HIV, which leads to AIDS, is one of the most nasty viruses the human race has encountered. Once it establishes an infection, barring a few reported cases, HIV is impossible to eliminate from the body.
That said, in the 30 or so years since its emergence, we have discovered a variety of medications to treat it.
Of these, so far, the most effective option has proven to be a single tablet pill that combines three other medications.
This article discusses the treatment of HIV/AIDS.
Treatments and Their Basis
HIV is a retrovirus, which means that it works by inserting RNA into a cell then turns that RNA into DNA which incorporates itself into the host genome.
Specifically, there are several steps which lend themselves to targeting.
Step 1: Entering the cell
First, the virus must attach to the cell and get inside of it. To do so, it tends to attach to CCR5, a special receptor present in the immune system cells it targets. After that, it is taken into the cell by an automatic, fusion response.
Two new, but lesser used treatments, maraviroc and enfuvirtide work by blocking the CCR5 receptor or uptake interaction.
Step 2: Creating DNA from RNA
After entry into the cell, the virus uses an enzyme called reverse transcriptase to turn its RNA into a double-stranded DNA molecule. This process is extremely important to target because it is specific to retroviruses and is essential to its replication.
That is, your body does not need or use reverse transcriptase naturally, so targeting it is a relatively easy task.
There are two main classes of inhibitors for this process. 1) Nucleoside/Nucleotide reverse-transcriptase inhibitors 2) Non-nucleoside reverse-transcriptase inhibitors
Nucleoside/Nucleotide reverse-transcriptase inhibitors (NRTIs/NtRTIs) work by mimicking vital components of DNA in the cell. They are, however, defective.
While they are similar enough for the virus to include them in its replication cycle, the NRTIs/NtRTIs do not work and cause the virus particle to fail. They work to directly disrupt and target reverse transcriptase’s action.
Some key medications in these two classes include tenofovir, lamivudine, and zidovudine.
Non-nucleoside reverse-transcriptase inhibitors (NNRTIs) work on a very similar principle – if you disrupt reverse transcriptase, the virus is useless.
That said, they do not directly mimic the DNA components and instead work by a process of indirect inhibition known as allosteric inhibition.
They stop the enzyme by inhibiting it in non-direct ways.
Some key NNRTIs include efavirenz and etravirine.
Step 3: Infecting the cell’s genome
After the viral DNA is created, it is taken into the nucleus of the cell the host’s DNA is stored. At this point, the enzyme integrase is essential. Integrase takes the viral DNA and inserts it into the host’s genome.
This step can be blocked by integrase inhibitors. A relatively new class of medication, one example is raltegravir.
Step 4: Creation and Assembly of Virus Particles
After infection of the host’s DNA, the cell will start producing viral components. However, these viral components need to be processed and modified to form virus particles.
To do that, the virus has an enzyme known as protease. Protease inhibition is an important way to stop the virus from being effective.
Saquinavir and ritonavir are examples of protease inhibitors.
In the 90s, scientists realized that the best way to treat HIV is by using multiple medications at one time. This is to avoid the disease becoming resistant to one treatment.
The problem with this approach, however, is that while more effective, multiple drug treatment can cause unpleasant side effects and is hard to adhere to.
As a result, researchers developed a single dose, single tablet medication that can be taken once daily. In particular, in 2006, the FDA approved Atripla, which combines tenofovir, emtricitabine and efavirenz.
Atripla is a highly effective treatment, and other, new single tablet combination therapies are being researched.
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