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HIV Life Cycle (http://aids.about.com/cs/aidsfactsheets/a/hivlife.htm)

The treatments and medications we have for HIV and AIDS are possible due to our understanding of HIV and its life cycle. Knowing how HIV makes copies of itself allows us to develop ways to block the process, and in turn preserve our immune system. This article will explain the process of HIV replication and what our medications due to stop it. HIV Live Cycle

Introduction of HIV
Obviously, before HIV can do damage it must enter the body. We all know that exposure to infected bodily fluids through sexual contact or sharing of neeedles is the primary way HIV enters the body. Infection through child birth and breast feeding are also ways people become exposed to HIV.

Viral Attachment
Once in the body, HIV needs a host to help it reproduce. The host in the case of HIV is the T-cell or CD4 cell. HIV seeks out CD4 cells and must attach to them by way of a "lock and key" type system. Proteins on the surface of HIV attach to complimentary proteins on the CD4 cell much like the way a key fits into a lock. The class of drugs called entry inhibitors (Fuzeon, T-20) block this attachment, preventing HIV from using the T-cell. Once allowed to attach, HIV uses the cell for the next steps in reproduction. Viral Fusion
Once attached to the cell, HIV injects proteins of its own into the cellular fluids (cytoplasm) of the T-cell. This causes a fusion of the cell membrane to the outer envelope of the HIV. Again, the class of drugs called entry inhibitors or fusion inhibitors (Fuzeon, T-20) block this fusion between cell and HIV. The Uncoating
In order to use its genetic material (RNA) for reproduction, the protective coating surrounding the RNA must be dissolved. Without this step, conversion of RNA to DNA can't take place, and reproduction is halted. Reverse Transcription
Once in the cell, the single stranded RNA of the HIV must be converted to the double stranded DNA. It accomplishes this with the help of the enzyme reverse transcriptase. Reverse transcriptase uses building blocks from the T-cell to help change the HIV RNA to DNA. The DNA contains the genetic information needed for HIV reproduction. Drugs called reverse transcriptase inhibitors block HIV's reverse transcriptase from using these building blocks. Nucleoside and nucleotide analog reverse transcriptase inhibitors (NRTIs) -- such as Zerit, Epivir, and Viread -- contain faulty imitations of the nucleotides found in a T-cell's cytoplasm. Instead of incorporating a nucleotide into the growing chain of DNA, the imitation building blocks in NRTIs are inserted, which prevents the double strand of DNA from becoming fully formed. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) -- such as Viramune and Sustiva -- block reverse transcription by attaching to the enzyme in a way that prevents it from functioning. Integration
To use the cell to reproduce, it must integrate the newly formed DNA into the cell nucleus. While the process is not fully understood, it is thought to be aided by transport proteins supplied by HIV. Viral Latency
Once integration has occurred, HIV must wait for more protein building blocks to be formed by the cells...in other words, HIV is waiting for materials it needs to complete the reproductive process. Final Assembly
Now that all the materials are available, they must be separated (cleavage) and assembled into new HIV. This process is possible because of the enzyme protease. This enzyme separates the parts allowing them to be reassembled into new HIV. Drugs called protease inhibitors -- such as Kaletra, Crixivan, and Viracept -- bind to the protease enzyme and prevent it from separating, or cleaving, the subunits. Budding
The final step of the viral life cycle is called budding. With its genetic material tucked away and a new outer coat made from the host (CD4) cell's membrane, the newly formed HIV pinches off and enters into circulation, ready to start the whole process again.





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What are Rapid HIV Tests? (http://aids.about.com/cs/hivtesting/f/rapid.htm)

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