be cleared using HAART.[76] Current HAART options are combinations (or "cocktails") consisting of at least three drugs belonging to at least two types. such as poor access to medical care. more aggressive treatment is recommended for children than adults. return once treatment is stopped.[93] In those countries where CD4 counts are not available.[78] HAART allows the stabilisation of the patient’s symptoms and viremia.[85] However." of anti-retroviral agents. There is no question that treatment should be started before the patient's CD4 count falls below 200. how fast CD4 declines. in some circumstances being effective in less than fifty percent of patients. and patient readiness. doctors assess their patients thoroughly: measuring the viral load. prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. nor alleviates the symptoms. inadequate social supports. but there is some evidence from cohort studies that treatment should be started before the CD4 count falls below 350. Major psychosocial issues.2 months. The complexity of these HAART regimens.[76][82][83] A computer based study in 2006 projected that following the 2004 United States treatment guidelines gave an average life expectancy of an HIV infected individual to be 32.[84] This study was limited as it did not take into account possible future treatments and the projection has not been confirmed within a clinical cohort setting. but it neither cures the patient. many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life.[92][82] There is also evidence to say that treatment should be started before CD4 percentage falls below 15%. when the protease inhibitor-based HAART initially became available. psychiatric disease and drug abuse contribute to nonadherence. which has led to a large reduction in HIV-associated morbidity and mortality in the developed world.[90][91] The timing for starting HIV treatment is still debated. these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). and most national guidelines say to start treatment once the CD4 count falls below 350. However.[87][88][89] The side effects include lipodystrophy. patients with WHO stage III or IV disease[94] should be offered treatment. insulin resistance. non-adherence and non-persistence with antiretroviral therapy is the major reason most individuals fail to benefit from HAART. . an increase in cardiovascular risks and birth defects.[79][80] Moreover. This is due to a variety of reasons such as medication intolerance/side effects. particularly in young infants. progression from HIV infection to AIDS has been observed to occur at a median of between nine to ten years and the median survival time after developing AIDS is only 9.[86] The reasons for non-adherence and non-persistence with HAART are varied and overlapping.[81] Despite this.many HIV-infected individuals since its introduction in 1996.

6 million] AIDS orphans living in sub-Saharan Africa 2005.000 children in this region.0 million] of them are children younger than 15 years of age. thus being affordable for developing countries.[95] Research to improve current treatments includes decreasing side effects of current drugs.7 million infections (estimated 3. The National Institute of Allergy and Infectious Diseases published a report that gave details of a potential region on HIV's surface that is a potential target for a vaccine. and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS. further simplifying drug regimens to improve adherence. between 33. making India the country with the highest number of HIV infections in the world. This is because a vaccine would cost less. .4 and 6. with an estimated 5.[95]In February 2007.1% no data 15–50% 5–15% UNAIDS and the WHO estimate that AIDS has killed more than 25 million people since it was first recognized in 1981.Anti-retroviral drugs are expensive.5–3.1 million) (11. [95] However.6–13.1–0. between 3.[96] Epidemiology Main article: AIDS pandemic Prevalence of HIV among adults per country at the end of 2005 1–5% 0. the AIDS pandemic claimed an estimated 2. there were 12. only a vaccine is thought to be able to halt the pandemic. after over 20 years of research.[3] In 2005.2 million people were newly infected and between 2.000) were children.0% 0. Unfortunately. Two million [1. as are more than three quarters of all women living with HIV. More than 64% of all people living with HIV are in sub-Saharan Africa. AIDS accounts for the deaths of 500.[3] Globally.9% of population) infections.5 million (4.0 million [10. an increase from 2004 and the highest number since 1981. and determining the best sequence of regimens to manage drug resistance. making it one of the most destructive pandemics in recorded history.4 and 3. Sub-Saharan Africa remains by far the worst-affected region. and would not require daily treatment. Two-thirds of HIV/AIDS infections in Asia occur in India.4 million) (0. with an estimated 21.3 million) lives in 2005 of which more than half a million (570. Despite recent improved access to antiretroviral treatment and care in many regions of the world.5–1. surpassing South Africa's estimated 5.3 million people with AIDS died.[3] South & South East Asia are second-worst affected with 15% of the total.5% <0.4–9.9% of population).4 and 46 million people currently live with HIV.4 million people currently living with HIV.8 million (between 2.4 and 3.6 to 27.[97] In the 35 African nations with the highest prevalence. In 2005. HIV-1 remains a difficult target for a vaccine.9–6.

