What'sitlike having HIV/Aids? Like how does it make you feel? What are the stages of it?
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Answers:
You get sick often, apparently you feel normal though
HIV infects certain human cells by binding its envelope glycoproteins gp120 and gp41 to specific molecules on the surface of the cells. Only cells that carry the appropriate molecules are susceptible to infection by HIV. In the 1980s, scientists quickly recognized that a molecule called CD4, which is found particularly on certain T-lymphocytes (a type of white blood cell), was the primary binding site, but it was only in 1996 that other co-receptors that are also required for infection were identified. Fusion of the virus with the cell membrane permits the viral nucleoid to enter the cell.
One of the co-receptors is called chemokine receptor 5 (CCR5). Because of their inherited genetic make-up, about 14 per cent of Caucasians have unusually small numbers of these receptors on the surface of their cells and a smaller proportion do not express CCR5 on their cells at all, rendering these cells less susceptible to infection with HIV. Studies suggest that this may help to explain why some people appear to be resistant to HIV infection and remain HIV-negative despite multiple exposures to the virus, and why some HIV-positive people experience slower disease progression than others.
As HIV disease progresses, HIV variants called syncytium-inducing (SI) strains evolve within the individual's body. SI variants can use an additional co-receptor on human cells, called CXCR4. This may allow HIV to infect a wider range of cells and may help to explain why the emergence of SI variants is associated with a worse prognosis. Again, a small proportion of Caucasians (about 1 per cent) do not produce this co-receptor.
Once fusion has taken place, reverse transcription then occurs to convert the viral genomic RNA into double-stranded DNA. The viral DNA is transported to the cell nucleus and is integrated, or inserted, into the normal cellular chromosomal DNA. When the right activation signals are present, the process of making new virions begins. Using the replication machinery of the host cell, the integrated viral DNA is transcribed to make messenger RNA (mRNA) and new strands of viral genomic RNA. The viral mRNA is then translated into a protein string that is cleaved into specific viral proteins. Assembly of new virions then takes place within the cell, and the new HIV particles are released by budding from the cell surface, taking a piece of the cell membrane as their envelope.
HIV replication can directly kill CD4+ T-lymphocytes. The loss of these cells paralyses the immune system and is one mechanism by which HIV infection causes AIDS.
A number of anti-HIV drugs have been developed, each targeting a different stage in this viral life cycle. By 2001, nine reverse transcriptase inhibitors and six protease inhibitors had been developed, with more in development. The widespread use of combinations of these agents in the developed world has resulted in dramatic reductions in rates of HIV-related illness and death. Several members of a new class of drugs, which inhibit the binding or fusion of HIV to host cells, are now in clinical development.
One person is infected with HIV in every 6.4 seconds. Do your part.
Please see the webpages for more details on HIV/AIDS.
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