question: How is HIV/AIDS treated? How do the HIV antivirals work?
comment: You answered the first part of your question with the second part, which is antiretroviral medications. Antiretrovirals work in a number of different ways to try to get a person's viral load as low as possible. Some of them work by preventing the virus from entering cells in the first place. Others work by preventing the viral RNA from replicating once inside the cell, and others work by preventing the virus from emerging from the cell so it can't go infect new cells. Most HIV treatment protocols call for the use of 2 or more of these different types of antiretrovirals to attack the virus in as many ways as possible. This is usually very effective, and can reduce a person's viral load to the point of being undetectable, although this isn't a cure, because unfortunately, no antiretroviral is 100% effective, and so there will always be some of the virus present, and stopping the medications could cause the viral load to increase. Also, some strains of the virus are resistant to certain drugs, and the virus can mutate to become resistant to a drug a person is currently taking.
passages: The failure of vaccine candidates to protect against HIV infection and progression to AIDS has led to a renewed focus on the biological mechanisms responsible for HIV latency. A limited period of therapy combining anti-retrovirals with drugs targeting the latent reservoir may one day allow for total eradication of HIV infection. Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.
  
  Section::::New developments.
   Human Immunodeficiency Virus Infection (HIV) is treated by using a combination of medications to fight against the HIV infection in the body. This is called antiretroviral therapy (ART). ART is not a cure, but it can control the virus so that a person can live a longer, healthier life and reduce the risk of transmitting HIV to others around him. ART involves taking a combination of HIV medicines (called an HIV regimen) every day, exactly as prescribed by the doctor. These HIV medicines prevent HIV Virus from multiplying (making copies of itself in the body), which reduces the amount of HIV in the body. Having less HIV in the body gives the immune system a chance to recover and fight off infections and cancers. Even though there is still some HIV in the body, the immune system is strong enough to fight off infections and cancers. By reducing the amount of HIV in the body, HIV medicines also reduce the risk of transmitting the virus to others. ART is recommended for all people with HIV, regardless of how long they’ve had the virus or how healthy they are. If left untreated, HIV will attack the immune system and eventually progress to AIDS.
   The first cases of AIDS were reported in 1981, and HIV, the retrovirus causing it, was identified in 1983 by Luc Montagnier, Françoise Barré-Sinoussi and Robert Gallo. Tests detecting HIV infection by detecting the presence of HIV antibody were developed. Subsequent tremendous research efforts turned HIV into the best studied virus. Human Herpes Virus 8, the cause of Kaposi's sarcoma which is often seen in AIDS patients, was identified in 1994. Several antiretroviral drugs were developed in the late 1990s, decreasing AIDS mortality dramatically in developed countries. Treatment that exists for HIV includes a multitude of different drugs collectively termed Highly Active Antiretroviral Therapy (HAART). HAART attacks many different aspects of the HIV virus, effectively reducing its effects below the limit of detection. However, when the administration of HAART is discontinued, HIV will bounce back. This is because HAART does not attack latently infected HIV cells, which can reactivate.
   HIV is a member of the genus "Lentivirus", part of the family "Retroviridae". Lentiviruses have many morphologies and biological properties in common. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded enzyme, reverse transcriptase, that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded enzyme, integrase, and host co-factors. Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system, for an indeterminate amount of time. The HIV virus can remain dormant in the human body for up to ten years after primary infection; during this period the virus does not cause symptoms. Alternatively, the integrated viral DNA may be transcribed, producing new RNA genomes and viral proteins, using host cell resources, that are packaged and released from the cell as new virus particles that will begin the replication cycle anew.
   There are six classes of drugs, which are usually used in combination, to treat HIV infection. Antiretroviral (ARV) drugs are broadly classified by the phase of the retrovirus life-cycle that the drug inhibits. Typical combinations include 2 Nucleoside reverse-transcriptase inhibitors (NRTI) as a "backbone" along with 1 Non-Nucleoside reverse-transcriptase inhibitor (NNRTI), protease inhibitor (PI) or Integrase inhibitors (also known as integrase nuclear strand transfer inhibitors or INSTIs) as a "base."
  