3. 4. . (2002). 2. ^ a b c d Joint United Nations Programme on HIV/AIDS (2006). (1986).): State of The Art: AIDS and Economics (PDF). "What to call the AIDS virus?". Nature 321 (6065): 10. Temin. ^ Rick Sowadsky (1999).[100] In Africa. This has created the misperception that the disease has vanished. R. which include the distribution of antiretroviral therapy.. A. where governmental acceptance of AIDS denialism has been blamed for an ineffective response to that country's AIDS epidemic.[99] This is the first comprehensive evaluation of the World Bank's HIV/AIDS support to countries. analytic work. J. "Overview of the global AIDS epidemic". Oroszlan.[103] although they have had a political impact. Levy...000 in 1996. H. and lending with the explicit objective of reducing the scope or impact of the AIDS epidemic.. K. The development of HAART as effective therapy for HIV infection and AIDS has substantially reduced the death rate from this disease in those areas where these drugs are widely available. Forsyth (ed. R. and Weiss. A. the number of persons with AIDS increased from about 35. Teich.[104][105][106] Notes and references 1. the number of persons living with AIDS has increased substantially. particularly in South Africa. L.[101] the existence of HIV itself. These claims have been examined and widely rejected by the scientific community. H... the number of MTCT and the prevalence of AIDS is beginning to reverse decades of steady progress in child survival.3 years—6. PMTCT (prevention of mother-to-child transmission) and ANC (ante-natal care) services. A. Haase. What is HTLV-III?. PMID 3010128.5 years less than it would be without the disease. J..[98] The latest evaluation report of the World Bank's Operations Evaluation Department assesses the development effectiveness of the World Bank's country-level HIV/AIDS assistance defined as policy dialogue. In fact. from the beginning of the epidemic through mid-2004. 2006 Report on the global AIDS epidemic (PDF format). Montagnier. Retrieved on 2006-08-24. S. ^ Greener. Toyoshima. In the United States. Because the Bank aims to assist in implementation of national government programmes. in S. Vogt. 49-55.000 in 1988 to over 220. P. their experience provides important insights on how national AIDS programmes can be made more effective. "AIDS and macroeconomic impact". Varmus. Countries such as Uganda are attempting to curb the MTCT epidemic by offering VCT (voluntary counselling and testing).. ^ Coffin.average life expectancy is 48. IAEN. N. as the life expectancy of persons with AIDS has increased in countries where HAART is widely used.[102] or the validity of current testing and treatment methods. Alternative hypotheses Main article: AIDS reappraisal A small minority of scientists and activists question the connection between HIV and AIDS..

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TIME magazine.S. 2006 | Reuters on Topix.Building Community AIDSPortal . Chermann JC (1998). Department of Health and Human Services HIV InSite . DOI:10.Galéa P. ^ Watson J (2006). 2006 Frontline • Everything you wanted to know about HIV and AIDS — Provided by New Scientist. 104.University of California San Francisco AIDS.gov Portal for all Federal domestic HIV/AIDS information and resources News media • "The Age of Aids" March 30. o External links • • • • • • • • • Wikimedia Commons has media related to: HIV External links UNAIDS .Joint United Nations Programme on HIV/AIDS webpage o 2006 Report on the Global AIDS Epidemic by UNAIDS o UNAIDS document regarding three scenarios for HIV/AIDS in Africa for the year 2025 (Large PDF file) Division of Acquired Immunodeficiency Syndrome (DAIDS) .HIV/AIDS Information . PMID 12672319. Genetica 104 (2): 133-42. PMID 10896606.U. Nat. Science 288 (5474): 2168-70. ^ Baleta A (2003). Med.net Online textbooks • HIV Medicine 2006. "HIV as the cause of AIDS and associated diseases". PMID 16397537. ^ Cohen J (2000). 12 (1): 6. "South Africa's new enemy".1038/nm0106-6a. medical textbook. "Scientists. research.Older Americans living with HIV face unique challenges . • "The Graying of AIDS" . 825 pages (free download) • "The Molecules of HIV" information resource Advocacy . PMID 10220906.National Institute of Allergy and Infectious Diseases (NIAID) at NIH History of AIDS research at the NIH Medecins Sans Frontieres/Doctors Without Borders HIV/AIDS Pages AIDSinfo .Aug 16. "S Africa's AIDS activists accuse government of murder". 14th edition.ORG: Educating .Raising HIV Awareness . guidelines and case studies AIDS. activists sue South Africa's AIDS 'denialists'".Latest policy. 106. 105. Lancet 361 (9363): 1105. 08/14/06 • "Elite" HIV patients mystify doctors .

