Posts tagged HIV therapy

Existing Prescription Drug Has Potential to Fight HIV

HIV-positive individuals can lead long, happy lives. They are, however, dependent on the prescription drugs that keep the infection at bay. This dependency is a lifelong one. Current therapies aid the immune system to contain the virus. If left alone, the immune system would soon be overwhelmed by the virus – thus the constant need for assistance. This was the fact that researchers focused on when examining the reaction of the immune system towards the virus when this prescription drug was applied. The results have many hopeful that in the near future, lifelong therapies will not be necessary to fight off or protect against infection.

What Prescription Drug?

The enzyme adenosine deaminase is the prescription drug getting the attention here. It already exists in the pharmaceutical world, and scientists are looking to repurpose it to target HIV. What the studies proved was that exposure to this enzyme empowered the immune system in a couple of different ways.

First, immune response was increased. Important CD4 and T cells hurried to the call and took care of the invading virus. The next observation was also impressive, as it showed an increase in memory for the T cells. Next time they encounter HIV, the cells will remember and be able to eliminate it from the host. This is crucial information for researchers investigating how to reduce treatment length. If the immune system can respond efficiently on its own, and then recall that response when threatened again, lifelong therapies may be done away with.

Should adenosine deaminase be able to boost the immune system to the point researchers have seen, it could mean better control of HIV infection. This control could also rely mostly on the immune system, with little fear of a reoccurring infection. Long-term management of the disease could see less dependency on antiretroviral therapies. It is hoped that further study and advocating for the prescription drug is expedited to help out in this regard.

Until the time comes when such medications are ready for use, though, it is vital for those with HIV to stick to their daily treatment routine in order to halt disease progression.

Why Millions of HIV-Positive Individuals Go Undiagnosed

As HIV prevention, testing and treatment continue to advance, HIV positive patients on a treatment plan remain healthier, living longer lives. As new information pours in, researchers scramble to further progress their understanding and approach to the disease. Methods used to slow disease progression and curb mortality rates are proving more and more successful. Yet, in spite of such advances, the struggle with HIV is still a slow, tragic war. Why might you ask?

What Is Holding Us Back from Defeating HIV?

More cases are reported every year, and it is estimated that millions have the infection without knowing it. Herein lies the danger. Those unaware HIV carriers often infect others. Spreading of the virus is one of the major roadblocks to its eradication.

Why Individuals Avoid Testing

Studies on why so many people with HIV refuse testing or treatment have come to a simple conclusion: fear. Fear is helping HIV survive the war. Whether it’s fear of the disease or the associated social stigmas, it remains the number one reason people do not get tested.

The psychology behind the behavior needs to change. Any chronic condition carries with it a strong measure of fear. HIV is no exception. However, those advances mentioned earlier are reason for hope. Hope supported by reality. Today, HIV testing can be performed at home. If the result is positive, treatments are available. What once arrived with a death sentence is now a treatable condition. Slowing the progression from HIV to AIDS is now a regular occurrence. HIV positive people can enjoy a long life and enjoy a full and happy one too. And more than every the public needs to understand this new chapter in the war on HIV.

Courage Reaps Benefits

Fear of a diagnosis is no reason to put off testing. Hope lives. Fear kills. Early detection leads to more positive outcomes, like HIV prevention, and management of the viral infection. This is the message healthcare professionals encourage. Educating the public on the facts, rather than the fears of HIV, saves lives, prevents future infections, and will help us to one day eliminate the virus for good.

New Understanding of Microbicide’s Effectiveness Against HIV Transmission

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

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.

Target Found in HIV Cells

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.

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