  Section::::Classes of medication.:Entry inhibitors.
   HIV is a member of the genus "Lentivirus", part of the family "Retroviridae". Lentiviruses share many morphological and biological characteristics. Many species of mammals are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factors. Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.
   A very early stage of viral infection is viral entry, when the virus attaches to and enters the host cell. A number of "entry-inhibiting" or "entry-blocking" drugs are being developed to fight HIV. HIV most heavily targets the immune system's white blood cells known as "helper T cells", and identifies these target cells through T-cell surface receptors designated "CD4" and "CCR5". Attempts to interfere with the binding of HIV with the CD4 receptor have failed to stop HIV from infecting helper T cells, but research continues on trying to interfere with the binding of HIV to the CCR5 receptor in hopes that it will be more effective.
   Previous treatment guidelines recommended that anyone with a viral load greater than 100,000 copies/mL of blood should begin treatment. It is now standard of care in the United States to begin anti-retroviral treatment upon discovery of HIV positive status. HIV is a retrovirus, an RNA virus that enters a host cell and uses the host DNA replication machinery and the enzyme reverse transcriptase to produce DNA from the viral RNA genome. HIV also produces an integrase enzyme which is used to integrate the newly produced viral DNA into the host’s DNA. The virus is then replicated every time the host cell's DNA replicates. 
   There is currently no cure or effective HIV vaccine. Treatment consists of highly active antiretroviral therapy (HAART) which slows progression of the disease. more than 6.6 million people were taking them in low and middle income countries. Treatment also includes preventive and active treatment of opportunistic infections.
  
  Section::::Treatment.:Antiviral therapy.
   The management of HIV/AIDS normally includes the use of multiple antiretroviral drugs in an attempt to control HIV infection. There are several classes of antiretroviral agents that act on different stages of the HIV life-cycle. The use of multiple drugs that act on different viral targets is known as highly active antiretroviral therapy (HAART). HAART decreases the patient's total burden of HIV, maintains function of the immune system, and prevents opportunistic infections that often lead to death. HAART also prevents the transmission of HIV between serodiscordant same sex and opposite sex partners so long as the HIV-positive partner maintains an undetectable viral load.
   In a study published by the Proceedings of the National Academy of Sciences (PNAS), Dr. Khalili and colleagues detail how they created molecular tools to delete the HIV-1 proviral DNA. When deployed, a combination of DNA-snipping enzyme called a nuclease and targeting strand of RNA called a guide RNA (gRNA) hunt down the viral genome and excise the HIV-1 DNA. From there, the cell's own gene repair machinery takes over, soldering the loose ends of the genome back together – resulting in virus-free cells.
   Section::::Immunomodulatory agents.
  
  Complementing efforts to control viral replication, immunotherapies that may assist in the recovery of the immune system have been explored in past and ongoing trials, including IL-2 and IL-7.
   Section::::Classes of medication.:Nucleoside/nucleotide reverse-transcriptase inhibitors.
   Even with all latent virus deactivated, it is thought that a vigorous immune response will need to be induced to clear all the remaining infected cells. Current strategies include using cytokines to restore CD4+ cell counts as well as therapeutic vaccines to prime immune responses. One such candidate vaccine is Tat Oyi, developed by Biosantech. This vaccine is based on the HIV protein tat. A brief report of their phase I/II clinical trial reported it was safe and well tolerated in 48 HIV-positive patients. Animal models have shown the generation of neutralizing antibodies and lower levels of HIV viremia.
   Highly active antiretroviral therapy (HAART) is the current recommended treatment for HIV. HAART entails taking a combination (regimen) of three or more ART medications from at least two different classes of drugs. There are six classes of ART medications: 
  
  BULLET::::- non-nucleoside reverse transcriptase inhibitors (NNRTIs)
  
  BULLET::::- Nucleoside reverse transcriptase inhibitors (NRTIs)
  
  BULLET::::- protease inhibitors (PIs)
  
  BULLET::::- entry inhibitors
  
  BULLET::::- Fusion inhibitors
  
  BULLET::::- Integrase inhibitors
   Many governments and research institutions participate in HIV/AIDS research. This research includes behavioral health interventions, such as research into sex education, and drug development, such as research into microbicides for sexually transmitted diseases, HIV vaccines, and anti-retroviral drugs. Other medical research areas include the topics of pre-exposure prophylaxis, post-exposure prophylaxis, circumcision and HIV, and accelerated aging effects.
  
  Section::::Treatment and transmission.
  
  The management of HIV/AIDS normally includes the use of multiple antiretroviral drugs. In many parts of the world, HIV has become a chronic condition in which progression to AIDS is increasingly rare.
   Section::::See also.
  
  BULLET::::- Antiviral drug
  
  BULLET::::- Discovery and development of HIV-protease inhibitors
  
  BULLET::::- Discovery and development of non-nucleoside reverse-transcriptase inhibitors
  
  BULLET::::- Discovery and development of nucleoside and nucleotide reverse-transcriptase inhibitors
  
  Section::::External links.
  
