Why it’s so hard to cure HIV/AIDS - Janet Iwasa

In 2008, something incredible happened: a man was cured of HIV. In over 70 million HIV cases, that was a first and, so far, a last. We don’t yet understand exactly how he was cured. We can cure people of various diseases, such as malaria and hepatitis C, so why can’t we cure HIV?

Well, first let’s examine how HIV infects people and progresses into AIDS. HIV spreads through exchanges of bodily fluids. Unprotected sex and contaminated needles are the leading cause of transmission. It, fortunately, cannot spread through air, water, or casual contact. Individuals of any age, sexual orientation, gender and race can contract HIV.

Once inside the body, HIV infects cells that are part of the immune system. It particularly targets helper T cells, which help defend the body against bacterial and fungal infections. HIV is a retrovirus, which means it can write its genetic code into the genome of infected cells, co-opting them into making more copies of itself.

During the first stage of HIV infection, the virus replicates within helper T cells, destroying many of them in the process. During this stage, patients often experience flu-like symptoms, but are typically not yet in mortal danger. However, for a period ranging from a few months to several years, during which time the patient may look and feel completely healthy, the virus continues to replicate and destroy T cells.

When T cell counts drop too low, patients are in serious danger of contracting deadly infections that healthy immune systems can normally handle. This stage of HIV infection is known as AIDS.

The good news is there are drugs that are highly effective at managing levels of HIV and preventing T cell counts from getting low enough for the disease to progress to AIDS. With antiretroviral therapy, most HIV-positive people can expect to live long and healthy lives, and are much less likely to infect others.

However, there are two major catches. One is that HIV-positive patients must keep taking their drugs for the rest of their lives. Without them, the virus can make a deadly comeback. So, how do these drugs work? The most commonly prescribed ones prevent the viral genome from being copied and incorporated into a host cell’s DNA. Other drugs prevent the virus from maturing or assembling, causing HIV to be unable to infect new cells in the body.

But HIV hides out somewhere our current drugs cannot reach it: inside the DNA of healthy T cells. Most T cells die shortly after being infected with HIV. But in a tiny percentage, the instructions for building more HIV viruses lies dormant, sometimes for years. So even if we could wipe out every HIV virus from an infected person’s body, one of those T cells could activate and start spreading the virus again.

The other major catch is that not everyone in the world has access to the therapies that could save their lives. In Sub-Saharan Africa, which accounts for over 70% of HIV patients worldwide, antiretrovirals reached only about one in three HIV-positive patients in 2012. There is no easy answer to this problem. A mix of political, economic and cultural barriers makes effective prevention and treatment difficult. And even in the U.S., HIV still claims more than 10,000 lives per year.

However, there is ample cause for hope. Researchers may be closer than ever to developing a true cure. One research approach involves using a drug to activate all cells harboring the HIV genetic information. This would both destroy those cells and flush the virus out into the open, where our current drugs are effective. Another is looking to use genetic tools to cut the HIV DNA out of cells genomes altogether.

And while one cure out of 70 million cases may seem like terrible odds, one is immeasurably better than zero. We now know that a cure is possible, and that may give us what we need to beat HIV for good.