Therefore, retroviruses cannot replicate themselves like normal viruses do. HIV always fuses with T-cells. These cells are a group of white blood cells known as lymphocytes. For a HIV-cell to fuse with the cell, it requires the presence of certain receptors on the cell surface. In this case, CD4 – receptors and co-receptors such as CCR5 or CXCR4. When the cell fuses with the T-cell, it releases two RNA-strands and 3 different replication enzymes. Integrase, protease and reverse transcriptase. Reverse transcriptase begins the reverse transcription of the viral RNA-strands.
In this process, one RNA-strand is transcribed to a RNA-DNA double helix. Now the integrase cuts the 3’ at each end of the DNA. This causes the DNA to remain two sticky ends. Integrase transfers the DNA and facilitates integration into the host cell. Now the host cell contains the genetic information of HIV in its DNA. From now on, when DNA replication occurs, the information of HIV is being replicated with it. Now the cell also contains mRNA with this information. The mRNA then migrates into the cytoplasm where building blocks for a new virus are synthesized. Here is where the protease comes in action.
Protease cleaves long proteins into smaller core proteins. Those smaller core proteins are crucial in this whole process. Two RNA strands and these three replication enzymes come together. The smaller core proteins now gather around these molecules and transfer the formed capsule through the plasmid membrane. From now on, the infected cell will keep producing these virus molecules. This causes more T-cells to get infected and so on.  T-cells are lymphocytes. These cells have a central role in the cell-mediated immunity. HIV causes T-cells to practically self-destruct. The cells cannot attack other bacteria and viruses anymore.
One who has AIDS runs faster risk of infection then one who has not. An innocent flu can be fatal for a HIV-patient. How can HIV/AIDS be treated? For AIDS, there a five major types of medicines. The first are Reverse Transcriptase inhibitors. These medicines keep the infected cells from copying the RNA strands. The second ones are protease inhibitors. These medicines make sure that the long proteins don’t get cut into smaller core proteins. This is the most important part of the whole replication-process. Without these smaller core proteins, the virus-molecules are unable to get out of the host cell.
The third ones are fusion inhibitors. The outer cell surface of the HIV-virus is covered with gp120 or gp41 proteins. These attach to the receptors of T-cells(host cell). Some fusion inhibitors target these proteins, other target the receptors on the host cell. Either way, it prevents both cells to fusion with each other. The fourth ones are integrase inhibitors. These prevent the integrase to cut the 3’ ends. This causes the DNA not to integrate with the DNA of the host cell. The fifth ones are multidrug combinations. These are combinations of two or more medicines that have been mentioned.
These medicines limit the production of HIV-molecules. They do not cure HIV/AIDS.  Natural immunity for HIV There is a small amount of people in the world who are naturally immune for HIV. People with two copies of the CCR5 delta32 gene are immune to HIV infection. The HIV-virus cannot enter the T-cells. Instead, the T-cells attack and disarm the HIV-molecules.  People who have this rare mutation could cure a HIV-patient by getting stem cell transplantation. The HIV-patient gets the stem cells injected in his marrow where they can divide. The stem cells will attack the virus and block it out of the human system.
However, stem cell transplantations have always been dangerous and this has never been done before.  Bibliography : (Basis presentation HIV/AIDS)http://www. mayoclinic. com/health/hiv-aids/DS00005 : (What is HIV? )http://www. avert. org/stages-hiv-aids. htm : (What is a retrovirus? ) http://std. about. com/od/glossary/g/What-Is-A-Retrovirus. htm : (Virus replication) http://biology. about. com/od/virology/ss/Virus-Replication. htm : (The evolving genetics of HIV)http://genetics. thetech. org/original_news/news13 : [ (HIV/AIDS medicines) ]http://www. nlm. nih. gov/medlineplus/hivaidsmedicines. html