Posts tagged HIV breakthrough
Immune Exhaustion and HIV
8 years ago
HIV infection has long been known to cause immune exhaustion. Even with current therapies, this is a chronic issue. Finding ways to lessen the burden on the immune system, while still keeping the virus at bay, have been studied. Recently, some new experimental treatments have brought to light some interesting conclusions on the matter. It is hoped that the information thus gathered will help control the problem for many in the near future.
What the Research Reveals About Immune Exhaustion
Delicate balances keep everything in existence – from the largest systems to the smallest organisms. The interactions between the medications that keep the HIV counts low, the immune T cells, and the proteins that signal immune exhaustion are extremely precise and particularly balanced. Researchers have studied the effects of blocking the protein pathways, which are known to signal the exhaustion. In doing so, they have discovered that people can recover from immune exhaustion. However, a number of things must be in place for this to happen.
The exhausted T cells are the ones that have the protein, PD-1, which signals the exhaustion. The partner to that protein binds to it, and this is how researchers can identify the exhausted cell. By blocking the path between these two proteins, the immune system has a chance to regain normal function.
A Very Specific Process
When tested, this strategy was effective, but only under specific circumstances. First, if viral levels in the blood were high, adding the protein blockade actually increased viral production. Best results were yielded when the viral load was low. Also important is how the T cells react, as their numbers also increase. However, with low viral load and cooperating immune cells, restoring a measure of strength back to the immune system is possible with this method.
Further testing is underway, as are trials to see just how effective this approach can be. Of course, if implemented in the future, patient screening will be necessary. In the meantime, antiretroviral therapies continue to be an important part of both managing viral count and slowing disease progression.
Protein HIV Used to Hijack Human Genes
8 years ago
Four years ago, it was estimated that 1.2 million people living in the United States had HIV. Add to that an average of 50,000 new cases per year, and the results are staggering. As the disease progresses into AIDS, the outlook is bleak. One estimate put the number of patients with the advanced stages of HIV at over 26,000. While it is true that therapy can give a person who is HIV-positive a promising future, these treatments are lifelong, and the effects of the infection still manifest themselves in different ways as a patient ages.
A Protein Called Tat
In order to better understand how this wily virus is able to get such a strong hold on its host, experts meticulously performed experiments and studies. The results have brought to light how HIV uses a tiny protein, called Tat, to shut down certain human genes. HIV (a retrovirus) does not have many of its own genes, which is why it searches out and eventually takes over a host cell’s genes. Here is where the small protein, Tat, comes in. Once the command center of the cell has been overtaken, Tat manipulates the genes in order to create a more appealing environment for the virus. Studies show that nearly 400 human genes bind with Tat—and then shut down. When the scientists compared the symptoms of an HIV infection to the genes that were shut down, the two were compatible.
What this tiny protein is able to accomplish is astounding. It does provide useful knowledge that could be applied to halt infection and keep the disease from progressing to AIDS. One European country has already begun working on a vaccine which inhibits Tat in order to try and stop HIV. The results have been promising. However, it will take some more time for anything concrete to be established. In the meantime, more information is being gathered and used to come up with even more effective ways to treat, prevent, and hopefully completely eradicate HIV in the future.
HIV Vaccine? Antibodies from Pregnant, HIV Positive Mothers
9 years ago
Not every child of HIV positive mothers ends up with the disease. The reasons for this have been hotly debated since it is hoped that the mechanism could be duplicated as some form of HIV vaccine. At first, a certain antibody response was considered a possible way that the disease was held at bay. While this was later discounted as being incorrect, new data has researchers once again believing that this antibody response is, in fact, the answer they have been searching for all along.
Each year, about a quarter of a million babies are born with HIV, having been infected during pregnancy by HIV positive mothers. This number, however, is only a small fraction of the babies born to HIV positive mothers during a year. The fact that something prevents most babies from infection certainly caught the attention of researchers who are always on the lookout for an HIV vaccine that can prevent infection.
The Notable Antibody Response
When infants are not infected with HIV due to transmission, the common variable seems to be what is referred to as a V3 neutralizing antibody (due to the fact that it responds to the V3 loop on the HIV envelope). This antibody had been written off by researchers in the past because it does seem to be a strong enough response to prevent transmission. In fact, it has proved ineffective in certain lab tests. So why does it prevent transmission from mother to child?
