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HIV vaccine is in tests, but results are promising

HIV vaccine is in tests, but results are promising

Despite the very earlier origin, when the human immunodeficiency virus (HIV) was identified in the early 1980s, it was already an epidemic world. At this time, the HIV-positive diagnosis was a death sentence, and as a medical student I remember well when, day after day, I took a job with 10 or 15 infected young people and, 12 hours later, I delivered it with , a survivor. There was simply nothing to be done and so from 1981 until today, HIV has spread all over the globe and devastated continents, accumulating 36 million infected and 24 million dead, securing for itself a place as one of the great plagues of mankind .

But mankind was not passive. After a troubled beginning, in record time, we identified the virus and mapped its life cycle, which allowed the creation of treatments that transformed it from lethal infection to chronic disease. Still, with all the successes heavy, the most we can say is that the fight is tied, as the number of infected continues to rise, generating an unsustainable weight in the economic, social and hygienic structures of several countries, perpetuating misery, hunger, crime, violence and underdevelopment.

As already demonstrated with other diseases, a vital weapon to break this impasse would be an effective vaccine - and no effort was spared to produce it. For years, the HIV vaccine has been a priority for entities such as the World Health Organization (WHO) or the Gates Foundation, but the repeated failures just prove how formidable our adversary is ... Until now. Recently, a publication in the journal Nature has unveiled a new strategy with the potential to generate the vaccine capable of preventing the spread of HIV.

It is impossible to deny that more than ever there is a strong hope that soon we will dispatch HIV in the same The aim of this article is to explain in a very simplified and summarized way why there is still no effective vaccine against HIV and why this discovery can make it possible.

In his famous book "The Art of War," Sun Tzu writes: "If you know yourself and your enemy, , you need not fear the outcome of 100 battles. " This is also true in the fight against infectious diseases, where knowing the enemy means understanding how microbes penetrate our organism, evading our defenses and subverting our physiology to our own advantage. Sun Tzu also stresses the importance of knowing the terrain of his battlefield, and in this case our battles occur not in the macroscopic world with which the reader is accustomed, but in the field of biology, which is significantly different. macroscopic, most events occur in a simple, visible, direct and predictable way, for example: you go to a restaurant every day, order your favorite dish, the kitchen prepares it, the waiter serves you, you eat, you pay and you leave.

In the world of biology, reality is not always directly visible and can fluctuate in a partially unpredictable way. So in this reality, the situation above could go like this: you go to a restaurant every day, but today it's on the other side of the street and the front door has shrunk in half. You enter through it, but go out in the bathroom, find your table, but the menu is in Sanskrit, order your favorite dish, but the kitchen prepares another that the waiter serves the next customer. Without eating, you pay twice what you paid yesterday, it takes five hours to find the way out, and you leave knowing that tomorrow everything may be different.Well, the first step to being a biologist is to understand that in the biology world only once in a while one plus two equals two, and one reason for this is that no matter how small an organism, your DNA is a dynamic structure and interactive with many possibilities to be exercised in response to internal and external stimuli. It is quite different from a physicist who thinks bad when the 25th decimal place of the result of his experiment does not exactly match his prediction. How does this interfere with the HIV vaccine? Directly because of its survival and transmission strategy

Why it is difficult to get an effective vaccine, part 2: the biology of HIV

In order to spread, infectious agents need to continuously infect new hosts - but each host is like a safe whose door is protected by a lock. To penetrate this safe, each microbe has its strategy. Some, like salmonella bacteria, dispense with subtleties and blow the door. Others, like herpes, have the key. HIV does not waste a second thinking about the right key - it goes to the lock with ten billion of them, so it's almost certain that at least one will work and that's enough. But to be able to understand exactly what we are talking about, we are going to name the steers.

What we call a lock are actually 3 proteins on the surface of white blood cells, called CD4, CCR5, and CXCR4. What we call the key is an HIV protein called gp120, and what we call infection is the process by which HIV uses its gp120 as a clamp to attach itself to the cell's CD4, CCR5 and CXCR4, thereby gaining the support it needs to penetrate the cell and settle in.

