In June 1981, disease detectives at the CDC published the first description of a pneumonia-like illness afflicting five Los Angeles men. The syndrome was later called AIDS. AIDS turns 30 this month, and its death toll in the United States has passed 600,000.
Some are asking: Why don't we have an HIV vaccine yet?
Put aside for a moment debates about money, politics and sexual behavior that complicate the challenge to protect people from HIV. Instead consider the complexity of the virus itself.
Remember: The abbreviation stands for Human Immunodeficiency Virus.
"In HIV, it infects the immune system, so if you ramp up the immune system you, you ramp up the part of the body that is infected by HIV," said Dr. Robert Bettiker. He cares for people with HIV at Temple University Hospital.
The virus can lead to Acquired Immune Deficiency Syndrome but powerful medicines help many people live for decades without progressing to AIDS. Bettiker says in the mid-80s, health officials thought it would take just a few years to find a vaccine, even though scientists knew the virus was elusive.
"We were so confident in our ability to create a vaccine, that if we just threw a lot of resources and a lot of minds and a lot of money at it we would be able to solve that," he said.
Pitted against most viruses, humans are usually good at fighting off infection. We rally from flu. Colds get better.
Philadelphia physician-researcher Ian Frank says few viruses stay in the body for a lifetime. The exceptions: hepatitis B, C and HIV.
"The thing about HIV that is different from other viruses is that it can get into a cell and live there lifelong in a dormant state, and all of a sudden, get activated from that dormant state at some point in the future," Frank said.
Frank is a vaccine researcher at the University of Pennsylvania. He says HIV infects a white blood cell called the T helper lymphocyte.
"That cell is responsible for coordinating the immune response that we make to any infection that we get exposed to in our lives," Frank said.
HIV depletes T helper cells, and without treatment, the virus wins the war against the immune system.
"Over the years they are living with HIV, people become vulnerable to all sorts of infections or they get a cancer they wouldn't likely get otherwise," Frank said.
Many vaccines work by exposing us to a weakened version of a virus. That introduction prods the immune system to get to work fighting off infection. Eventually the body develops immunity.
Bettiker says that strategy isn't possible with HIV.
"We are asking vaccines to do something that they've never been able to do before," he said.
When scientists were designing the first AIDS vaccine studies, they looked to a small population of people with HIV, who are able, without medicine, to tamp down the virus in their bodies.
"We call them elite controllers, these people have no virus that's replicating in their body. Their viral load is undetectable; we can't see any evidence of the virus," Frank said.
Scientists hoped to duplicate that response in other people by programming white blood cells to kill off already-infected cells. Experts call that a cellular immune response.
Early studies failed to control infection, but sent researchers on a new path. Next, vaccine designers worked to get the immune system to make better antibodies.
"Antibodies are very specific, sort of like a glove. You have a left-handed glove and a right-handed glove, and if the virus is right-handed and you hit it with a bunch of left-handed gloves, you aren't going to hurt the virus very much," Bettiker said.
Antibody blood proteins are resistance fighters uniquely armed to hunt down a specific virus, but HIV has a suite of tricks to hide. First, the virus has a glycan shield; a sugar coating that is slippery to antibodies.
"The virus can just shrug them off," Bettiker said.
Frank said: "The sugars represent basically a camouflage, because antibodies don't necessarily bind to sugars they would rather bind to proteins."
The virus also changes a lot. As HIV copies itself, it makes mistakes. Those constant mutations make it hard for the body to keep up and manufacture the required perfect-match antibodies.
The most promising HIV vaccine trial, so far, was conducted in Thailand. But scientists don't completely understand the mechanism behind that limited success.
"If it worked is has something to do with triggers on making more effective antibodies," Frank said.
It's possible those antibodies were able to neutralize HIV, or maybe they somehow just slowed down the virus.
Frank calls that a gang attack.
"By just having so many antibodies that glom on to the surface of the virus, that a virus can't infect another cell," Frank said.
Frank's team in Philadelphia is testing the next generation of candidate HIV vaccines. It's a combo approach. The researchers are hoping for both a cellular and antibody response.
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