Additional Factors for HIV Positive Mothers
It is believed one of the factors that makes this immune response more effective in warding off transmission from mother to child lies in the effectiveness of the mother’s antibodies because they can neutralize HIV infection. Obviously, testing will now continue to determine if experimental vaccines can be boosted by this V3 neutralizing antibody. While every child is not kept safe from transmission by this antibody response, researchers hope to use this as a jumping point, something they can use one day to increase the effectiveness of an HIV vaccine someday.
HIV May Evolve into an Ineffective Virus
9 years ago
HIV, like most viruses, evolves continually and at a rapid pace. Its process of replication is through constant mutation, so HIV cells can generate thousands of mutations of themselves. Some mutations die off before they take control over the virus cells of a host body, and some mutations become a dominant factor in the local virus population. Mutations that help the cells survive the longest have the best chance of dominating, and although some believe this may make HIV a stronger virus over time, there is evidence now emerging that shows the possibility that HIV may evolve – eventually – into a weaker, more treatable, and possibly ineffective virus.
The research showing this new evidence comes out of Africa. Philip Goulder, from the University of Oxford, and his team of researchers looked at the HIV epidemics in Botswana and South Africa. The epidemic started in Botswana roughly ten years before it hit South Africa, so the researchers took blood samples from roughly 2,000 HIV positive women from these two countries to compare the DNA structures of the viruses in each population. HIV cells in infected Botswanan women had developed mutations which helped them evade the immune system. Although this sounds like a bad sign, the mutations – in helping the virus evade detection – crippled the virus in many ways. Mutations in the Botswanan women slightly slowed down the replication speed of the virus cells, causing a 10% decrease in replication time. This slight variation helped the women’s immune systems keep up with the virus for a few years longer, causing a longer period between initial infection and when the virus caused AIDS to develop (meaning the immune system had been compromised completely).
This mutation only occurred over 10 years between when Botswana had its HIV outbreak and when the HIV outbreak spread to South Africa, so in a relatively short amount of time (one decade), HIV naturally evolved into a weaker virus. Goulder, of the research team looking at these mutations, says, “HIV can generate any mutation in the book, on any day,” so he’s not surprised that big mutations like this could occur so quickly. This mutation changes the time that the virus causes AIDS in untreated infected individuals to go from roughly 10 years to 12.5 years, which could mean the difference of life and death for those awaiting treatment. These mutations are already showing researchers where to focus their attacks on the virus, possibly leading to the development of an effective HIV vaccine. And, with the virus already mutating in this fashion, HIV may evolve to the point where the virus never completely compromises the natural human immune system, and where the immune system alone could maintain and control the HIV virus indefinitely.
Target Found in HIV Cells
9 years ago
by ADMIN
in HIV Research
Target Found in HIV Cells: New and Promising Results
HIV treatment is something researchers and scientists are continually pursuing. This is because, as the HIV cells mutate and become resistant to some medications, new medications need to be developed and varied types of treatment need to be utilized. In this pursuit, researchers have identified a new target for eliminating HIV replication and preventing the spread of the HIV cells in the body. This promising target found in HIV cells deals with the ‘activation’ period HIV has after a dormant phase. The virus cells can lay dormant for months, even several years, before it suddenly ‘awakens.’ HIV then begins its erratic replication process, destroying the body’s immune system in the process.
Scientists believed for many years that this activation process – the awakening of the HIV cells in the body – is caused by two components, the protein that HIV produces, called Tat, and the CycT1 protein. Indeed, they thought CycT1 protein was the only activation protein which caused Tat to activate the HIV cell and start the replication process. The most recent discovery is of a new protein – Ssu72 phosphatase – which seems to also be intimately connected to this activation process.
After this discovery, and subsequent studies to identify that this protein is indeed involved in the activation process of HIV cells, several new treatments are now thought to be possible. The first protein involved in causing Tat to start the HIV replication process – CycT1 – is used by the body for normal activity. Therefore, it cannot be a target of anti-HIV drugs (without disrupting the normal bodily activities it is involved in). Ssu72, however, is not used in normal body processes and can be targeted by anti-HIV drugs. This target found in HIV cells is now being studied as a means to eliminate or disable this protein—long before it starts the Tat’s process of HIV cell replication.
