Posts tagged HIV breakthrough

New HIV Antibody

New HIV Antibody: Reveals New HIV Vulnerability

It has recently been discovered that a new HIV antibody, known as 35O22, binds itself to a spot on the HIV cell walls—one that was not previously recognized as a vulnerable location. This viral spike, which is located in an area straddling the proteins gp41 and gp120, is weak to the antibody. Because of this, 35O22 is able to bind to the HIV cell and actually neutralizes several strains of the virus. This new HIV antibody has many researchers cautiously hopeful, as the discovery could turn out to be extremely significant.

Over half of the known HIV strains, roughly 60 percent, are affected by the 35O22 antibody. In laboratory tests, moreover, the antibody actually prevented these strains of HIV from infecting other cells. More good news is that the antibody is very potent, which means only a small amount of the antibody is needed to neutralize the virus. After discovering 35O22, scientists and researchers have identified other 35O22-like antibodies that are common in groups of HIV-infected people. Indeed, their blood contains antibodies that could potentially neutralize most of the known HIV strains. This suggests that a vaccine could elicit 35O22 much easier than other less common bNAbs (Broadly Neutralizing HIV-1 Antibodies) – the grouping of antibodies 35O22 belongs in.

Researchers also report that the strains of HIV that 35O22 neutralizes compliments the strains neutralized by other bNAbs. This means that combining 35O22 with some of the other bNAbs in a vaccine, prevention treatment, or therapy could produce a single solution to the problem of HIV: the complete neutralization of the vast majority of HIV strains found around the globe. This new HIV antibody and the exposure of a new vulnerability in the HIV cell is therefore very significant. In fact, it could mean a potential cure for HIV by way of preventing all known strains of the virus from replicating.

Computers Against HIV

Computers Against HIV: A Striking Ally

Research into eliminating HIV and AIDS has always been a battle against time. Certain compounds that were once successful in destroying the virus cells, or in causing them to become sterile or inefficacious, are now worthless against the virus. This is a direct result of the ability of HIV to constantly mutate and adapt. Thus, new compounds are continually needed, and new methods of treatment are constantly sought after. One group of researchers, based at the University of Southern Denmark, are exploring methods that would accelerate the very process of finding new compounds that can be used against the HIV cells. What they’ve successfully done is to use computers to find potential compounds against HIV—at a rate magnified by several hundred percent! It might be said, then, that the use of computers against HIV has enlisted a formidable new ally in the war against HIV.

The problem is not the lack of compounds that have the potential to destroy or effectively stop the HIV cells. These days, scientists are able to reproduce almost anything imaginable in their laboratories. The problem is to effectively find and identify those compounds. By using computers based on quantum physics – which speed up processing times by several fold – the researchers at USD were able to pinpoint compounds that have varied effects on the HIV cells.

Many of these compounds do not kill the cells outright but, instead, stop HIV cells from being able to reproduce. ‘HIV is a retrovirus that contains enzymes which make it able to copy itself with the help of host genetic material and thus reproduce. If you can block these enzymes’ ability to replicate itself, the virus cannot reproduce.’ This is according to Vasanthanathan Poongavanam, a member of the research team at Southern Denmark. The group was able to identify 25 promising compounds. When the 25 compounds were then tested using the group’s advanced computer systems the field was narrowed to 14, which inhibited the virus’s ability to reproduce. ‘It took us only a few weeks to find these 14 very interesting compounds, whereas before it would have taken years.’ All of this illustrates that using computers against HIV has brought a daunting new player onto the field.

Mutating HIV Into Extinction

Mutating HIV into Extinction: One Answer to the Dilemma of HIV

In the late 1990’s a group of scientists and researchers faced with the dilemma of HIV and its resistance to a cure, decided to try to force the virus to over-mutate. The idea was to cause HIV to mutate at a rate much greater than the average HIV cell normally does, thus making the cells weaker and more prone to being eradicated. Essentially, they were attempting to cure people by mutating HIV into extinction. Many thought this approach would ultimately prove fruitless, but they pressed on.

Fast forward to 2011 and we find that, indeed, the group has developed a drug that causes rapid mutation in HIV cells. In the lab the drug forced a mutation explosion such that the HIV cells could no longer produce enough protein to survive. This essentially ‘killed’ the virus (although, technically, viruses are not alive in the first place, which is one of the reasons they are so difficult to eliminate). In clinical trials, however, the mutation was not great enough to cause the test patients’ HIV cells to collapse.

