Antiretroviral Drugs: How HIV Medications Work

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  • 0:07 Human Immunodeficieny Virus
  • 2:40 Entry/Fusion Inhibitors
  • 3:33 Reverse Transcriptase…
  • 6:13 Integrase Inhibitors
  • 6:59 Protease Inhibitors
  • 7:59 Lesson Summary
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Lesson Transcript
Instructor: Katy Metzler

Katy teaches biology at the college level and did her Ph.D. work on infectious diseases and immunology.

In recent years, HIV infection no longer means certain death from AIDS. This is because there are many effective drugs to fight HIV. In this lesson, see how these antiretroviral drugs work, and why they must always be used in combination instead of alone.

Human Immunodeficiency Virus

If someone asked you which infection in the whole world you most wanted to avoid getting, what would you say? Many of us would say HIV, or Human Immunodeficiency Virus, the virus that causes AIDS, which is a disease that devastatingly weakens the human immune system. HIV is a really scary virus to most people and for good reason.

It stays quiet in the body for years before causing any symptoms, so people who don't even know they have it can transmit it to others through their blood and bodily fluids. If it's allowed to run its course and develop into AIDS, it eventually weakens the immune system so much that the patient will die of rare infections that would never be a problem for a healthy person.

And perhaps even more frightening, the HIV virus is designed for fast evolution because it makes a lot of mistakes when copying its own genome to make new virus particles. In an infected person, a mutation is most likely made at every single position in the HIV genome several times each day. Stop and think about that for a minute.

The viruses in an infected person's body are constantly changing, which helps HIV become resistant both to the immune system and to drugs that are used to treat it. As a result, HIV infections must always be treated with a combination of drugs, so that if a virus arises that is resistant to one drug, it is most likely still susceptible to the other drugs in the treatment regimen.

Every hour, nearly 300 people become infected with HIV worldwide. And 97% of HIV-infected people live in low- and middle-income countries where they often do not have access to good healthcare and expensive drugs. That said, the drugs that are currently available to fight HIV have drastically changed the outlook of the disease. For people who are fortunate enough to have access to the best medications, HIV infection no longer means certain death from AIDS. However, they must stick religiously to a complicated drug regimen that can include as many as 40 pills a day.

In this lesson, we will learn about Antiretroviral Drugs and how they work. The name 'antiretroviral' really means a drug that is used to fight any retrovirus, or RNA virus that inserts a DNA copy of its genetic material into a host cell's genome. However, nowadays, the term 'antiretroviral drugs' refers specifically to drugs that are used to treat HIV, since it is such an important retroviral disease.

As we discuss the various different drugs, we will see where they act in the replication cycle of the virus. It's not so important to remember all of the names of the drugs that are mentioned here. The most important thing is to learn the different strategies that can be used to block HIV infection.

Entry/Fusion Inhibitors

At the beginning of its replication cycle, HIV attaches to receptor molecules on the outsides of helper T cells, which are an important type of immune cell in our body. After attaching to these receptors, the membrane of HIV fuses with the plasma membrane of the T cell, and the viral contents enter the cell.

These are key steps in HIV infection. Like all viruses, HIV cannot replicate, or make copies of itself, if it doesn't get into host cells. So, drugs that can prevent HIV from entering T cells would be very promising indeed.

So far, only a few antiretroviral drugs use this strategy. The first is maraviroc, which attaches to one of HIV's receptors on T cells, preventing the virus from binding. The second is enfuvirtide, which blocks the fusion of the viral membrane with the T cell's plasma membrane. You can envision these drugs' strategies as locking all of the doors of a house so that the virus can't get inside.

Reverse Transcriptase Inhibitors

Once HIV is inside a T cell, it needs to use its genetic material to create new copies of itself. HIV is an RNA virus, and it needs to convert its genetic material into DNA first so that its proteins can be expressed by the cell. Conveniently, HIV has brought along its own enzyme called reverse transcriptase, which makes a DNA copy of the virus's RNA genome.

Many important antiretroviral drugs target reverse transcriptase. Two important classes of HIV drugs are the Nucleoside and Nucleotide Reverse Transcriptase Inhibitors (NRTIs/NtRTIs). Remember that a nucleoside is a nucleotide without the phosphate group, so it's a pentose sugar attached to a nitrogenous base. When one or more phosphate groups are added to a nucleoside, it becomes a nucleotide. DNA and RNA are made of strings of nucleotides.

NRTIs are analogs of nucleosides and nucleotides. It turns out that nucleoside and nucleotide analogs can inhibit reverse transcription very well. These analogs are like false, decoy components of the DNA strand that the virus needs to make. They compete with the real nucleosides and nucleotides in the cell. Here's how: when reverse transcriptase inserts one of the analogs into the growing DNA chain, instead of a real nucleotide, DNA synthesis stops. This is because the analogs don't have the right chemical structure for the next nucleotide to be added into the chain. Examples of these drugs are zidovudine (AZT), a nucleoside analog, and tenofovir, a nucleotide analog.

But hold up just a minute, what about selective toxicity? Our cells have to synthesize DNA, too, when they replicate. If a patient is being treated with a nucleoside or nucleotide analog, what will happen to their normal cells? It turns out that this is not too much of a problem because DNA polymerase, the enzyme that our cells use to synthesize DNA, doesn't bind very well to these analog drugs.

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