Answers: There are a few classifications of antiretroviral medications used to treat HIV infection and they work within different ways. They're often combined into "cocktails" for maximum worth. These are complicated but I'll do my best to make it simpler.
Nucleoside reverse transcriptase inhibitors (NRTIs), which are also certain as nucleoside analogs, include stavudine (d4T) and zidovudine (used to be called AZT but is in a minute called ZDV).
When HIV infects a cell, reverse transcriptase copies the viral single stranded RNA genome into a double-stranded viral DNA. The viral DNA is consequently integrated into the host chromosomal DNA which then allows host cellular processes, such as transcription and translation to reproduce the virus. NRTIs block reverse transcriptase's enzymatic function and prevent completion of synthesis of the double-stranded viral DNA thus preventing HIV from multiplying.
Nonnucleoside reverse transcriptors (NNRTIs) include delavirdine, efavirenz and nevirapine. Unlike the nucleoside analogs, the NNRTIs interfere beside HIV-1 reverse transcriptase by noncompetitively binding directly to the enzyme downstream from the active catalytic site.
Then nearby are nucelotide reverse transcriptase inhibitors, such as tenofovir. The mechanism of tenofovir is similar to that of nucleoside analogs, which interfere near RT (reverse transcription) and prevent translation of viral genetic material into viral DNA. Unlike the nucleoside analogs, the nucleotide reverse transcriptase inhibitors are chemically pre-activated next to the presence of phosphate group. Since the phosphorylation step is not necessary, nucleotide analogs can incorporate into viral DNA tie up more rapidly than nucleoside analogs. More importantly, this will bypass a viral apparatus of nucleoside resistance. In short, they terminate the DNA cuff of an HI virus.
This leads us to protease inhibitors (PIs), similar to nelfinavir, atazanavir, lopinavir/ritonavir, indinavir, saquinavir, fosamprenavir and ritonavir. PIs prevent viral replication by inhibiting the activity of HIV-1 protease, an enzyme used by the virus to cleave nascent proteins for final assembly of new virons. This is neccessry for replication.
Finally, in that are fusion inhibitors, such as enfurvirtide. Fusion inhibitors are a new class of drugs that perform against HIV. They got that autograph because they prevent the virus from fusing with the inside of a cell and so stop it from replicating.
None of these drugs have a direct effect on the immune system itself but it's evident that the immune system benefits from the mechanism of each. Render the virus incapable of replicating (reproducing) or prevent the virus from fusing beside a healthy body cell and the immune system will be protected and unsuppressed. It should be said, however, that the virus can become resistant to a specific drug protocol.