HIV Research
Vitamin D Helps with Resistance to HIV
9 years ago
When it comes to the poorest nations of the world, an inexpensive means of fighting the spread of HIV is vital. Researchers may have found just such an ally according to a recent study of how vitamin D affects the immune system response to HIV. What did they find?
The Test Subjects
The study was performed using 100 young individuals, half from the Cape area in Africa and the other half from the Xhosa indigenous tribe. Blood samples were taken from the healthy individuals during the sunny summer months when vitamin D levels are the highest and again during the winter when they are at a seasonal low due to less sun exposure. During the winter, both groups proved to be vitamin D deficient, and the women who were in the study suffered even more from the deficiency than men.
Exposure to HIV-1
Next, these blood samples were exposed to HIV-1. After giving the virus nine days to work, the samples were tested. The amazing result was that the vitamin D deficient winter samples were more prone to infection than the summer samples with normal vitamin D levels.
The deficient individuals were next given a six-week supply of vitamin D supplements to get their levels back to normal. Then their blood was taken and tested again. Infection rate was reduced back to what it had been for the summer samples. The results were clear – vitamin D was helping ward off the disease.
Implications
While there is no immunization for HIV, this study reveals that vitamin D can reduce the chances of infection. Since vitamin supplements are far less expensive than vaccinations, this is also a far more viable solution for reducing the risk of infection in developing countries. Also, additional health benefits associated with vitamin D would be achieved by combating deficiency. It’s a win-win for some of the underdeveloped countries that are the hardest hit by the spread of HIV.
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.
New Understanding of Microbicide’s Effectiveness Against HIV Transmission
9 years ago
Researchers of HIV and AIDS have long known that semen has an enhancing quality on the infectiousness of HIV, as it causes the virus cells to cluster together and bind themselves to certain protein strands within the semen fluids, thus increasing their ability to attach to – and infect – host cells. This is a major reason, researchers have learned through studies, why anal sex has the highest risk potential in the transmission of HIV from one person to another. The other major reason for the high risk involved in anal sex is rupturing of anal tissue during intercourse, which causes bleeding and raises the infection potential for both partners. Recently, researchers learned that semen is further problematic in stopping the spread of HIV, as it has been shown to lessen certain antiretroviral microbicide’s effectiveness against HIV.
An antiretroviral microbicide is a new form of anti-HIV gel which is meant to be applied to the vaginal walls prior to sexual intercourse, and which was proven to effectively eliminate the HIV cells – either by killing them or causing them to be unable to bind to any host cells – but this success is only seen in the laboratory. When they started clinical trials in areas of Africa with high infection rates, they noticed that not only were the microbicides ineffective in stopping infection, sometimes they seemed to have the reverse effect, causing it to be more likely for infection to occur. They now know why this happened. The microbicide’s effectiveness against HIV was compromised by proteins within the semen which, while strengthening the HIV cell’s infectiousness, caused the microbicides to be up to twenty times less effective against stopping transmission of the virus. The researchers who conducted the study that lead to this observation are hoping to help women in the Sub-Saharan countries of Africa who, many times, have no choice about safe sex or condom use. If they can work around the negative effects of semen, which some new antiretroviral microbicides are already promising, they can help curb the spread of the disease, in these countries and around the world. As one of the authors of the study says, “This study sheds light on why these microbicides did not work, and it provides us with a way to fix this problem by creating a new compound drug combining antivirals and amyloid inhibitors.” The more they know about each step of the infection process, the more they can break these steps down and stop HIV transmission.
Possible New HIV Therapies with the Discovery of Viral Insertion Variants
9 years ago
The human immunodeficiency virus (HIV) has the ability to attach its DNA to the host’s immune system’s DNA and manipulate the host cells to continue its replication process. This ultimately kills the affected cells, destroying the host’s immune system along the way. Researchers had long ago discovered that the HIV protein integrase is responsible for the HIV’s cell’s ability to attach itself to a host cell’s DNA, but for over twenty years they were not able to learn how this process actually happened. New discoveries into this process have shown that new HIV therapies are possible, because they are now attempting to retarget the entry points of the initial HIV cells, and thus weaken the virus’s ability to replicate so rapidly.
Researchers at KU Leuven’s Laboratory for Molecular Virology and Gene Therapy have learned that two amino acids are responsible for the integrase’s integration of the viral DNA to the host DNA. “HIV integrase is made up of a chain of more than 200 amino acids folded into a structure,” says Jonas Demeulemeester, one of the doctoral researchers working on this project. These amino acids, which are all folded in on each other, manipulate themselves in such a way that only two of the amino acids come into direct contact with the host’s DNA, and this becomes the initial entry point of the HIV cell.
The process of how HIV links to a host cell’s DNA is similar to related animal-borne viruses. Using this model to look at the animal-borne viruses, the researchers were able to learn that by manipulating and re-targeting the amino acids that make up the integrase they can cause the HIV cells to enter the host’s DNA at variant points. They learned that some entry points are more susceptible to a rapid replication and destruction of the host cells, and at the same time there are “safer” entry points of the host’s DNA which cause for a very slow and manageable reproduction rate of the viral cells. Now possible new HIV therapies exist because of this discovery, as we can now target the individual amino acids within the viral DNA, hopefully manipulating them into extinction.
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.
