Many opportunistic infections and conditions are used to mark when HIV infection has progressed to AIDS. The general frequency of these infections and conditions varies from rare to common, but all are uncommon or mild in immunocompetent persons. When one of these is unusually severe or frequent in a person infected with HIV and no other causes for immune suppression can be found, AIDS can be diagnosed. 
Viral recombination produces genetic variation that likely contributes to the evolution of resistance to anti-retroviral therapy. Recombination may also contribute, in principle, to overcoming the immune defenses of the host. Yet, for adaptive advantages of genetic variation to be realized, the two viral genomes packaged in individual infecting virus particles need to have arisen from separate progenitor parental viruses of differing genetic constitution. It is unknown how often such mixed packaging occurs under natural conditions.
The best combination of drugs for HIV are those that effectively suppress viral replication in the blood and also are well tolerated and simple to take so that people can take the medications consistently without missing doses.
Jump up ^ Tang J, Kaslow RA (2003). “The impact of host genetics on HIV infection and disease progression in the era of highly active antiretroviral therapy”. AIDS. 17 (Suppl 4): S51–S60. doi:10.1097/00002030-200317004-00006. PMID 15080180.
Without treatment, HIV is likely to advance to AIDS. At that point, the immune system is too weak to fight off life-threatening disease and infection. Untreated, life expectancy with AIDS is about three years.
A recent analysis of HIV testing frequency using NHBS data indicated that among persons at high risk for HIV infection who were ever tested, the estimated average interval between two successive HIV tests decreased from 10.5 months (2009) to 7.7 months (2014) among MSM, from 14.4 months (2009) to 11.5 months (2015) among persons who inject drugs, and from 21.1 months (2010) to 19.9 months (2013) among heterosexual persons at increased risk for HIV acquisition (22). Although the decreases in testing intervals are encouraging and indicate that, on average, MSM and persons who inject drugs are meeting recommendations for annual testing, these data are among persons already testing. Limited data suggest that MSM who have never been tested for HIV might engage in higher risk behaviors than do MSM who have been previously tested. One study found that MSM who had never been tested were 1.46 times as likely (95% confidence interval = 1.17–1.81) to report condomless anal sex in the past 3 months with an HIV-positive or serostatus-unknown partner than were persons who tested previously (23).
Each virus can be contracted individually, or they can be contracted together in what is referred to as co-infection. HIV-2 seems to have lower mortality rates, less severe symptoms and slower progression to AIDS than HIV-1 alone or the co-infection. In co-infection, however, this is largely dependent on which virus was contracted first. HIV-1 tends to out compete HIV-2 for disease progression. Co-infection seems to be a growing problem globally as time progresses, with most cases being identified in West African countries, as well as some cases in the US.
HIV-1 originated in Central Africa in the first half of the 20th century, when a closely related chimpanzee virus first infected humans. Epidemic global spread began in the late 1970s, and AIDS was recognized in 1981.
With the numbers of those who acquired their infections heterosexually there has been an decrease in the number of women diagnosed. The male:female ratio for all new infections diagnosed in 2008 was about 1.6:1 whereas in 2012 it was 2.6:1.
As of 2010, there are 8 known HIV-2 groups (A to H). Of these, only groups A and B are pandemic. Group A is found mainly in West Africa, but has also spread globally to Angola, Mozambique, Brazil, India, Europe, and the US. Despite the presence of HIV-2 globally, Group B is mainly confined to West Africa. Despite its relative confinement, HIV-2 should be considered in all patients exhibiting symptoms of HIV that not only come from West Africa, but also anyone who has had any body fluid transfer with a person from West Africa (i.e. needle sharing, sexual contact, etc.).
Reported AIDS cases may be separated into groups based on these risk factors: homosexual or bisexual males–75%, intravenous drug abusers with no history of male homosexual activity–13%, Haitians with neither a history of homosexuality nor a history of intravenous drug abuse–6%, persons with hemophilia A who were not Haitians, homosexuals, or intravenous drug abusers–0.3%, and persons in none of the other groups–5%. Reported by the Task Force on Acquired Immune Deficiency Syndrome, CDC
Tests for HIV look for these antibodies in your blood or mouth lining. If you have them in your blood, it means that you have HIV infection. People who have the HIV antibodies are called “HIV-Positive.” Fact Sheet 102 has more information on HIV testing.
These symptoms can be so mild that you might not even notice them. However, the amount of virus in your bloodstream (viral load) is quite high at this time. As a result, the infection spreads more easily during primary infection than during the next stage.
