The classical process of infection of a cell by a virion can be called “cell-free spread” to distinguish it from a more recently-recognized process called “cell-to-cell spread”. In cell-free spread (see figure), virus particles bud from an infected T cell, enter the blood or extracellular fluid and then infect another T cell following a chance encounter. HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread, for which two pathways have been described. Firstly, an infected T cell can transmit virus directly to a target T cell via a virological synapse. Secondly, an antigen-presenting cell (APC), such as a macrophage or dendritic cell, can transmit HIV to T cells by a process that either involves productive infection (in the case of macrophages) or capture and transfer of virions in trans (in the case of dendritic cells). Whichever pathway is used, infection by cell-to-cell transfer is reported to be much more efficient than cell-free virus spread. A number of factors contribute to this increased efficiency, including polarised virus budding towards the site of cell-to-cell contact, close apposition of cells, which minimizes fluid-phase diffusion of virions, and clustering of HIV entry receptors on the target cell to the contact zone. Cell-to-cell spread is thought to be particularly important in lymphoid tissues where CD4+ T cells are densely packed and likely to interact frequently. Intravital imaging studies have supported the concept of the HIV virological synapse in vivo. The hybrid spreading mechanisms of HIV contribute to the virus’ ongoing replication in spite of anti-retroviral therapies.
The replication of HIV can only take place inside human cells. The process typically begins when a virus particle bumps into a cell that carries a special protein called CD4 on its surface. The spikes on the surface of the virusparticle stick to the CD4 to allow the viral envelope to fuse with the cell membrane. HIV particle contents are then released into the cell, leaving the envelope behind.
Jump up ^ Keele BF, Van Heuverswyn F, Li Y, Bailes E, Takehisa J, Santiago ML, Bibollet-Ruche F, Chen Y, Wain LV, Liegeois F, Loul S, Ngole EM, Bienvenue Y, Delaporte E, Brookfield JF, Sharp PM, Shaw GM, Peeters M, Hahn BH (Jul 28, 2006). “Chimpanzee reservoirs of pandemic and nonpandemic HIV-1”. Science. 313 (5786): 523–6. Bibcode:2006Sci…313..523K. doi:10.1126/science.1126531. PMC 2442710 . PMID 16728595.
The genome of HIV-1 is dimeric, unsegmented and contains a single molecule of linear. The genome is -RT and is positive-sense, single-stranded RNA. The complete genome is fully sequenced and of one monomer 9200 nucleotides long. The genome has terminally redundant sequences that have long terminal repeats (LTR) of about 600 nt. The 5′-end of the genome has a methylated nucleotide cap with a sequence of type 1 m7G5ppp6’GmpNp. The 3′-terminus has a poly (A) tract and has a tRNA-like structure and accepts lysin. Two copies of the genome are present in the virion in a dimeric configuration with two copies per particle being held together by hydrogen bonds to form a dimer. (source: ICTV db Descriptions)
12. Francioli, P. et al (1982) ‘Acquired immunologic deficiency syndrome, opportunistic infections and homosexuality. Presentation of 3 cases studied in Switzerland’ Schweizerische medizinische Wochenschrift 112(47):1682-1687
HIV/AIDS is diagnosed via laboratory testing and then staged based on the presence of certain signs or symptoms. HIV screening is recommended by the United States Preventive Services Task Force for all people 15 years to 65 years of age including all pregnant women. Additionally, testing is recommended for those at high risk, which includes anyone diagnosed with a sexually transmitted illness. In many areas of the world, a third of HIV carriers only discover they are infected at an advanced stage of the disease when AIDS or severe immunodeficiency has become apparent.
Your doctor can monitor how well your HIV treatment is working by measuring the amount of HIV in your blood (also called the viral load.) The goal of treatment is to get the viral load undetectable on labs tests; ideally less than 20 copies. This does not mean the virus is gone or cured, it means the medication is working and must be continued.
Measures to prevent opportunistic infections are effective in many people with HIV/AIDS. In addition to improving current disease, treatment with antiretrovirals reduces the risk of developing additional opportunistic infections. Adults and adolescents who are living with HIV (even on anti-retroviral therapy) with no evidence of active tuberculosis in settings with high tuberculosis burden should receive isoniazid preventive therapy (IPT), the tuberculin skin test can be used to help decide if IPT is needed. Vaccination against hepatitis A and B is advised for all people at risk of HIV before they become infected; however it may also be given after infection. Trimethoprim/sulfamethoxazole prophylaxis between four and six weeks of age and ceasing breastfeeding in infants born to HIV positive mothers is recommended in resource limited settings. It is also recommended to prevent PCP when a person’s CD4 count is below 200 cells/uL and in those who have or have previously had PCP. People with substantial immunosuppression are also advised to receive prophylactic therapy for toxoplasmosis and MAC. Appropriate preventive measures have reduced the rate of these infections by 50% between 1992 and 1997. Influenza vaccination and pneumococcal polysaccharide vaccine are often recommended in people with HIV/AIDS with some evidence of benefit.
