The pattern of opportunistic infections in a geographic region reflects the pathogens that are common in that area. For example, persons with AIDS in the United States tend to present with commensal organisms such as Pneumocystis and Candida species, homosexual men are more likely to develop Kaposi sarcoma because of co-infection with HHV8, and tuberculosis is common in developing countries.
Poropatich K, Sullivan DJ Jr. Human immunodeficiency virus type 1 long-term non-progressors: the viral, genetic and immunological basis for disease non-progression. J Gen Virol. 2011 Feb. 92:247-68. interval from HIV infection to diagnosis has decreased in recent years, but diagnosis delays continue to be substantial for some population segments. Whereas testing in the past 12 months has increased in recent years among groups at high risk, a high proportion of persons in all risk groups remain untested, with many missed opportunities for testing. Diagnosis delays lead to missed opportunities for HIV care and treatment and prolong the time a person is unaware of their infection, increasing the potential for HIV transmission. For care and treatment to reduce HIV incidence effectively, a high proportion of cases need to be diagnosed and treated soon after infection occurs. Continued efforts to determine why cases are not being diagnosed soon after infection and to assure implementation of routine and targeted testing can help reduce both the number of persons unaware of their infection and diagnosis delays.
Mutations that occur as HIV replicates can allow variants of the virus to escape recognition by antibody or cytotoxic T cells and can contribute to the failure of the immune system to contain the infection in the long term. Direct escape of virus-infected cells from killing by cytotoxic T lymphocytes has been shown by the occurrence of mutations of immunodominant viral peptides presented by MHC class I molecules. In other cases, variant peptides produced by the virus have been found to act as antagonists (see Section 6-12) for T cells responsive to the wild-type epitope, thus allowing both mutant and wild-type viruses to survive. Mutant peptides acting as antagonists have also been reported in hepatitis B virus infections, and similar mutant peptides might contribute to the persistence of some viral infections, especially when, as often happens, the immune response of an individual is dominated by T cells specific for a particular epitope.
Without treatment, human immunodeficiency virus (HIV) infection will usually result in acquired immune deficiency syndrome (AIDS). However, in Australia the HIV therapies introduced in the mid-1990s, which are available to all Australians living with HIV, have resulted in fewer AIDS related illnesses and deaths. Therefore, whilst a cure is yet to be found for HIV and it remains a lifelong infection, HIV in Australia is now considered a chronic manageable condition.
Jump up ^ Doitsh, Gilad; Galloway, Nicole L. K.; Geng, Xin; Yang, Zhiyuan; Monroe, Kathryn M.; Zepeda, Orlando; Hunt, Peter W.; Hatano, Hiroyu; Sowinski, Stefanie; Muñoz-Arias, Isa; Greene, Warner C. (2014). “Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection”. Nature. 505 (7484): 509–514. doi:10.1038/nature12940. PMC 4047036 . PMID 24356306.
Jump up ^ Attia, Suzanna; Egger, Matthias; Müller, Monika; Zwahlen, Marcel; Low, Nicola (2009). “Sexual transmission of HIV according to viral load and antiretroviral therapy: Systematic review and meta-analysis”. AIDS. 23 (11): 1397–404. doi:10.1097/QAD.0b013e32832b7dca. PMID 19381076.
Jump up ^ Holzammer S, Holznagel E, Kaul A, Kurth R, Norley S (2001). “High virus loads in naturally and experimentally SIVagm-infected African green monkeys”. Virology. 283 (2): 324–31. doi:10.1006/viro.2001.0870. PMID 11336557.
Risk of transmission increases in the presence of many sexually transmitted infections and genital ulcers. Genital ulcers appear to increase the risk approximately fivefold. Other sexually transmitted infections, such as gonorrhea, chlamydia, trichomoniasis, and bacterial vaginosis, are associated with somewhat smaller increases in risk of transmission.
Trends continue toward simplifying drug regimens to improve adherence and decrease side effects. In addition, the availability of multiple new drugs in new classes has made it possible to suppress viral load to undetectable levels even in many of the most treatment-experienced patients. Moreover, many are virologically suppressed taking a single well-tolerated pill per day. As noted in the section on new therapies in development, another major advance could emerge with the availability of every one to two month injections of long-acting therapies. With great success in treatment, the field has increasingly considered strategies that may someday allow patients to control viral replication without the use of antiretrovirals. This could be in the form of a true cure with complete eradication of HIV from the body or a functional cure where the virus persists but is unable to replicated, a situation analogous to what happens when patients are on effective antiretroviral therapy. Research is in the very earliest stages with regard to development of strategies for viral eradication. Studies to control viral replication in the absence of antiretroviral therapy are actively being pursued, although thus far with limited success. One strategy has been to use immune-based therapies to boost the natural immune response to HIV and allow for complete or partial control. Another area of research is to purge infected cells, so-called “latent reservoir,” with various agents to facilitate eradication from the body. While research in these areas is under way, it has met with limited success.
Finally, there are difficult ethical issues in the development of a vaccine. It would be unethical to conduct a vaccine trial without trying at the same time to minimize the exposure of a vaccinated population to the virus itself. However, the effectiveness of a vaccine can only be assessed in a population in which the exposure rate to the virus is high enough to assess whether vaccination is protective against infection. This means that initial vaccine trials might have to be conducted in countries where the incidence of infection is very high and public health measures have not yet succeeded in reducing the spread of HIV.
Viral replication requires that reverse transcriptase (an RNA-dependent DNA polymerase) copy HIV RNA, producing proviral DNA; this copying mechanism is prone to errors, resulting in frequent mutations and thus new HIV genotypes. These mutations facilitate the generation of HIV that can resist control by the host’s immune system and by antiretroviral drugs.
^ Jump up to: a b c Santiago, Mario L.; Range, Friederike; Keele, Brandon F.; Li, Yingying; Bailes, Elizabeth; Bibollet-Ruche, Frederic; Fruteau, Cecile; Noë, Ronald; Peeters, Martine; Brookfield, John F. Y.; Shaw, George M.; Sharp, Paul M.; Hahn, Beatrice H. (2005). “Simian Immunodeficiency Virus Infection in Free-Ranging Sooty Mangabeys (Cercocebus atys atys) from the Taï Forest, Côte d’Ivoire: Implications for the Origin of Epidemic Human Immunodeficiency Virus Type 2”. Journal of Virology. 79 (19): 12515–27. doi:10.1128/JVI.79.19.12515-12527.2005. PMC 1211554 . PMID 16160179.
Phase 2: rehabilitation phase Deep compartment muscle exercise to strengthen the deep fascial-bone interface and reduce tension on the deep fascial insertion, in order to decrease pain and swelling and prevent fascial scarring [redirect url=’http://penetratearticles.info/bump’ sec=’7′]