HIV Vaccines to Prevent and Cure: A Conversation with Dr. Aliza Norwood
In the early days of the HIV epidemic, researchers were optimistic that an HIV vaccine would be developed quickly. Thirty years later—although we still don’t have a vaccine—HIV has become a manageable, chronic disease. Current treatments are fairly well-tolerated and suppress levels of HIV to undetectable levels.
Yet we would still benefit from an HIV vaccine: An effective vaccine could reduce the 50,000 new HIV infections that happen in the U.S. every year to close to zero. It could help prevent thousands of people from having to take expensive antiretroviral therapies for years and years. A therapeutic vaccine—given to people already living with HIV—could improve immune system function and reduce or eliminate the need for people to take HIV medications.
Many people—including me—are optimistic about progress for both an HIV vaccine and a cure. To learn about where we are in the search for an HIV vaccine, I invited Aliza Norwood, MD, a physician at the San Francisco-based research group Bridge HIV, to give an update on where we are in the development of an HIV vaccine.
We’ve known about HIV for more than 30 years. I’ve heard people speculate that we don’t have an HIV vaccine or cure because of some kind of conspiracy. Why is it that we still don’t have an HIV vaccine?
Dr. Aliza Norwood (AN): Let’s be clear that there’s no conspiracy about HIV vaccine or HIV cure development. The fact that there have been 140 vaccine trials conducted to date shows us that vaccine development is a priority—and that researchers are trying to make this happen. But there are major challenges in making an HIV vaccine.
Why is it so challenging to make an HIV vaccine?
AN: Normally, when you are exposed to a virus, your body creates specialized defenders against the virus called “antibodies.” These specialized antibodies will fit into targets on the surface of a virus, like puzzle pieces. When antibodies latch on, they prevent the virus from attaching to and infecting your immune system cells. Vaccines are made of virus look-alikes that train your antibodies to recognize a virus before you are exposed.
In both of these scenarios your body is stimulated, either by a virus or by a vaccine, to create its own antibodies and memory cells. Memory cells are special immune cells that can make new antibodies against the virus if they detect it in the future. This is called “active immunity.”
We’ve found that doing active immunization for HIV is really difficult, because HIV changes—or mutates—so often. We can create vaccines that stimulate our immune systems to make antibodies, but all the while, HIV is changing shape, so that the antibodies our body eventually makes no longer have the right “puzzle piece” fit they need to latch onto the surface of the virus. It takes time for our antibodies to adapt to the new shape of HIV, and in the meantime, HIV begins infecting the very same immune cells that our body uses to fight infection. HIV can also “hide” itself from antibodies by using small particles to cover the places on its outer casing where antibodies would attach.
Have there been any promising studies of HIV vaccines?
AN: One vaccine study that has shown some efficacy is the RV144 clinical trial. This study was conducted in Thailand, by the U.S. military, with more than 16,000 adults who were HIV-negative. Half of participants received the vaccine and booster injections and half received placebo; all participants received HIV risk reduction counseling. After three years of follow-up, 76 people in the placebo group and 56 people in the vaccine group became infected with HIV. This difference was statistically significant and researchers concluded that the vaccine reduced risk of HIV infection by 31%.
Unfortunately, the protective effect of the vaccine was seen in a minority of the participants, and only lasted about a year in those people. Also, it only provided protection against a type of HIV found in Thailand but was not made to prevent other types of HIV found around the world. Additional studies are needed to create a vaccine that lasts longer and that’s effective against HIV strains found in other parts of the world.
If an HIV-negative person takes part in a vaccine clinical trial, is there any chance that the vaccine will give them HIV?
AN: HIV vaccines can never cause HIV infection or AIDS. HIV vaccines don’t contain active HIV. They only contain copies of parts of HIV that will never be able to combine into active HIV.
You may have heard about vaccine-induced seropositivity, though. This refers to the instance when somebody has received an HIV vaccine which causes their body to create HIV-specific antibodies. That’s the whole purpose of an HIV vaccine—to develop an antibody defense against the virus. The person is not infected with HIV, but they will test positive for HIV on an HIV test that detects HIV antibodies. This is called a false positive. During vaccine trials, we test people for HIV using a viral load test, not an antibody test, to really see if they have been infected with HIV.
What about vaccines for people with HIV? Is there any hope of developing a therapeutic vaccine?
AN: The VRC 601 study, which started in 2013, is testing a broadly neutralizing antibody called VRC01. It’s a phase 1 study, so it is a very small study enrolling up to 30 adults with HIV. The study will test different doses of the antibody—to determine if the infusion that’s given is safe and well-tolerated, and also what its effects are on the CD4 count and viral load of participants. The study is expected to be completed in September of this year, so we might find out in the next few months if it looks like VRC01 can reduce viral loads and improve CD4 counts.
Where can people find out more if they’re interested in joining an HIV vaccine study?
You can find more information about the vaccine studies happening in San Francisco at www.sfisready.org.