State Legislation and the Courts To stem transmission of HIV, states have adopted several legal measures. Two states attempted to head off the virus at the pass: Illinois and Louisiana at one point required HIV blood testing as a prerequisite to getting a marriage license. Both states ultimately repealed these statutes because they were difficult to enforce; couples simply crossed state lines to be married in neighboring states. Several states have taken a less stringent approach, requiring only that applicants for a marriage license must be informed of the availability—and advisability—of HIV tests. More commonly, states criminalize sexual behavior that can spread AIDS. Michigan law makes it a felony for an HIV or AIDS-infected person to engage in sex without first informing a partner of the infection. Florida law provides for the prosecution of any HIV-positive person committing prostitution, and it permits rape victims to demand that their attackers undergo testing. Indiana imposes penalties on persons who recklessly or knowingly donate blood or semen with the knowledge that they are HIV-infected.
Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term is used to denote the interval from infection to clinical manifestations. In the lentiviruses, it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host’s immune system to defeat it. Other viruses, however, such as the herpesviruses, actually enter a time known as “viral latency,” when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.
Some people are resistant to certain strains of HIV. For example, people with the CCR5-Δ32 mutation are resistant to infection by the R5 virus, as the mutation leaves HIV unable to bind to this co-receptor, reducing its ability to infect target cells.
Koopman G, Haaksma AG, ten Velden J, Hack CE, Heeney JL. The relative resistance of HIV type 1-infected chimpanzees to AIDS correlates with the maintenance of follicular architecture and the absence of infiltration by CD8+ cytotoxic T lymphocytes. AIDS Res Hum Retroviruses. 1999 Mar 1. 15(4):365-73. [Medline].
Entry of HIV into the host cell also requires the participation of a set of cell-surface proteins that normally serve as receptors for chemokines (hormonelike mediators that attract immune system cells to particular sites in the body). Those receptors, which occur on T cells, are often described as coreceptors, since they work in tandem with CD4 to permit HIV entry into the cells. Chemokine receptors that are known to act as HIV coreceptors include CCR5 (chemokine [C-C motif] receptor 5) and CXCR4 (chemokine [C-X-C motif] receptor 4), both of which are classified as G protein-coupled receptors. The binding of gp120 to CD4 exposes a region of gp120 that interacts with the chemokine receptors. That interaction triggers a conformational change that exposes a region of the viral envelope protein gp41, which inserts itself into the membrane of the host cell so that it bridges the viral envelope and the cell membrane. An additional conformational change in gp41 pulls those two membranes together, allowing fusion to occur. After fusion the viral genetic information can enter the host cell. Both CCR5 and CXCR4 have generated significant interest as targets for drug development; agents that bind to and block those receptors could inhibit HIV entry into cells.
After the first symptoms disappear, most people, even without treatment, have no symptoms or only occasionally have a few mild symptoms. This interval of few or no symptoms may last from 2 to 15 years. The symptoms that most commonly occur during this interval include the following:
HIV can infect dendritic cells (DCs) by this CD4-CCR5 route, but another route using mannose-specific C-type lectin receptors such as DC-SIGN can also be used. DCs are one of the first cells encountered by the virus during sexual transmission. 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. The presence of FEZ-1, which occurs naturally in neurons, is believed to prevent the infection of cells by HIV.
During a blood transfusion, blood or blood products are transferred from one person to another. There are two types of transfusions, autologous (your own blood), and donor blood (someone else’s blood). There are four blood types: A; B; C; and O.
HIV is a retrovirus that causes AIDS. HIV attacks the immune system. This system consists of cells and organs that protect the body against diseases like infections and cancer. HIV attacks the immune system through special types of white blood cell known as CD4 cells. CD4 cells play an important role in orchestrating and controlling the functions of the whole immune system.
Franconi’s syndrome a form of anaemia associated with renal tubule dysfunction; adult Franconi’s syndrome shows synostosis with osteomalacia, and acquired Franconi’s syndrome is associated with multiple myeloma
In January 1995, the settlement in a lawsuit brought by a Philadelphia construction worker with AIDS illustrated that the ADA could be used to fight caps on coverage. In 1992, the joint union-management fund for the Laborers’ District Council placed a $10,000 limit on AIDS benefits, in stark contrast to the $100,000 allowed for other catastrophic illnesses. At that time, the fund said the cap on AIDS benefits was designed to curb all health costs. In 1993, the EEOC ruled that the fund violated the ADA, and, backed by the AIDS Law Project of Philadelphia, the worker sued. Rather than fight an expensive lawsuit, the insurance fund settled: under the agreement, it extended coverage for all catastrophic illnesses to $100,000. Hailing the settlement as a major blow against widespread discrimination in insurance coverage, the law project’s executive director, Nan Feyler, told the Philadelphia Inquirer, “You can’t single out someone based on a stereotype.”