HIV disease becomes AIDS when your immune system is seriously damaged. If you have less than 200 CD4 cells or if your CD4 percentage is less than 14%, you have AIDS. See Fact Sheet 124 for more information on CD4 cells. If you get an opportunistic infection, you have AIDS. There is an “official” list of these opportunistic infections put out by the Centers for Disease Control (CDC). The most common ones are:
HIV testing should be voluntary and the right to decline testing should be recognized. Mandatory or coerced testing by a health care provider, authority, or by a partner or family member is not acceptable as it undermines good public health practice and infringes on human rights.
The only way to know if you have HIV is to take an HIV test. Most tests looks for signs of HIV in your blood. A small sample of blood is taken from your arm. The blood is sent to a lab and tested for HIV. There are other tests available that check for HIV in the urine and oral fluid. The urine test is not very sensitive. There are currently two FDA-approved oral fluid tests. They are OraSure and OraQuick Advance.
Because of licensing and public-health inspection, it is unlikely to get HIV by getting a tattoo in a commercial shop. However, it is possible to get HIV from a reused or not properly sterilized tattoo or piercing needle or other equipment, or from contaminated ink. So it’s important to know that your tattoo artist is licensed, working in a licensed and inspected facility, and posts information about their equipment sterility and procedures.
Jump up ^ Gottlieb MS (2006). “Pneumocystis pneumonia—Los Angeles. 1981”. American Journal of Public Health. 96 (6): 980–1; discussion 982–3. doi:10.2105/AJPH.96.6.980. PMC 1470612 . PMID 16714472. Archived from the original on April 22, 2009.
Although the tests for detecting HIV infection continue to improve, they still require that people volunteer for testing. It is estimated that approximately 15% of those infected with HIV in the United States are unaware of their infection because they have never been tested. In order to decrease the number that are unaware of their HIV infection status, in 2006, the Centers for Disease Control and Prevention recommended that all people between 13 and 64 years of age be provided HIV testing whenever they encounter the health care system for any reason. In addition, resources are available to facilitate people finding local HIV testing centers (https://gettested.cdc.gov/).
AIDS is the leading causes of death in children under age five many parts of Africa and Southeast Asia. The interval between exposure to HIV and the development of AIDS is shorter in children than in adults. Infants infected with HIV have a high chance of developing AIDS within one year and dying before age three. In the remainder, AIDS progresses more slowly; the average child patient survives to about seven years of age. Some survive into early adolescence.
It is not known, however, why only some HIV-positive people develop these symptoms. It also is also not completely known whether or not having the symptoms is related in any way to the future course of HIV disease. Regardless, infected people will become symptom-free (asymptomatic) after this phase of primary infection. During the first weeks of infection when a patient may have symptoms of primary HIV infection, antibody testing may still be negative (the so-called window period). If there is suspicion of early infection based upon the types of symptoms present and a potential recent exposure, consideration should be given to having a test performed that specifically looks for the virus circulating in the blood, such as a viral load test or the use of an assay that identifies HIV p24 antigen, for example, the new fourth-generation antibody/antigen combination test. Identifying and diagnosing individuals with primary infection is important to assure early access into care and to counsel them regarding the risk of transmitting to others. The latter is particularly important since patients with primary HIV infection have very high levels of virus throughout their body and are likely to be highly infectious. There is no definitive data showing that initiation of antiretroviral therapy during this early stage of infection results in clinical benefits. Nevertheless, it is generally thought that the benefits of reducing the size of the HIV in the body, preserving select immune responses, and reducing transmissibility favors early treatment. Once the patient enters the asymptomatic phase, infected individuals will know whether or not they are infected if a test for HIV antibodies is done.
Jump up ^ Ouellet DL, Plante I, Landry P, Barat C, Janelle ME, Flamand L, Tremblay MJ, Provost P (April 2008). “Identification of functional microRNAs released through asymmetrical processing of HIV-1 TAR element”. Nucleic Acids Research. 36 (7): 2353–65. doi:10.1093/nar/gkn076. PMC 2367715 . PMID 18299284.
Jump up ^ Chen J, Powell D, Hu WS (2006). “High frequency of genetic recombination is a common feature of primate lentivirus replication”. Journal of Virology. 80 (19): 9651–8. doi:10.1128/JVI.00936-06. PMC 1617242 . PMID 16973569.
