Entry Inhibitors
Interfere with the virus’s ability to bind to the outer surface of the CD4+ T-cell co-receptor and prevent HIV from entering the CD4+ T-cell.
Fusion Inhibitors
Interfere with the virus’s ability to fuse with the outer surface of the CD4+ T-cell membrane and prevent HIV from entering the CD4+ T-cell.
Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
In order for HIV-1 to make more copies of itself, HIV needs to convert its RNA to DNA by using reverse transcriptase enzyme. NRTIs are fake DNA building blocks. When one of the fake building blocks is added to a growing HIV-1 DNA chain, the real DNA building blocks cannot be added on and the building of HIV-1 DNA stops. Thus, HIV-1 RNA can't be converted into HIV-1 DNA and inhibits reverse transcriptase.
Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
In order for HIV-1 to make more copies of itself, HIV needs to convert its RNA to DNA by using reverse transcriptase enzyme. NNRTIs bind to the reverse transcriptase (RT) enzyme, interfering with its ability to convert HIV-1 RNA into HIV-1 DNA.
Integrase Strand Transfer Inhibitors (INSTIs)
Interfere with the HIV enzyme integrase, which the virus uses to insert ("integrate") its genetic material (HIV-1 DNA) into the genetic material (DNA) of the CD4+ T-cell it has infected.
Protease Inhibitors (PIs)
Interfere with the HIV enzyme called protease. When protease does not work properly, new HIV virus particles cannot be assembled.
Even though the total number of gut bacteria is not different when you compare HIV-negative and HIV-positive people, it's the composition of the microorganisms that change with HIV infection.
HIV-positive people who are not on antiretroviral therapy do have different gut microbiomes compared to those people who are HIV-negative. There is a larger percentage of gut CD4 cells that have a protein on their surface that the virus can use to bind and enter the cell which makes the CD4 cells in the gut are more susceptible to the HIV virus than CD4 cells circulating in the blood.
There is one type of CD4 cell in the gut that is called Th17 cells that HIV enters and kills off. These cells usually work to keep the intestinal barrier efficient. Destruction of these Th17 CD4 cells by HIV results in something that is called “microbial translocation” which means that there are harmful bacteria leaking into the blood stream.