Knowing this, it seems obvious that the solution to prevent infection is to neutralize gp120, correct? So correct was this exactly the intent of the first anti-HIV vaccines to inject the individual with purified fragments of gp120 in order to generate anti-gp120 antibodies that neutralize their ability to bind to cellular proteins. Just for those who do not know, antibodies are defense proteins produced by our immune system to stick to invaders or substances foreign to the body for the purpose of: if alive, kill them. If active, neutralize them. If circulating, remove them. And vaccines do this? Yes! Yes! Yes! ... That's your specialty, practically your reason for existing, so theory aligned to a plan, let's fight.

The anti-gp120 vaccine test was performed and ... Exactly like in the restaurant metaphor, even doing everything sense, failed. The level of neutralization of the anti-gp120 antibodies was not sufficient to prevent infection and, if this were not enough, once an antibody proved effective, HIV used its enormous mutational ability to exchange that version of gp120 for another and escape. This proved to be the greatest difficulty in getting a vaccine: the target, gp120, simply does not stop and undergo changes faster than our ability to chase it with antibodies. Unfortunately, a similar scenario was repeated with other HIV proteins administered alone or together.

Exhausted this possibility of frontal attack, the scientists went out in search of new strategies and a good place to start was to analyze how people naturally immune to infection by HIV can defeat him. From the study of this group we learned two things: the first is that without CCR5 and / or CXCR4 on the surface of the cell HIV infection does not progress, and the second was that the neutralizing efficacy of the anti-gp120 antibodies identified in some of these individuals was exponentially higher to the mean found in the infected and / or vaccinated population. Thus, a new strategy emerged which consisted in the creation of a vaccine that generated not any antibody but one of these superantibodies. This idea failed not because the anti-gp120 superantibody was bad, but first because the vaccine to generate this superantibody is much more complex. Second, the minimal protective blood concentration of vaccine superantibody was not reached, as it exceeds the body's average antibody production capacity. Third, although the superantibody protects very well against some viruses, it does not cover everyone, leaving a protection gap.Finally, the metaphor of the restaurant reappears: paradoxically, in some cases, treatment with the superantibody appears to have facilitated HIV infection. Similar strategies based on the attempt to prevent HIV binding with CCR5 and CXCR4 also failed to achieve satisfactory levels of protection. That is, we essentially tested everything our studies suggested as effective in blocking HIV infection and, in the end, we ended up empty-handed. It is at such times of maximum frustration, when the alternatives seem to be running out and despair strikes, that the crazy ideas that eventually save the day come up.

Then a group of scientists looked at what we had done and thought, if everything we tested works partially, why not make a vaccine that combines all these actions? A complete madness, and why? You know, if a vaccine to generate a superantibody is already difficult, imagine the difficulty of creating a vaccine to produce a superantibody, and in the middle of it you artificially insert another protein to block CCR5, which, in order to function, needs to be modified by yet a third protein that does not exist in the cell and therefore needs to be co-administered in the form of a second combined vaccine and all of this needs to work simultaneously and coordinated. This simply does not exist, it is impossible, a recipe for disaster. The nearest comparable thing would be to dispatch tons of materials and people into Earth's orbit to build there a permanent station ... Wow? But we did it, did not we? Exactly, daring crazy things sometimes pays well and likewise, the researchers in this group have been progressively identifying and disarming problems and adjusting the vaccine so that in animal testing it has generated effective, safe and lasting protection against HIV. > Again invoking the metaphor of the restaurant, it is true that the fact of working in animals does not mean that it will work in humans, but it can. All we can do is test and verify. Still, it is impossible to deny that more than ever, there is a strong hope that we will soon dispatch HIV on the same path in which we send smallpox, polio, mumps, chicken pox, HPV, measles, among others. With few exceptions, only those who refuse vaccination will get HIV.


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