from Data360 • Resources for HIV/AIDS and Sexual and Reproductive Health Integration Johns Hopkins Bloomberg School of Public Health. articles.Patient/clinician information & Historical news and treatment database • AIDS Community Research Initiative of America .Community-based research and education for people living with HIV • Data about people living with HIV/AIDS in the world (regional totals and percentage of adults with AIDS that are women). • POZ provides information and networking opportunities for the HIV community.com provides a comprehensive collection of HIV and AIDS information. and forums.org: AIDS Education Global Information System. • AIDSmeds is a place to find complete and easy-to-read information on treating HIV & AIDS. • AEGiS. statistics. Center for Communication Programs HIV/AIDS related topics HIV · AIDS · HIV structure and genome · HIV test · CDC Classification System for HIV Infection · HIV disease HIV progression rates · HIV vaccine · WHO Disease Staging System for HIV Infection and Disease · AIDS dementia complex · Antiretroviral drug AIDS origin · AIDS pandemic · AIDS Museum · Timeline of AIDS · History Oral polio vaccine AIDS hypothesis · Reappraisal of HIV– AIDS Hypothesis · Duesberg hypothesis International AIDS Conference · International AIDS Society · World AIDS Day · Treatment Action Campaign · UNAIDS · PEPFAR · NAMES Project AIDS Memorial Quilt · HIV and Culture AIDS misconceptions · List of HIV-positive people · People With AIDS Self-Empowerment Movement · HIV–positive fictional characters . Los Alamos National Laboratory Multimedia/video • How Aids Works (with animation) • Watch an animated tutorial on the life cycle of HIV • Video of Treatment Update 2006 from the Conference on Retrovirus' Other sites • HIV/AIDS at About.• • • Be the Generation .Information on HIV Vaccine Clinical Research in 20 American Cities Media Campaign: HIV leads to AIDS FightAIDS@Home Articles • The Mechanism of HIV-1 Core Assembly: Insights from Three-Dimensional Reconstructions of Authentic Virions • Unsafe Health Care and the HIV/AIDS Pandemic 2003 • The role of dendritic cells in HIV pathogenesis • The HIV databases.

Sub-Saharan Africa (in South Africa • Uganda) · Asia (in China • India • Myanmar • Pakistan • Taiwan • Japan) · in Latin America (in Brazil) · AIDS pandemic in Caribbean · Eastern Europe and Central Asia (in Russia) · Western Europe · United States · List of countries by HIV/AIDS adult prevalence rate Sexually transmitted diseases and infections (STD/STI) (primarily A50A64.HIV n. the leading user-contributed encyclopedia. . 090-099) Chancroid (Haemophilus ducreyi) • Chlamydia (Chlamydia trachomatis) • Donovanosis (Granuloma Inguinale) • Bacterial Lymphogranuloma venereum (LGV) (Chlamydia trachomatis) • Gonorrhea (Neisseria gonorrhoeae) • Syphilis (Treponema pallidum) • Ureaplasma urealyticum Protozoal Trichomoniasis (Trichomonas vaginalis) Parasitic Crab louse/crabs • Scabies AIDS (HIV-1/HIV-2) • Cervical cancer & Genital warts (condyloma) (Human papillomavirus (HPV)) • Hepatitis Viral B • Herpes simplex virus (HSV1/HSV2) • Molluscum contagiosum (MCV) Cervicitis • Epididymitis • Ectopic pregnancy • Infertility • NonOther conditions gonococcal urethritis (NGU) • Pelvic inflammatory disease (PID) • Premature birth • Proctitis • Prostatitis • Reactive arthritis • Urethritis This entry is from Wikipedia.(Med.human immundefekt virus Nederlands (Dutch) HIV(-virus) Français (French) abbr. .ιός ανθρώπινης ανοσολογικής ανεπάρκειας . .) menschliches/r Immunschwächevirus n. . . .) Aids-Virus Ελληνική (Greek) abbr.(Med. It may not have been reviewed by professional editors (see full disclaimer) Donate to Wikimedia Translations Home > Library > Words > Translations Translations for: Hiv Dansk (Danish) abbr. .(abrév = human immunodeficiency virus) VIH séro-positif n.séro-positif Deutsch (German) abbr.

