HIV is a virus that damages the immune system. The immune system helps the body fight off infections. HIV is a lifelong condition and currently there is no cure, although many scientists are working to find one. At that point, the immune system is too weak to fight off other diseases and infections. Untreated, life expectancy with AIDS is about three years.
Doctors' beliefs about treatment affect patients' experience of pain. Archived PDF from the original on February 9, Inas part of an overall reform of marriage and population legislation, it became legal for people with AIDS to marry in China. Uganda 2. New York Hiv or other virus.
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The first step in fusion involves the high-affinity attachment of the CD4 binding domains of gp to CD4. Ohher condition can become progressive disseminated histoplasmosis and can impact on organs outside of the respiratory system. HIV is different from other viruses because it uses the part of our body that fights disease to othre. No effective cure currently exists, but with proper medical care, HIV can be controlled. Note : When the statement and list of endorsements was retrieved, it had last been updated on 23 August and included "over organizations from nearly countries. Hiv or other virus infections are diseases caused by viruses, fungi, or bacteria that would not make a person with Speed freak os x undamaged immune Hiv or other virus sick. Can I get HIV from otner drugs? Each of the very small number of documented cases has involved severe trauma with extensive tissue damage and the presence of blood. The six remaining genes, tatrevnefvifvprand vpu or vpx Shit in anal the case of HIV-2are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus replicateor cause disease. These mRNAs are exported Hiv or other virus the nucleus into the cytoplasmwhere they are translated into the regulatory proteins Tat which encourages new virus production and Rev. Over decades, the virus slowly spread across Africa and later into other parts of the world. Stomach Flu. American Association for the Advancement of Science. You may need help to stop or cut down using drugs, but many resources are available.
These special cells help the immune system fight off infections.
- HIV is a virus that targets and alters the immune system, increasing the risk and impact of other infections and diseases.
- So, once you have HIV, you have it for life.
- Research has shown for both same-sex and opposite-sex couples that HIV is untransmissable through condomless sexual intercourse if the HIV-positive partner has a consistently undetectable viral load.
So, once you have HIV, you have it for life. In the U. Once someone has a dangerous opportunistic illness, life expectancy without treatment falls to about 1 year. The only way to know for sure if you have HIV is to get tested.
Testing is relatively simple. You can ask your health care provider for an HIV test. Many medical clinics, substance abuse programs, community health centers, and hospitals offer them too. You can also buy a home testing kit at a pharmacy or online. Content Source: HIV. Many Federal agencies have developed public awareness and education campaigns to address HIV prevention, treatment, care, and research.
Also included is information about campaigns related to the prevention and diagnosis of hepatitis B and C. El VIH es una amenaza de salud grave para las comunidades latinas, quienes se encuentran en gran desventaja respecto de la incidencia de esta enfermedad en los Estados Unidos. Want to stay abreast of changes in prevention, care, treatment or research or other public health arenas that affect our collective response to the HIV epidemic? Or are you new to this field?
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What can we improve? Next We thank you for your time spent taking this survey. Your response has been recorded. Campaigns Many Federal agencies have developed public awareness and education campaigns to address HIV prevention, treatment, care, and research. Ver Mas Recursos. Learning Opportunities Want to stay abreast of changes in prevention, care, treatment or research or other public health arenas that affect our collective response to the HIV epidemic?
This improves quality of life, extends life expectancy, and reduces the risk of transmission, according to the WHO's guidelines from June Treatment plans will be different between people. May 15, Campaigns Many Federal agencies have developed public awareness and education campaigns to address HIV prevention, treatment, care, and research. HIV vs.
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HIV and AIDS: Overview, causes, symptoms, and treatments
Research has shown for both same-sex and opposite-sex couples that HIV is untransmissable through condomless sexual intercourse if the HIV-positive partner has a consistently undetectable viral load.
HIV is a member of the genus Lentivirus ,  part of the family Retroviridae. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. 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. 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.
