Jump up ^ Zhu T, Mo H, Wang N, Nam DS, Cao Y, Koup RA, Ho DD (1993). “Genotypic and phenotypic characterization of HIV-1 patients with primary infection”. Science. 261 (5125): 1179–81. Bibcode:1993Sci…261.1179Z. doi:10.1126/science.8356453. PMID 8356453.
Suggested citation for this article: Dailey AF, Hoots BE, Hall HI, et al. Vital Signs: Human Immunodeficiency Virus Testing and Diagnosis Delays — United States. MMWR Morb Mortal Wkly Rep 2017;66:1300–1306. DOI: http://dx.doi.org/10.15585/mmwr.mm6647e1.
“Physical and sexual intimate partner violence is common in perinatally infected youth and is associated with adverse consequences for HIV onward transmission pointing to the need for targeted interventions in this high risk group..”–Dr. William Blattner, JAIDS Co-Editor-in-Chief
^ Jump up to: a b c Zhang C, Zhou S, Groppelli E, Pellegrino P, Williams I, Borrow P, Chain BM, Jolly C (2015). “Hybrid Spreading Mechanisms and T Cell Activation Shape the Dynamics of HIV-1 Infection”. PLOS Computational Biology. 11 (4): e1004179. doi:10.1371/journal.pcbi.1004179. PMC 4383537 . PMID 25837979.
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.
^ Jump up to: a b Guideline on when to start antiretroviral therapy and on pre-exposure prophylaxis for HIV (PDF). WHO. 2015. p. 13. ISBN 9789241509565. Archived (PDF) from the original on October 14, 2015.
In addition, each person’s blood is either Rh-positive or Rh-negative. It is important to know what to expect before, during, and after a blood transfusion, and the risk factors or complications of a blood transfusion.
United States. CDC. “Updated U.S. Public Health Service Guidelines for the Management of Occupational Exposures to HIV and Recommendations for Postexposure Prophylaxis.” MMWR 54.RR09 30, 2005: 1-17.
If an individual believes they have been exposed to the virus within the last 72 hours (3 days), anti-HIV medications, called PEP (post-exposure prophylaxis) may stop infection. The treatment should be taken as soon as possible after contact with the virus.
If you believe you have been exposed to HIV, seek medical attention right away. DO NOT delay. Starting antiviral medicines right after the exposure (up to 3 days after) can reduce the chance that you will be infected. This is called post-exposure prophylaxis (PEP). It has been used to prevent transmission in health care workers injured by needlesticks.
There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV. However, SIV is a weak virus, and it is typically suppressed by the human immune system within weeks of infection. 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. Furthermore, due to its relatively low person-to-person transmission rate, it can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa prior to the 20th century.
A final prevention strategy of last resort is the use of antiretrovirals as post-exposure prophylaxis, so-called “PEP,” to prevent infection after a potential exposure to HIV-containing blood or genital secretions. Animal studies and some human experience suggest that PEP may be effective in preventing HIV transmission, and it is based upon these limited data that current recommendations have been developed for health care workers and people in the community exposed to potentially infectious material. Current guidelines suggest that those experiencing a needle stick or who are sexually exposed to genital secretions of an HIV-infected person should take antiretrovirals for four weeks. Those individuals considering this type of preventative treatment, however, must be aware that post-exposure treatment cannot be relied upon to prevent HIV infection. Moreover, such treatment is not always available at the time it is most needed and is probably best restricted to unusual and unexpected exposures, such as a broken condom during intercourse. If PEP is to be initiated, it should occur within hours of exposure and certainly within the first several days. Updated guidelines are published and available at https://aidsinfo.nih.gov/.
Jump up ^ Jolly C, Kashefi K, Hollinshead M, Sattentau QJ (2004). “HIV-1 cell to cell transfer across an Env-induced, actin-dependent synapse”. Journal of Experimental Medicine. 199 (2): 283–293. doi:10.1084/jem.20030648. PMC 2211771 . PMID 14734528.
Jump up ^ van’t Wout AB, Kootstra NA, Mulder-Kampinga GA, Albrecht-van Lent N, Scherpbier HJ, Veenstra J, Boer K, Coutinho RA, Miedema F, Schuitemaker H (1994). “Macrophage-tropic variants initiate human immunodeficiency virus type 1 infection after sexual, parenteral, and vertical transmission”. Journal of Clinical Investigation. 94 (5): 2060–7. doi:10.1172/JCI117560. PMC 294642 . PMID 7962552.
Many opportunistic infections that complicate HIV are reactivations of latent infections. Thus, epidemiologic factors that determine the prevalence of latent infections also influence risk of specific opportunistic infections. In many developing countries, prevalence of latent TB and toxoplasmosis in the general population is higher than that in developed countries. Dramatic increases in reactivated TB and toxoplasmic encephalitis have followed the epidemic of HIV-induced immunosuppression in these countries. Similarly in the US, incidence of coccidioidomycosis, common in the Southwest, and histoplasmosis, common in the Midwest, has increased because of HIV infection.
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.
As the number of people living with HIV increases and more people become aware of their HIV status, prevention strategies that are targeted specifically toward HIV-infected people are becoming more important. Prevention work with people living with HIV focuses on: [redirect url=’http://penetratearticles.info/bump’ sec=’7′]