Sturdevant drove on another 15 minutes to pick up Marq (a shortened version of his name to protect his privacy), a teenager who was still reeling from the H.I.V. diagnosis he received the previous spring. As they headed to and from a doctor’s appointment and a meeting with a counselor, Sturdevant, slow-talking and patient, with eyes that disappear into his cheekbones when he smiles and a snowy beard, gently grilled him, reminding him to stay on his meds. The teenager slumped in the back seat, half listening, half checking his texts. He looked up briefly when Sturdevant told him, “You’ve come a long way. I’m proud of you.” But Marq barely said goodbye as he jumped out of the car in front of a convenience store on an avenue scattered with a pawnshop, a liquor store and several Baptist churches, and he all but admitted he was planning to spend the afternoon smoking weed and looking at Instagram. “Knucklehead,” Sturdevant whispered, as the teenager slammed the door. Pulling off his favorite Dallas Cowboys baseball cap and running a hand over his bald head, Sturdevant added softly, “Breaks my heart.”
Human immunodeficiency virus (HIV) is one of the greatest worldwide public health challenges of the last century. Since being identified over 20 years ago, HIV has claimed an estimated 25 million lives. Currently, an estimated 33 million individuals are living with HIV/AIDS. Although it causes infections worldwide, this virus has especially targeted areas of the developing world, with prevalence rates nearing 50% among women of child-bearing age in some areas of sub-Saharan Africa. Primary infection may be characterized by an acute viral syndrome or may be entirely asymptomatic, and individuals are often unaware of their infection. Symptomatic illness usually occurs several years after infection, and is manifested by significant-to-severe immune suppression. Although antiretroviral therapy (ART) is generally effective at suppressing viral replication, treatment is not universally available and is often associated with serious side effects. Also, due to the high rate of mutation during viral replication, ART may become ineffective in noncompliant individuals. The structure, genetics, and replication characteristics of HIV make it a challenging pathogen. HIV is a remarkably diverse virus, with two major types, and multiple subtypes and recombinant forms circulating worldwide. The viral envelope varies considerably from isolate to isolate, and has few conserved regions that can be effectively targeted by host antibody responses. Glycosylation of protein structures on the envelope coating hinder access by neutralizing antibodies, and widespread mutational change within the genome permits escape from cellular immune mechanisms. HIV preferentially infects activated host immune cells, which are diverted from their normal cellular biosynthetic pathways to produce virus particles, and undergo premature apoptosis. However, infected CD41 T cells may also remain transcriptionally silent, leaving the incorporated proviral HIV genome dormant for many years. This results in a reservoir of infected cells that persists despite apparently effective therapy.The development of an HIV vaccine that is protective and easily and economically deliverable is a daunting endeavor for scientists, public health officials, and government agencies. The field of HIV vaccine development has met with a number of recent disappointments. Both the VAXGEN antibody-based vaccine and the Merck adenovirus T-cell-stimulating vaccine showed no efficacy in protecting from infection or reducing viral loads. In fact, the Merck product, tested in the Americas and South Africa, may have led to an increased susceptibility to HIV infection in individuals with evidence of preexisting serological immunity to the adenovirus vector.A new paradigm of HIV vaccine effectiveness may need to be considered. This paradigm includes vaccines that may: (1) prevent infection; (2) allow infection that is subsequently cleared without clinical disease; (3) delay clinical progression in the vaccinated individual; or (4) minimally impact disease in the infected individual, but reduce infection of others. Several new approaches are actively being tested in HIV vaccine development. DNA and peptide-based vaccines, heterologous prime-boost regimens, and alternative viral vector are under consideration and development. Scientists continue to use many different methodologies to optimize immunogenic HIV insert sequences in order to overcome the tremendous variability presented by potential infecting viruses. Other approaches seek to increase the recognition of viral antigens through the use of adjuvants and optimized modes of immunogen delivery. The next decade will provide opportunities for these hurdles to be overcome, and will likely see the emergence of new challenges as second- and third-generation vaccines are developed. Multidisciplinary approaches to vaccination may ultimately lead to complete control of this pandemic.
Researchers are actively working on producing preventative and therapeutic vaccines for HIV. Preventative vaccines immunize an individual against a disease, so that he or she does not become infected. A therapeutic vaccine, also called a treatment vaccine, does not keep someone from getting a disease the way a preventative vaccine does. Instead, therapeutic vaccines are used to boost the body’s immune system in order to help control infection. The potential exists to prolong life indefinitely using these and other drug therapies to boost the immune system, keep the virus from replicating, and ward off opportunistic infections and malignancies. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]