The infection is very difficult to treat because the virus combines its genetic information with the genetic information of a type of white blood cell called CD4 cells. HIV can continue to replicate without treatment, generating more than 10 billion new virus particles per day.
HIV has three primary stages:
- Acute HIV. A large amount of HIV is present in your blood. Some people develop flu-like symptoms like chills, fever, and a sore throat. It occurs about 2 to 4 weeks after exposure.
- Chronic HIV. After the acute symptoms subside, you enter the chronic stage where HIV replicates at low levels. You’re still contagious in this stage, but you may not have symptoms.
- AIDS. AIDS is the last stage of HIV and severely impairs your immune system. It’s characterized by a CD4 count under 200 cells per cubic millimeter of blood.
The replication cycle, or life cycle, of HIV can be divided into seven stages. Medications that treat HIV interrupt one of the seven stages of the HIV lifecycle.
In an actively infected cell, the entire life cycle only lasts 1 or 2 days. But some cells can become latently infected, meaning that HIV can potentially be present in them for years without producing new virus particles. At any time, these cells may activate and begin making viruses.
In this article, we break down what happens during each of the seven stages of HIV’s life cycle and how medications interrupt these processes.
During the first stage of HIV’s life cycle, the virus binds to receptors on the surface of CD4 cells. CD4 cells, also called helper T cells, are a type of white blood cell that alerts other immune cells that there’s an infection in your body.
HIV is an enveloped virus, meaning that its genetic information is protected by both a protein shell and a lipid layer called an envelope.
Once HIV binds to receptors on CD4 cells, it initiates the fusion of its envelope with the membrane of the CD4 cell using a glycoprotein called
Fusing with the membrane of your CD4 cells allows the virus to enter the cell.
Reverse transcription is a process of converting genetic information in the form of RNA into DNA. RNA and DNA contain similar genetic information but are structurally different. RNA is typically made up of one long chain of genetic information, while DNA is made up of a double strand.
The virus converts its RNA into DNA by releasing an enzyme called reverse transcriptase. This process allows the virus’ genetic information to enter the nucleus of your CD4 cell.
Once HIV has converted its RNA into DNA, it then releases another enzyme called integrase inside the nucleus of your CD4 cell. The virus uses this enzyme to combine its DNA into the DNA of your CD4 cell.
At this point, the infection is still considered latent and is difficult to detect even with sensitive laboratory tests.
Because HIV is now integrated into your CD4 cell’s DNA, it can use that cell’s machinery to generate viral proteins. During this time, it can also produce more of its genetic material (RNA). These two things allow it to create more viral particles.
In the assembly stage, new HIV proteins and RNA are sent to the edge of your CD4 cell and become immature HIV. These viruses are non-infectious in their current form.
During the budding stage, the immature viruses push out of your CD4 cell. They then release an enzyme called protease that modifies proteins in the virus and creates a mature and infectious version.
The primary goals of antiretroviral therapy are to prevent HIV from replicating and suppressing your viral load to a point where it’s no longer detectable.
Antiretroviral drugs are divided into seven drug classes depending on which part of HIV’s lifecycle they interrupt. At least two different drug classes are used during antiretroviral therapy. Each medication typically has two or three of the drugs in it.
Binding stage antivirals
CCR5 antagonists block the CCR5 coreceptor on the surface of your CD4 cells to disrupt the binding phase. CCR5 is the primary coreceptor used by the GP120 glycoprotein on the surface of HIV to enter your cells.
A coreceptor is a particular type of receptor required by the virus to enter a cell.
Post-attachment inhibitors bind to the receptors on CD4 cells. This activity blocks HIV from binding to two types of coreceptors called CCR5 and CXCR4 and prevents the virus from entering your CD4 cells during the binding stage.
Fusion stage antivirals
Fusion inhibitors block the ability of the HIV envelope to combine itself with the membrane of a CD4 cell. This action prevents the virus from entering your cells.
Reverse transcription stage antivirals
Nucleoside reverse transcriptase inhibitors (NRTIs)
NRTIs block HIV from using the reverse transcriptase enzyme to replicate. Reverse transcriptase allows the virus to convert its RNA to DNA in the reverse transcription stage of its life cycle. The drug prevents the virus from copying its RNA into DNA accurately.
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
NNRTIs disable a key protein that HIV uses to replicate. They work in a similar way to NRTIs by stopping the virus from replicating itself.
Integration stage antivirals
Integrase strand transfer inhibitors
Integrase strand transfer inhibitors block the enzyme integrase that HIV uses to combine its reverse-transcribed DNA with the DNA of your cell during the integration stage.
Budding stage antivirals
Protease inhibitors block the enzyme protease during the budding stage. Protease is an enzyme that allows immature HIV to become mature viruses that can infect other CD4 cells.
HIV replicates by combining its genetic information with the genetic information of your CD4 white blood cells.
The replication process, or HIV lifecycle, has seven stages.
Antiretroviral therapy includes medications from at least two types of drug classes. Each drug class prevents the virus from replicating by inhibiting a particular part of the HIV lifecycle.