Resistance to HIV infection - How a Mutation May Help Fight AIDS

A rare genetic mutation called CCR5-delta32 can make a person highly resistant to HIV by removing the doorway the virus uses to enter immune cells. The same idea explains the only documented HIV cures so far — stem-cell transplants from delta32 donors. It's not a treatment you can get, but it's reshaping how researchers chase a real cure.

How the CCR5-delta32 mutation blocks HIV

HIV is a virus that attacks the body's immune system, and it can't just float into a cell — it has to dock onto specific proteins on the cell surface first CDC. The main target is a CD4 immune cell, and the virus uses CD4 as its primary handle plus a second protein, called a co-receptor, to actually fuse and get inside. For most strains of HIV, that co-receptor is CCR5.

The delta32 mutation deletes a small piece of the CCR5 gene. People who inherit the deleted version from both parents make a CCR5 protein that never reaches the cell surface properly — so the virus shows up with its key, but the lock is gone. Without a working CCR5 co-receptor, the common CCR5-tropic strains of HIV can't enter CD4 cells, and the infection mostly can't get a foothold.

It's not magic and it's not absolute. The protection is strongest against CCR5-using virus; some HIV strains use a different co-receptor (CXCR4) and can sidestep the block. The mutation is also far more common in people of Northern European descent than in other populations, and you need two copies for the strong effect — one copy slows disease but doesn't stop infection.

How this connects to the only documented HIV cures

There is no cure for HIV — ART (antiretroviral therapy) can drive the virus down to undetectable, but that's control, not eradication, and people who get HIV have it for life CDC. A small number of people are the dramatic exception. Several have been documented in long-term remission after stem-cell (bone-marrow) transplants: the Berlin patient, the London patient, and a New York woman who was the third documented case and the first woman NIH, 2022.

Here's the link to the mutation: those transplants were done to treat cancer or leukemia, not HIV, and the donor cells were chosen from rare people who carry two copies of CCR5-delta32. The patient's own HIV-vulnerable immune system was wiped out and rebuilt from HIV-resistant donor cells. The new immune system literally had no working CCR5 lock for the virus to use.

This matters because it's proof of concept — it shows that taking CCR5 out of the equation can produce lasting, ART-free remission in a human. But a stem-cell transplant is brutal: it's high-risk, sometimes life-threatening, requires a matched donor who also happens to carry this rare deletion, and is only justified when someone needs the transplant for cancer anyway. It is not a scalable or generally available cure, and no clinician would do it just to treat HIV.

Sterilizing cure vs. functional cure

Researchers split the goal into two kinds of cure NIAID. A sterilizing cure means clearing every replication-competent copy of HIV from the body. A functional cure means the virus still hides somewhere but stays controlled without daily medication. What's available today is neither — it's lifelong treatment.

The reason even an undetectable viral load isn't a cure is the latent reservoir: HIV parks silent copies of itself inside long-lived cells and tissues HHS clinicalinfo. Treatment keeps active virus suppressed, but those dormant copies aren't touched, and if treatment stops the virus rebounds. Clearing or permanently silencing that reservoir is the central problem a cure has to solve.

How researchers are trying to copy the mutation

You can't hand someone the delta32 mutation at birth, but you can try to recreate its effect. An HIV cure is an active research goal, not a current option, and the experimental strategies under study include several approaches aimed at the reservoir or at CCR5 NIAID:

• Gene/CCR5 editing — using tools like CRISPR to knock out the CCR5 gene in a person's own immune cells, essentially engineering the delta32 effect without a transplant.
• Latency-reversing ('shock and kill') — waking up the dormant reservoir so the virus reveals itself and can be cleared by the immune system or drugs.
• Broadly neutralizing antibodies — lab-made antibodies that target many HIV strains at once.
• Therapeutic vaccines — training the immune system to control the virus on its own.

None of these is an available cure. They're promising research, and CCR5 editing in particular grows directly out of what the delta32 mutation taught us — but they aren't something you can ask for at a clinic today.

What actually protects you right now

Since you can't choose your genes, the proven prevention you can use matters far more than any future cure. The core CDC tools are condoms, PrEP, PEP, treatment-as-prevention (U=U), and regular testing CDC.

U=U is the headline. A person with HIV who takes their medicine and stays virally suppressed will not transmit HIV to sex partners — treatment is both health and prevention. This isn't hope; across the PARTNER, Opposites Attract, and PARTNER2 studies, mixed-status couples logged more than 125,000 condomless sex acts with zero linked transmissions while the partner was undetectable (under 200 copies/mL) PARTNER, Lancet. Most people reach undetectable within about six months of starting ART.

PrEP is for people without HIV who are exposed through sex or injection drug use; taken as prescribed it cuts HIV risk from sex by about 99%. Daily options include Truvada and Descovy, and there's a long-acting injectable, cabotegravir (Apretude). Newer long-acting prevention is a real step change — twice-yearly injectable lenacapavir produced zero infections among women in the PURPOSE 1 trial WHO.

If you think you've just been exposed

This is the one situation where the clock matters more than anything in this article. PEP (post-exposure prophylaxis) can prevent infection, but it must start within 72 hours and is taken daily for 28 days CDC PEP. Treat it as a same-day urgent-care or ER conversation, not a wait-and-test one — the original occupational study found a 28-day course cut seroconversion by about 81%. After the window, plan testing: see when to test after exposure.

When to see a clinician and get tested

The USPSTF gives HIV screening a Grade A recommendation: everyone ages 15 to 65 should be tested at least once, and people at increased risk at least annually USPSTF. Acute HIV is easy to miss and highly contagious — about 90% of people get flu-like symptoms 2 to 4 weeks after infection, right when viral load peaks. Those symptoms can't confirm or rule out HIV, so if you've had a risk and feel sick, get an urgent test. The honest framing: only a test settles it. You can get tested through a clinic, your doctor, or at home.

Modern HIV is compatible with a near-normal lifespan — a 20-year-old who starts treatment before their CD4 count falls below 200 now has a life expectancy approaching the general population's Lancet HIV. That's the whole case for testing and starting early. If you're navigating a new diagnosis or supporting someone who is, our guides on whether is early hiv treatment in babies safe and effective, how earlier hiv treatment can help prevention, and why older hiv individuals face serious financial and emotional hardships can help.