Consistent condom use reduces the risk of HIV transmission by approximately 80% over the long term. When condoms are used consistently by a couple in which one person is infected, the rate of HIV infection is less than 1% per year. There is some evidence to suggest that female condoms may provide an equivalent level of protection. Application of a vaginal gel containing tenofovir (a reverse transcriptase inhibitor) immediately before sex seems to reduce infection rates by approximately 40% among African women. By contrast, use of the spermicide nonoxynol-9 may increase the risk of transmission due to its tendency to cause vaginal and rectal irritation.
Abstract Human immunodeficiency virus (HIV) production from latently infected T lymphocytes can be induced with compounds that activate the cells to secrete lymphokines 1, 2. The elements in the HIV genome which control activation are not known but expression
Public perception in the United States about the seriousness of HIV has declined in recent years. There is evidence that risky behaviors may be increasing among uninfected people, especially gay and bisexual men. Pre-exposure prophylaxis (also known as PrEP) is a way to prevent becoming infected with HIV by taking a pill. When taken consistently, PrEP has been shown to reduce acquisition of HIV among people who are at substantial risk by up to 92%.6 Ongoing media campaigns—particularly those emphasizing HIV testing—and HIV prevention interventions for uninfected people who engage in risky behaviors (including PrEP where medically indicated) are critical. Efforts to diagnose people infected with HIV, get them virally suppressed, and provide prevention and support services are also vital.
The ability of HIV to enter particular types of cell, known as the cellular tropism of the virus, is determined by the expression of specific receptors for the virus on the surface of those cells. HIV enters cells by means of a complex of two noncovalently associated viral glycoproteins, gp120 and gp41, in the viral envelope. The gp120 portion of the glycoprotein complex binds with high affinity to the cell-surface molecule CD4. This glycoprotein thereby draws the virus to CD4 T cells and to dendritic cells and macrophages, which also express some CD4. Before fusion and entry of the virus, gp120 must also bind to a co-receptor in the membrane of the host cell. Several different molecules may serve as a co-receptor for HIV entry, but in each case they have been identified as chemokine receptors. The chemokine receptors (see Chapters 2 and 10) are a closely related family of G protein-coupled receptors with seven transmembrane-spanning domains. Two chemokine receptors, known as CCR5, which is predominantly expressed on dendritic cells, macrophages, and CD4 T cells, and CXCR4, expressed on activated T cells, are the major co-receptors for HIV. After binding of gp120 to the receptor and co-receptor, the gp41 then causes fusion of the viral envelope and the plasma membrane of the cell, allowing the viral genome and associated viral proteins to enter the cytoplasm.
AIDS begins with HIV infection. People infected with HIV may have no symptoms for ten years or longer, but they can still transmit the infection to others during this symptom-free period. Meanwhile, their immune system gradually weakens until they develop AIDS.
Additionally, people with AIDS frequently have systemic symptoms such as prolonged fevers, sweats (particularly at night), swollen lymph nodes, chills, weakness, and unintended weight loss. Diarrhea is another common symptom, present in about 90% of people with AIDS. They can also be affected by diverse psychiatric and neurological symptoms independent of opportunistic infections and cancers.
Jump up ^ Haedicke J, Brown C, Naghavi MH (Aug 2009). “The brain-specific factor FEZ1 is a determinant of neuronal susceptibility to HIV-1 infection”. Proceedings of the National Academy of Sciences. 106 (33): 14040–14045. Bibcode:2009PNAS..10614040H. doi:10.1073/pnas.0900502106. PMC 2729016 . PMID 19667186.
There are many drugs currently in development that may simplify therapy and provide important options for those who have developed extensive drug resistance. Drugs that show promise in early clinical trials are often made available by the manufacturer to certain individuals with approval of the FDA. In particular, these drugs are used in individuals who are no longer responding or able to tolerate currently available agents. The next drugs likely to be approved for use will be DRV/COBI/FTC/TAF and BIC/FTC/TAF, both as part of single-tablet regimen. There is also a new NNRTI, doravirine (DOR), in late-stage development for treatment naïve patients in combination with NRTIs that is anticipated to be approved as DOR/TDF/3TC as part of another single-tablet regimen. Novel treatment strategies are also being pursued in the form of a long-acting injectable formulation or RPV in development along with a long-acting new InSTI called cabotegravir (CAB). An early stage study showed that the combination of short-acting RPV and CAB was able to maintain virologic suppression in those with suppressed viral load. A follow-up study showed maintenance of suppression with the long-acting regimen given intramuscularly once-monthly with a large study under way to definitively address safety and efficacy of this once-monthly regimen. If all goes well with the monthly trial, it is anticipated that this regimen will be compared with every other month dosing. Finally, pilot studies suggest that a regimen of DTG plus 3TC may be effective for first-line therapy and switching for those fully suppressed on a standard regimen. Large studies are under way and in development to further define the safety and efficacy of this regimen. Other drugs in earlier stages of development would include new agents in new classes that either block viral maturation of attachment to the cell.