Some people will wish to use herbal remedies and a Cochrane review was able to find a small number of trials, some of which seemed to have adequate methodology.There was no significant clinical benefit and objective criteria such as CD4 count were unaffected. Since the review there have been a few studies in the literature suggesting some benefit from herbal remedies but larger trials are needed.[15, 16]
Jump up ^ Irlam, James H.; Siegfried, Nandi; Visser, Marianne E.; Rollins, Nigel C. (2013-10-11). “Micronutrient supplementation for children with HIV infection”. The Cochrane Database of Systematic Reviews (10): CD010666. doi:10.1002/14651858.CD010666. ISSN 1469-493X. PMID 24114375.
In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon. Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response. Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells.
ART extends the average life expectancy, and many people with HIV can expect to live for decades with proper treatment. An increasing number have a normal life expectancy if they adhere carefully to medication regimens. Medications help the immune system recover and fight infections and prevent cancers from occurring. If ART is not taken regularly and doses are missed, the virus may become resistant, and the manifestations of AIDS may develop.
After acute infection, the virus appears to become dormant, and the person feels normal. This stage of HIV infection may last an average of eight to 10 years, but it can vary among individuals and strains of HIV. A recently identified aggressive HIV strain from Cuba has been found to progress to AIDS in as little as three years.
Sexual contact. In adults and adolescents, HIV is spread most commonly by sexual contact with an infected partner. The virus enters the body through the lining of the vagina, vulva, penis, rectum, or mouth through sexual activity.
Further evidence for the importance of chemokine receptors in HIV infection has come from studies in a small group of individuals with high-risk exposure to HIV-1 but who remain seronegative. Cultures of lymphocytes and macrophages from these people were relatively resistant to macrophage-tropic HIV infection and were found to secrete high levels of RANTES, MIP-1α and MIP-1β in response to inoculation with HIV. In other experiments, the addition of these same chemokines to lymphocytes sensitive to HIV blocked their infection because of competition between these CC chemokines and the virus for the cell-surface receptor CCR5.
Macrophage-tropic (M-tropic) strains of HIV-1, or non-syncytia-inducing strains (NSI; now called R5 viruses) use the β-chemokine receptor CCR5 for entry and are, thus, able to replicate in both macrophages and CD4+ T cells. This CCR5 co-receptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV infection. 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. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.
One interesting issue is that the co-receptor usage of the virus strains tends to change over time. The initial infection nearly always involves a strain that uses the chemokine receptor 5 (CCR5), is found on macrophages and dendritic cells, as a co-receptor with CD4. People who are homozygous for deletions in the CCR5 gene (ie, CCR5-delta32) tend to be resistant to infection, [46, 47] and those with heterozygosity for the polymorphism tend to show slower progression of disease. 
Jump up ^ Compared with overview in: Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C. (2007). Lippincott’s Illustrated Reviews: Microbiology. Lippincott’s Illustrated Reviews. Hagerstown, MD: Lippincott Williams & Wilkins. p. 3. ISBN 0-7817-8215-5.
^ Jump up to: a b Consolidated guidelines on the use of antiretroviral drugs for treating and preventing HIV infection (PDF). World Health Organization. 2013. pp. 28–30. ISBN 978-92-4-150572-7. Archived (PDF) from the original on February 9, 2014.
Currently, the risk of infection with HIV in the United States through receiving a blood transfusion or blood products is extremely low and has become progressively lower, even in geographic areas with high HIV prevalence.
A combination of these drugs will be used; the exact mix of drugs is adapted to each individual. HIV treatment is usually permanent and lifelong. HIV treatment is based on routine dosage. Pills must be taken on a regular schedule, every time. Each class of ARVs has different side effects, but some possible common side effects include:
Consider the drug Truvada. The drug emtricitabine-tenofovir (Truvada) can reduce the risk of sexually transmitted HIV infection in people at very high risk. You need to take it every day. It doesn’t prevent other STIs, so you’ll still need to practice safe sex. If you have hepatitis B you should be evaluated by an infectious disease or liver specialist before beginning therapy. You will need a blood test to check your kidney function before taking this drug.
HIV is spread primarily by unprotected sex (including anal and oral sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Some bodily fluids, such as saliva and tears, do not transmit HIV. Methods of prevention include safe sex, needle exchange programs, treating those who are infected, and male circumcision. Disease in a baby can often be prevented by giving both the mother and child antiretroviral medication. There is no cure or vaccine; however, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. Treatment is recommended as soon as the diagnosis is made. Without treatment, the average survival time after infection is 11 years.
In the United States, the face of the HIV/AIDS epidemic has changed dramatically. Adolescents and young adults less than 25 years of age now account for half the new HIV infections reported annually to the CDC and for most perinatally acquired infections. As a result, strategies to prevent new infection and manage the long-term effects of past infection have focused increasingly on the second and third decades of life.
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