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There are six main types (‘classes’) of antiretroviral drugs. Different classes work at different stages of the HIV lifecycle to stop it making new viruses. Generally, drugs from two (or sometimes three) classes are combined to ensure a combined attack on HIV.
The four main classes, which most people are treated with, target one of three viral proteins which control HIV’s lifecycle: reverse transcriptase, integrase and protease.
Historically, most people started HIV treatment with two drugs from the NRTI class combined with either one NNRTI, one protease inhibitor or one integrase inhibitor – hence, ‘triple therapy’. Increasingly, some people are offered a two-drug combination containing an integrase inhibitor and a drug from another class. These two-drug combinations containing an integrase inhibitor are just as effective as three-drug combinations.
Many of the HIV drug combinations used today combine two or three drugs in one pill (a ‘fixed-dose’ combination). Or you may be offered a combination that consists of two drugs in one pill, accompanied by a third drug in another pill.
Nucleoside reverse transcriptase inhibitors (NRTIs), and nucleotide reverse transcriptase inhibitors (NtRTIs), often all referred to as NRTIs, work by targeting the action of an HIV protein called reverse transcriptase.
After the HIV virus releases its genetic material into a host cell, reverse transcriptase converts the viral RNA into DNA, a process known as ‘reverse transcription’. NRTIs disrupt the construction of a new piece of proviral DNA, thereby stopping the reverse transcription process and halting HIV replication.
This class of medications is sometimes referred to as the ‘backbone’ of a first-line HIV treatment combination. It includes the following drugs:
Non-nucleoside reverse transcriptase inhibitors (NNRTIs) also target reverse transcriptase, but in a different way to NRTIs.
NNRTIs interfere with the reverse transcriptase enzyme by binding directly to it, blocking the reverse transcription process.
Integrase inhibitors target a protein in HIV called integrase which is essential for viral replication.
Integrase is responsible for inserting viral genomic DNA into the host chromosome. The integrase enzyme binds to host cell DNA, prepares an area on the viral DNA for integration, and then transfers this processed strand into the host cell’s genome.
Integrase inhibitors stop the virus from inserting itself into the DNA of human cells.
Protease inhibitors (PIs) block the activity of the protease enzyme, which HIV uses to break up large polyproteins into the smaller pieces required for assembly of new viral particles. While HIV can still replicate in the presence of protease inhibitors, the resulting virions are immature and unable to infect new cells.
Booster drugs are used to ‘boost’ the effects of protease inhibitors and other antiretroviral drugs. Adding a small dose of a booster drug to an antiretroviral makes the liver break down the primary drug more slowly, which means that it stays in the body for longer times or at higher levels. Without the boosting agent, the prescribed dose of the primary drug would be ineffective.
There are some fixed-dose pills that combine two or three antiretroviral drugs from more than one class into a single pill that is taken once a day. Find out more about these on our page One-pill-a-day HIV treatments.
Drugs from the following classes are mostly used when resistance has developed to first-line or second-line drugs. Because they work differently to existing drugs, they remain active against virus that has developed resistance to other antiretroviral classes.
A retroviral enzyme which converts genetic material from RNA into DNA, an essential step in the lifecycle of HIV. Several classes of anti-HIV drugs interfere with this stage of HIV’s life cycle: nucleoside reverse transcriptase inhibitors and nucleotide reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs).
Non-nucleoside reverse transcriptase inhibitor, the family of antiretrovirals which includes efavirenz, nevirapine, etravirine, doravirine and rilpivirine. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) bind to and block HIV reverse transcriptase (an HIV enzyme), preventing HIV from replicating.
An enzyme that HIV uses to break up large proteins into smaller ones from which new HIV particles can be made.
In relation to medicines, a drug manufactured and sold without a brand name, in situations where the original manufacturer’s patent has expired or is not enforced. Generic drugs contain the same active ingredients as branded drugs, and have comparable strength, safety, efficacy and quality.
A substance that acts against retroviruses such as HIV. There are several classes of antiretrovirals, which are defined by what step of viral replication they target: nucleoside reverse transcriptase inhibitors; non-nucleoside reverse transcriptase inhibitors; protease inhibitors; entry inhibitors; integrase (strand transfer) inhibitors.
Entry inhibitors stop HIV from entering human cells. These include fusion inhibitors, CCR5 inhibitors and attachment inhibitors.
In order to enter a host cell, HIV must bind to two separate receptors on the cell’s surface: the CD4 receptor and a co-receptor (CCR5 or CXCR4). Once HIV has attached to both, its envelope can fuse with the host cell membrane and release viral components into the cell. CCR5 inhibitors prevent HIV from using the CCR5 co-receptor by binding to it, blocking viral entry.
CCR5 inhibitors won’t work in everyone and are very rarely used for first-line treatment. You would have a test to see if this type of treatment would be effective before starting on it. One CCR5 inhibitor is licensed in Europe:
Fusion inhibitors works by stopping the fusion of the HIV envelope protein with the CD4 cell. One fusion inhibitor (enfuvirtide, also known as Fuzeon) is available, but is rarely used.
Attachment inhibitors bind to the gp120 portion of the HIV envelope protein that makes up the spikes on the surface of the virus. This prevents the virus from attaching to the CD4 receptor on T cells and other immune cells, which it uses to gain entry to the cells. One attachment inhibitor is available.
Post-attachment inhibitors bind to the CD4 receptor on T-cells. They prevent the HIV gp120 protein from changing its shape to engage with co-receptors after it engages with the CD4 receptor. One post-attachment inhibitor is available.
Capsid inhibitors interfere with multiple stages of the HIV lifecycle. The HIV capsid is a cone-shaped structure that provides a container for viral proteins and enzymes. When the virus enters a target cell, the capsid opens up in a pre-programmed sequence to allow HIV proteins to integrate into the host cell’s DNA. Capsid inhibitors interrupt the opening and unpacking of the capsid, preventing HIV infection of a cell, as well as the assembly of new capsids. One capsid inhibitor is available.
Full image credit: A variety of antiretroviral drugs used to treat HIV infection. Credit: NIAID. Image available at www.flickr.com/photos/niaid/31793869534 under a Creative Commons licence CC BY 2.0.
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