In a new study, released in July in Proceedings of the National Academy of Sciences (PNAS), the researchers discovered how the drug – currently known as KP1212 – was able to cause the HIV cells to mutate beyond their normal rate. Armed with this new knowledge, they are confident that they will be able to strengthen the effects of the drug and eliminate the HIV cells on a permanent basis. If they are successful we are talking about an actual cure for HIV.

HIV cells normally mutate quite frequently due to the way HIV reproduces. HIV makes copies of its genetic material, which is very error-prone and unstable, in a rapid mutation that actually helps the virus cells evade elimination from both the body’s immune system and man-made drugs. If HIV can essentially be forced into overdrive (roughly double the normal mutation rate), it will cause weaknesses that will result in the immediate elimination of HIV. Or, at the very least, cause the virus to become highly susceptible to drug elimination. This kind of forced over-mutation can, and in some cases already does, work for other viruses. For example, this is how Ribavirin works in patients with the hepatitis C virus. Similarly, some of the drugs developed for certain strands of influenza work in the same way. All of this good news suggests that we could be on the road to mutating HIV into extinction.

HIV to Treat HIV

HIV To Treat HIV: HIV ‘Cut and Paste’

Researchers recently applied the idea of ‘cut and paste’ to something completely different than word processing on their computers: the treatment of HIV. Of course, most of us use ‘cut-and-paste’ on a regular basis, whether for emails, documents, or filling in information. Certainly, it is a function that comes in handy. However, this cutting-edge technique could mean really big changes on the HIV battlefield. What we are talking about is using HIV to treat HIV. Obviously, this is an exciting idea. But, how does this process work? Moreover, how will this be beneficial in HIV treatment?

Within our cells are proteins, which are used to perform a variety of tasks. One of these proteins acts like a pair of scissors. It cuts away at the genome, grabbing and separating bits of information. The cell can then use the information as needed. For scientists, these natural ‘scissors’ can be used to help patch up damaged cells. The damaged cells, specifically those infected with HIV, have genetic bits of information missing. In order to patch up these holes, the ‘scissors’ could cut out patches from the virus and then use this to patch up the damaged cells. In effect, parts of the HIV would be cut away to repair the damage done by the disease. This may sound far-fetched, but recent testing gives reason for optimism.

HIV has been studied for nearly three decades and it may seem ironic to use HIV to treat HIV. However, it is a promising point of attack in the fight against HIV and AIDS, especially as this therapy looks particularly sound in the area of strengthening the immune system. Assisting the body to not only resist attack—but also to fend it off in such a manner—would be a big step in the fight against HIV. Should the cut and paste method prove successful, there may be other infections that could also be treated or prevented using similar methods.

Protein Mechanism That Inhibits HIV

Protein Mechanism That Inhibits HIV: SAMHD 1

The number of different functions a single cell carries out is staggering. New systems and operations continuously come to light, as researchers dig deeper into the profound workings of living things. This search has exposed a process within human cells that may prove useful in the fight against HIV. Current HIV treatments target the virus itself along with the proteins therein. What time has shown, however, is that these change and mutate. What is needed is a protein mechanism that inhibits HIV but doesn’t mutate. The new findings could do just this, as they could aid in developing new treatments that target human molecules that are not known or likely to mutate.

Within the cell, certain building blocks are used to make up new strands of DNA. These are nucleotides. When HIV infects a host cell, it sends two strands of RNA into the cell. These strands must be changed to DNA, in order for the infection to take place. However, before this task can be completed, nucleotides are necessary. It was found that a certain protein found in human cells is responsible for the amount of nucleotides present in that cell. Experiments have been done to map out the workings of the protein labeled SAMHD 1. Mechanisms have been identified that can trigger a sort of emptying of nucleotides from the cell. When this happens, there is no way for HIV to infect the cell.

Researchers are looking into developing inhibitors that can reduce the amounts of SAMHD 1 and therefore limit how many nucleotides reside in certain immune cells. If this protein mechanism that inhibits HIV is successful, a new generation of HIV therapy will be born. Should this happen, new treatments will be available that could be immune to mutations. Applying this science to other infections is another possibility too. Preventing infection and spread of HIV would go a long way to advancing us in the battle against the persistent virus.

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