HIV Research

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.

HIV and Heart Disease

HIV and Heart Disease

A recent study, underscoring the link between HIV and heart disease, has provided interesting findings. Heart disease is the number one cause of death in the US, with men having a slightly greater risk of developing the condition than women. However, people who have an even greater risk of developing heart disease are those who are infected with HIV. The link between HIV and heart disease is especially pronounced, in regard to plaque buildup in the arteries and actual heart attacks. Moreover, just like heart disease in the general population, men who are infected with HIV have a higher risk of heart disease than women.

Hundreds of HIV infected men, and a control group not infected with the virus, were studied. Background information was also taken into consideration, such as smoking and lifestyle. Advanced scanning techniques were used to gather images of the participants’ arteries, particularly the coronary arteries. These images were used to determine if plaque or a stenosis had developed. Researchers found that those who were HIV-positive had a higher rate of both of these conditions. When it came to non-calcified plaque, those with HIV showed higher rates and greater build-up. This can be dangerous, as this type of plaque buildup can rupture or break free. When this happens, it can cause a blockage in a vessel or even a heart attack. Those who had later stages of HIV, and who were also taking antiretroviral medications, had the most cases of heart disease as well as the most severe cases.

Exactly why HIV and heart disease present together and so often is not yet known. Researchers fully intend to keep investigating. However, now that it is clear what types of disease manifest themselves in men who test positive for HIV, physicians can keep a close eye on their vascular system in order to catch early signs of heart disease.

New Imagery of HIV

New Imagery of HIV: Electron Microscope Allows Up Close View of HIV Function

Research on how HIV works, infects cells, and responds to various forms of treatment, has now been ongoing for about three decades. Important information has been collected and better understood over the years, which has led to a series of advancements against the disease. The benefits of this research can be seen by the number of patients who are now able to not only enjoy a fairly normal lifestyle, but who also reach an almost average life expectancy. These are certainly great statistics that reflect the strides made against the disease. However, new imagery of HIV in action could revolutionize not only how research is done, but also allow insight into the best ways of how to continue fighting the epidemic.

A team of medical researchers recently used electron microscopy to view a 3D image of HIV in the digestive tract. This exciting step allowed the researchers to study the infection up close and live. Because of this ability to actually watch the virus in real-time, we now have greater insight into how HIV works and, thus, how it may be stopped.

Examining the infected tissue in this way, which gave scientists the opportunity to track both how human cells respond to the virus, and monitor how HIV itself functions, has given scientists a new understanding of the disease. The team could view concentrated areas in the gut where HIV pooled, leading to a greater appreciation of how the virus spreads and invades healthy tissue.

Another interesting observation involves our immune system. HIV appears to hide in the deep sections of the digestive tract, an area known to be associated with immune activity. Researchers believe an antibody attack using drugs could prove effective against wiping out these clusters of HIV. If so, this could have a massive impact on slowing further infection.

Seeing HIV live in infected tissue gives hope that more discoveries await on how this vicious virus functions. As with the new imagery of HIV from electron microscope imagery, new understanding of how the disease functions will almost certainly lead to even more effective ways of dealing with it. Researchers are hoping to continue to use electron microscopy to view other particulars of the infection and to monitor how it functions in those areas, as well. Thanks to the new imagery of HIV, and tracking how the HIV infection gains a foothold and grows, means that we are one step closer to closing the chapter on HIV.

 

 

Interfering with HIV

Interfering with HIV: Nef and HIV

Although progress against HIV has been slow, we seem to be in a new era, as we are beginning to reap the benefits from our years of research. Certainly, advancements have been made across the board. Perhaps this can best be illustrated by the lengthened life expectancy for people diagnosed with HIV. Increased life expectancy is the result of a number of factors. Some of these factors are greater understanding of the disease, new therapies and, especially, the effective cocktail of antiretroviral drugs that is now available. Many of these therapies are directly interfering with HIV and its ability to infect cells, thus keeping HIV from progressing to AIDS. Certainly, living with a chronic condition such as HIV, instead of facing a terminal illness, is a major advancement.

As stirring as this reality is, there is always the need for better treatment options. Moreover, as the fight against the disease has progressed, researchers are now facing viral mutation of HIV. This has led to certain strains of HIV that are developing resistance to antiretroviral therapies. This difficult challenge facing researchers has led to an exciting discovery; one which could lead to new drug therapies.

Nef is a protein that is not new in HIV research. However, it has received renewed focus as alternative mechanisms of HIV infection have been uncovered. Nef has an important role to play in the infection of cells, as it binds itself to other proteins in a cell. When this happens it then becomes impossible for anything else to enter and infect that cell. Because of a more complete understanding of this process, researchers now believe it may be possible to take advantage of the protein. The idea is for a drug to enter and bind with Nef, thus disabling HIV’s ability to infect other cells. We might describe this as an ‘immobilizing’ tactic. Moreover, this should work with already developed therapies. This type of therapy has an added benefit, as it would not have to harm the human cell. This is because the drugs would be targeting the HIV protein site.

New pharmaceuticals could be created effectively interfering with HIV and its ability to further infect the cell. Having this ability would make treating HIV much more effective. When we add to this the fact that healthy cells would not be affected, it is easy to see why researchers are so excited.

HIV and Drug-Resistant Mutations

HIV and Drug-Resistant Mutations

Antiretroviral therapies have come a long way in the treatment of HIV. Not only does the treatment slow the progress of the disease, in some cases even preventing AIDS for developing for years, it also allows for a rather normal life. This is all good news, and medical researchers are hoping that this upward trend continues. There is, however, a downside to the antiretroviral therapies being used. That is, HIV and drug-resistant mutations, or, in other words, viral mutation. Thankfully, the reason this mutation occurs may have been recently discovered.

A research team was imaging HIV and viewing computer models, in an effort to understand how and why these mutations were happening. HIV works by invading a host cell and then implanting its own blueprint into the cell’s information center. When this happens, the virus then programs the cell to make replicates of the virus, instead of a healthy human cell. Specific details that occurred during these complex procedures were noted. The team observed how certain common HIV drugs interact with the virus. In doing so, they came to some conclusions that may help explain why these HIV and drug-resistant mutations occur.

For example, when transferring information into the healthy cell, the drug attaches itself and creates a sort of bridge. The information that the HIV is trying to pass on is then put on this salt bridge. It then slides to and fro. Transfer of this important information becomes difficult and, usually, ineffective. This frustrates the replication of the HIV. Mutations seem to occur on the part of the virus in an effort to stop the bridge from forming. New, drug-resistant strains of HIV can prevent the bridge from being put up. This allows the virus’s information to be transmitted into the host cell, ultimately causing infection to occur.

Knowledge is power, so goes the saying. Scientists are delighted to have a new understanding of how and why these HIV and drug-resistant mutations occur. Armed with this information, they are increasingly confident that they can successfully create new medications that will counter the effects of mutated strains of HIV.

 

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