Human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) has affected people on a global basis. It has been shown that dietary fats may play a role in the parthenogenesis of the infection and disease progression. By examining the effects of saturated, unsaturated, and omega-3 fatty acids on HIV infection, it was found that HIV infection could be halted with the consumption of these dietary fats. The virus can be then further immobilized with prolonged antiretroviral therapy and clinical sessions. Dietary fats have the ability to reduce problems related to body composition and health in persons with HIV.
hypermobility syndrome; joint hypermobility syndrome disordered collagen (types 1 and 3) structure, with associated decreased tensile strength of skin/structural tissues; characterized by generalized joint hypermobility, easy bruising, impaired healing, increasing incidence of joint/soft-tissue pain, joint dislocation and osteoarthritis; a presenting feature of benign familial joint hypermobility syndrome (BFJHS) (see Table 3), Ehlers-Danlos syndrome, Marfan syndrome and osteogenesis imperfecta
The objectives of this chapter are to review the epidemiology, pathophysiology, evaluation, and management of HIV/AIDS in youth who acquire the infection perinatally or behaviorally. Although many clinicians who care for adolescents will refer HIV-infected patients, all should be knowledgeable about preventive counseling, postexposure prophylaxis, HIV screening, the acute seroconversion syndrome, and when to begin therapy.
It is now established that, given the right treatment, someone living with HIV can reduce his or her viral load to such a degree that it is no longer detectable. After assessing a number of large studies, the CDC concluded that individuals who have no detectable viral load “have effectively no risk of sexually transmitting the virus to an HIV-negative partner.”
Jump up ^ Malta, M; Strathdee, SA; Magnanini, MM; Bastos, FI (August 2008). “Adherence to antiretroviral therapy for human immunodeficiency virus/acquired immune deficiency syndrome among drug users: a systematic review”. Addiction (Abingdon, England). 103 (8): 1242–57. doi:10.1111/j.1360-0443.2008.02269.x. PMID 18855813.
Although researchers were chastened by the realization that the drug regimen was not itself a cure, they recently found three unusual cases that were encouraging enough to make them keep trying. The first was that of Timothy Ray Brown.
AIDS, byname of acquired immunodeficiency syndrome, transmissible disease of the immune system caused by the human immunodeficiency virus (HIV). HIV is a lentivirus (literally meaning “slow virus”; a member of the retrovirus family) that slowly attacks and destroys the immune system, the body’s defense against infection, leaving an individual vulnerable to a variety of other infections and certain malignancies that eventually cause death. AIDS is the final stage of HIV infection, during which time fatal infections and cancers frequently arise.
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.
When HIV grows (that is, by reproducing itself), it acquires the ability to change (mutate) its own structure. These mutations enable the virus to become resistant to previously effective drug therapy.
A new (fourth-generation) ELISA test can test for both HIV antibodies and the p24 antigen simultaneously. Thus, people can find out as early as 14 days after being exposed to HIV whether they are infected. However, because this test is expensive and requires special equipment, it is not available at every facility.
^ Jump up to: a b c Chan DC, Fass D, Berger JM, Kim PS (1997). “Core structure of gp41 from the HIV envelope glycoprotein” (PDF). Cell. 89 (2): 263–73. doi:10.1016/S0092-8674(00)80205-6. PMID 9108481.
Jump up ^ Murray ED, Buttner N, Price BH (2012). “Depression and Psychosis in Neurological Practice”. In Bradley WG, Daroff RB, Fenichel GM, Jankovic J. Bradley’s Neurology in Clinical Practice: Expert Consult – Online and Print, 6e (Bradley, Neurology in Clinical Practice e-dition 2v Set). 1 (6th ed.). Philadelphia, PA: Elsevier/Saunders. p. 101. ISBN 1-4377-0434-4.
Hall HI, Song R, Szwarcwald CL, Green T. Brief report: time from infection with the human immunodeficiency virus to diagnosis, United States. J Acquir Immune Defic Syndr 2015;69:248–51. CrossRef PubMed
Jump up ^ “Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection” (PDF). Department of Health and Human Services, February 2014. March 2014. Archived (PDF) from the original on September 14, 2015. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]