HIV is different in structure from other retroviruses. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle. This is, in turn, surrounded by the viral envelope , that is composed of the lipid bilayer taken from the membrane of a human host cell when the newly formed virus particle buds from the cell. The viral envelope contains proteins from the host cell and relatively few copies of the HIV Envelope protein,  which consists of a cap made of three molecules known as glycoprotein gp , and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.
As the sole viral protein on the surface of the virus, the Envelope protein is a major target for HIV vaccine efforts. The density is high as the glycans shield the underlying viral protein from neutralisation by antibodies. The molecular structure of the viral spike has now been determined by X-ray crystallography  and cryogenic electron microscopy.
Three of these genes, gag , pol , and env , contain information needed to make the structural proteins for new virus particles. The six remaining genes, tat , rev , nef , vif , vpr , and vpu or vpx in the case of HIV-2 , are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus replicate , or cause disease. Nef also interacts with SH3 domains.
The vpu protein p16 influences the release of new virus particles from infected cells. 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.
The Psi element is involved in viral genome packaging and recognized by gag and rev proteins. The SLIP element. The term viral tropism refers to the cell types a virus infects. Indeed, macrophages play a key role in several critical aspects of HIV infection. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In the tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.
Some people are resistant to certain strains of HIV. Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid , which enables the virus to be transmitted from a male to his sexual partner. The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process [ further explanation needed ] leads to a predominant transmission of the R5 virus through this pathway.
A number of studies with subtype B-infected individuals have determined that between 40 and 50 percent of AIDS patients can harbour viruses of the SI and, it is presumed, the X4 phenotypes. Adaptation to use normal cellular machinery to enable transmission and productive infection has also aided the establishment of HIV-2 replication in humans.
A survival strategy for any infectious agent is not to kill its host, but ultimately become a commensal organism. Entry to the cell begins through interaction of the trimeric envelope complex gp spike on the HIV viral envelope and both CD4 and a chemokine co-receptor generally either CCR5 or CXCR4 , but others are known to interact on the target cell surface. The first step in fusion involves the high-affinity attachment of the CD4 binding domains of gp to CD4.
Once gp is bound with the CD4 protein, the envelope complex undergoes a structural change, exposing the chemokine receptor binding domains of gp and allowing them to interact with the target chemokine receptor. This loop structure brings the virus and cell membranes close together, allowing fusion of the membranes and subsequent entry of the viral capsid. After HIV has bound to the target cell, the HIV RNA and various enzymes, including reverse transcriptase, integrase, ribonuclease, and protease, are injected into the cell.
They are currently thought to play an important role by transmitting HIV to T cells when the virus is captured in the mucosa by DCs. HIV-1 entry, as well as entry of many other retroviruses, has long been believed to occur exclusively at the plasma membrane. Shortly after the viral capsid enters the cell, an enzyme called reverse transcriptase liberates the positive-sense single-stranded RNA genome from the attached viral proteins and copies it into a complementary DNA cDNA molecule.
The integration of the viral DNA into the host cell's genome is carried out by another viral enzyme called integrase. These mRNAs are exported from the nucleus into the cytoplasm , where they are translated into the regulatory proteins Tat which encourages new virus production and Rev.
As the newly produced Rev protein is produced it moves to the nucleus, where it binds to full-length, unspliced copies of virus RNAs and allows them to leave the nucleus. Gag proteins bind to copies of the virus RNA genome to package them into new virus particles. Upon infection and replication catalyzed by reverse transcriptase, recombination between the two genomes can occur.
This form of recombination is known as copy-choice. Recombination events may occur throughout the genome. Anywhere from two to 20 recombination events per genome may occur at each replication cycle, and these events can rapidly shuffle the genetic information that is transmitted from parental to progeny genomes.
Viral recombination produces genetic variation that likely contributes to the evolution of resistance to anti-retroviral therapy. It is unknown how often such mixed packaging occurs under natural conditions.