click here.VIH .愛滋病病毒 n.ヒト免疫不全ウイルス. .Human Immunodeficient virus (인간 면역결핍 바이러스) n. . . Shopping hiv prevention hiv and aids prevention .virus de la inmunodeficiencia humana n.virus de la inmunodeficiencia humana Svenska (Swedish) abbr. .Italiano (Italian) HIV (Virus da immunodeficienza Umana . .AIDS) Português (Portuguese) abbr.vírus (m) da imunodeficiência humana (Patol. .VIH . . .‫)اختصار( فيروس‬ ‫( עברית‬Hebrew) abbr.human immunodeficiency virus 中文(简体) (Chinese (Simplified)) 爱滋病病毒 中文(繁體) (Chinese (Traditional)) abbr. To select your translation preferences click here. .愛滋病病毒 한국어 (Korean) abbr.) Русский (Russian) вирус иммунного дефицита человека Español (Spanish) abbr.‫כשל חיסוני‬/‫נגיף האיידס‬ n. . エイズウイルス idioms: • hiv positive HIV 陽性 ‫( العربيه‬Arabic) ‫ مرض الديدمز أو متلمزمه نقص المناعه المكتسبه‬.인체 면역 결핍 바이러스 日本語 (Japanese) abbr.‫כשל חיסוני‬/‫נגיף האיידס‬ If you are unable to view some languages clearly. .

Read more Genetics Encyclopedia. Inc. Published by Houghton Mifflin Company.columbia. Read more Britannica Concise Encyclopedia. Copyright © 2007. 2000 by Houghton Mifflin Company. Post a question or answer questions about "hiv" at WikiAnswers. human immunodeficiency virus (medical term). The New Dictionary of Cultural Literacy. Columbia University Press. Kett. Sixth Edition Copyright © 2003. Read more Wikipedia. Read more Get the FREE Answers. Copyrights: Dictionary. Joseph F. Hirsch. All rights reserved. Read more Columbia Encyclopedia. © 2006 Encyclopædia Britannica.home hiv tests Did you mean: AIDS (in medicine). The American Heritage® Dictionary of the English Language. Third Edition Edited by E.. WizCom Technologies Ltd. HIV (abbreviation) Join the WikiAnswers Q&A community.cc. Copyright © 2003 by The Gale Group. All rights reserved. Updated in 2007. www.edu/cu/cup/ Read more Health Dictionary. All rights reserved. Read more Translations. Jr. This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "HIV". Copyright © 2002 by Houghton Mifflin Company.D. Britannica Concise Encyclopedia. Fourth Edition Copyright © 2007. Published by Houghton Mifflin. Genetics. and James Trefil.com IE Toolbar! Download Now More Info Add Answers to the IE7 Toolbar Search Box! Add Now! . All rights reserved. Licensed from Columbia University Press. All rights reserved. Inc. The Columbia Electronic Encyclopedia. All rights reserved.

All rights reserved.On this page: E-mailE-mail Print Link Keep Reading Related Topics • Immune System Genetics • Retrovirus • Reverse Transcriptase Special Offers Stages of HIV • Aids Test • HIV 1 Real Time PCR • Viral Count HIV Aids in Sub Saharan Africa • • hiv Home Bloggers & Webmasters Sitemap About Advertise RSS What's new Blog Help Terms of Use Privacy Copyright © 2008 Answers Corporation. Policy IP Notices Disclaimer .