The HIV/AIDS Vaccine:
A few weeks ago I was sitting in the basement of the biomedical research center at my school, just having made it through another fascinating class on pharmacology. It was time for lunch, so I made for the exit, meeting my friend along the way.
“Hey,” she said. “Did you hear about the new AIDS vaccine that actually works?”
I would soon hear more about it.
The vaccine was given to 8,197 people, and not given to 8,198, for a total of more than 16,000 in the trial. Of those incredibly large numbers, 51 of the vaccinated people contracted HIV, while 74 of those not vaccinated did.
While small, that difference meant something. It meant that those given the vaccine had a 31% lower risk of infection. In my AIDS class, when the professor started discussing the vaccine briefly, I wrote in my notes in all caps, “FIRST EVER EFFECTIVE AIDS VACCINE!” and considered throwing a party. It felt like one of those pivotal days, when things were changing.
Problems with the Vaccines
The professor, a world renowned expert on viruses, pointed out several concerns with the vaccine. First, it did not confer additional protection to those who did catch HIV. So if you get the shot, then contract HIV, the disease will proceed according to its usual pattern. This is significant because you would expect the vaccine to confer some protection, even in those who do get infected.
Second, the vaccine was simply a merger of two other vaccines, both of which did not work by themselves. Why would you expect combining them to work? asked the professor.
Finally, the numbers, while statistically significant, were only barely so. If a few more vaccinated people had caught AIDS, or a few less non-vaccinated, then the entire study wouldn’t mean anything.
I disagreed with the professor on the first two points, most likely because I’m ignorant.
The key factor about HIV is that an immune response to it is not protective. The fact is that an infected person has a tremendous immune response to HIV – just it isn’t ever enough to wipe the disease out, as it constantly mutates to avoid the body’s attack.
This constant mutation to avoid destruction occurs for one major reason. HIV can lay dormant in cells, waiting for the chance to spring up. Once infection is established, permanent clearance, and immune response, is generally impossible. For instance, there is, shortly after initial infection, a major immune response, which almost removes the virus from the body entirely.
So an effective vaccine could prevent the virus from establishing the initial beachhead, so to speak, but not provide any benefits beyond that.
It’s also a generally accepted idea that effective vaccines can be combinations of targets. This occurs on several levels: first, a good vaccine can stimulate both the T and B cell lines in the immune system, which have different requirements for activation. And second, a good vaccine can target multiple parts of a virus, trying to overwhelm it.
The thinking I had then was that the HIV vaccine elicited a stronger initial response to infection that prevented the formation of a beachhead. And once that beachhead was established, the typical pattern where HIV disregards the immune system’s response, took over.
Professor Right, Student Wrong
Unfortunately, the professor’s third point was ultimately true. Recent news seems to throw doubt on the exact numbers and validity of the study, lowering an already small effect to the range where it is meaningless.
We’ll next cover what potential vaccination strategies for fighting HIV/AIDS are.