Bonhoeffer et al. In addition, Hu and Temin  suggested that recombination is an adaptation for repair of damage in the RNA genomes. Strand switching copy-choice recombination by reverse transcriptase could generate an undamaged copy of genomic DNA from two damaged single-stranded RNA genome copies. This view of the adaptive benefit of recombination in HIV could explain why each HIV particle contains two complete genomes, rather than one.
On the view that recombination in HIV is a repair process, the generation of recombinational variation would be a consequence, but not the cause of, the evolution of template switching. HIV-1 infection causes chronic inflammation and production of reactive oxygen species. For HIV, as well as for viruses in general, successful infection depends on overcoming host defensive strategies that often include production of genome-damaging reactive oxygen species.
Thus, Michod et al. The final step of the viral cycle, assembly of new HIV-1 virions, begins at the plasma membrane of the host cell. The Env polyprotein gp goes through the endoplasmic reticulum and is transported to the Golgi apparatus where it is cleaved by furin resulting in the two HIV envelope glycoproteins, gp41 and gp The Gag p55 and Gag-Pol p 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.
The budded virion is still immature as the gag polyproteins still need to be cleaved into the actual matrix, capsid and nucleocapsid proteins. This cleavage is mediated by the packaged viral protease and can be inhibited by antiretroviral drugs of the protease inhibitor class.
The various structural components then assemble to produce a mature HIV virion. Firstly, an infected T cell can transmit virus directly to a target T cell via a virological synapse. HIV differs from many viruses in that it has very high genetic variability.
This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day. When simultaneous infection occurs, the genome of progeny virions may be composed of RNA strands from two different strains. This hybrid virion then infects a new cell where it undergoes replication. As this happens, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes.
The closely related simian immunodeficiency virus SIV has evolved into many strains, classified by the natural host species. These hosts have adapted to the presence of the virus,  which is present at high levels in the host's blood, but evokes only a mild immune response,  does not cause the development of simian AIDS,  and does not undergo the extensive mutation and recombination typical of HIV infection in humans.
In contrast, when these strains infect species that have not adapted to SIV "heterologous" or similar hosts such as rhesus or cynomologus macaques , the animals develop AIDS and the virus generates genetic diversity similar to what is seen in human HIV infection.
Nef 's function in non-pathogenic forms of SIV is to downregulate expression of inflammatory cytokines , MHC-1 , and signals that affect T cell trafficking. Co-infection with distinct subtypes gives rise to circulating recombinant forms CRFs. In , the last year in which an analysis of global subtype prevalence was made, Many HIV-positive people are unaware that they are infected with the virus.
Specimens that are repeatedly ELISA-reactive occasionally provide an indeterminate western blot result, which may be either an incomplete antibody response to HIV in an infected person or nonspecific reactions in an uninfected person.
HIV deaths other than U. Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. Although much less commonly available, nucleic acid testing e. In these situations, a second specimen is collected and tested for HIV infection. Modern HIV testing is extremely accurate, when the window period is taken into consideration. This gives rise to four possible scenarios:. 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.
Previously it was said the chance of transmission was 'very low' or 'negligible' The 'Swiss Statement'. In total from the four studies, couples were enrolled over four continents and , acts of condomless sex were reported, there were zero phylogenetically linked transmissions of HIV where the positive partner had an undetectable viral load. This result is consistent with the conclusion presented by Anthony S.
In the beginning, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy , the disease after which the discoverers of HIV originally named the virus.
Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa, and are believed to have transferred to humans a process known as zoonosis in the early 20th century. HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O. There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV.
It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV. Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. An alternative view—unsupported by evidence—holds that unsafe medical practices in Africa during years following World War II, such as unsterile reuse of single-use syringes during mass vaccination, antibiotic, and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread.
From Wikipedia, the free encyclopedia. Human retrovirus, cause of AIDS. This article is about the virus. For other uses, see HIV disambiguation.