  BULLET::::- AIDSinfo – Comprehensive resource for HIV/AIDS treatment and clinical trial information from the U. S. Department of Health and Human Services
  
  BULLET::::- ASHM – Australian Commentary on HHS Guidelines for the use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents
  
  BULLET::::- Origins of antiretroviral combination therapy
  
  BULLET::::- Viral Load research papers, including effectiveness of HAART on reducing viral load
   A ribozyme antiviral to deal with hepatitis C has been suggested, and ribozyme antivirals are being developed to deal with HIV. An interesting variation of this idea is the use of genetically modified cells that can produce custom-tailored ribozymes. This is part of a broader effort to create genetically modified cells that can be injected into a host to attack pathogens by generating specialized proteins that block viral replication at various phases of the viral life cycle.
  
  Section::::Approaches by life cycle stage.:During viral synthesis.:Protein processing and targeting.
   Dr. Sadhna Joshi at the University of Toronto is working to discover
  
  ways to combat HIV through gene therapy. In her research, Dr.
  
  Joshi targets both the cells that are infected by HIV, and the virus
  
  itself. Dr. Joshi is experimenting with ways to prevent infection by
  
  removing receptors that HIV uses to enter immune cells. She is also
  
  targeting genes in HIV to prevent replication after infection.
  
  Dr. Clifford Lingwood from The Hospital for Sick Children and
  
  Dr. Donald Branch from Canadian Blood Services have identified
  
  a new resistance factor in the battle against HIV. They discovered
   More than 30 different drugs exist for treating HIV patients. Antiretroviral drugs can disrupt the virus’s replication process causing its numbers to decrease dramatically. While the virus cannot be eradicated completely, in small numbers it is harmless. Usually a patient is given a combination of three or four drugs, a treatment known as highly active antiretroviral therapy, or HAART. The main reason such a treatment might fail is the development of mutated strands of the virus, resistant to one or more of the prescribed drugs.
   The main obstacle to conventional antiretroviral therapy eliminating HIV infection is that HIV is able to integrate itself into the DNA of host cells and rest in a latent state, while antiretrovirals only attack actively replicating HIV. The cells in which HIV lies dormant are called the viral reservoir, and one of the main sources is thought to be central memory and transitional memory CD4+ T cells. Recent reports of the cure of HIV in two infants are presumably due to the fact that treatment was initiated within hours of infection, preventing HIV from establishing a deep reservoir. Currently there is work being done to try to activate reservoir cells into replication so that the virus is forced out of latency and can be attacked by antiretrovirals and the host immune system. Targets include histone deacetylase (HDAC) which represses transcription and if inhibited can lead to increased cell activation. The HDAC inhibitors valproic acid and vorinostat have been used in human trials with only preliminary results so far.
   Due to the nature of the virus the drugs used to treat HIV are called antiretroviral medicines, and the course of treatment is called antiretroviral therapy (ART). These potent medicines cannot cure an individual; they can however manage the virus and slow the progression of the HIV infection. Strict compliance with the prescribed ART regimen is vital to controlling the disease.
   In the Quantiplex bDNA or branched DNA test, plasma is centrifugated to concentrate the virus, which is then opened to release its RNA. Special oligonucleotides that bind to viral RNA and to certain oligonucleotides bound to the wall of the vessel are added. In this way, viral RNA is fastened to the wall. Then new oligonucleotides that bind at several locations to this RNA are added, and other oligonucelotides that bind at several locations to those oligonucleotides. This is done to amplify the signal. Finally, oligonucleotides that bind to the last set of oligonucleotides and that are bound to an enzyme are added; the enzyme action causes a color reaction, which allows quantification of the viral RNA in the original sample. Monitoring the effects of antiretroviral therapy by serial measurements of plasma HIV-1 RNA with this test has been validated for patients with viral loads greater than 25,000 copies per milliliter.
   Current HAART options are combinations (or "cocktails") consisting of at least three medications belonging to at least two types, or "classes," of antiretroviral agents. Initially treatment is typically a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two nucleoside analog reverse transcriptase inhibitors (NRTIs). Typical NRTIs include: zidovudine (AZT) or tenofovir (TDF) and lamivudine (3TC) or emtricitabine (FTC). Combinations of agents which include protease inhibitors (PI) are used if the above regimen loses effectiveness.
   The Division's basic research efforts have yielded significant scientific information about HIV. For example, in recent years, DAIDS-funded investigators have identified new structures for viral components of HIV, additional chemokine co-receptors, and the existence of multiple, persistent HIV reservoirs even with the use of highly active antiretroviral therapy (HAART). Despite these advances, questions still remain about the molecular interactions involved in the regulation of HIV expression and replication. More information is also needed about how the virus evades the immune system in order to identify additional targets against which therapeutic interventions and vaccines can be directed.
  
  Section::::Scientific areas of focus.:Therapeutics.
  