Posts tagged controlling HIV
New Potential Route to a Cure for HIV/AIDS
9 years ago
by ADMIN
in HIV Management
So much of the early research in finding a cure for HIV pointed towards the virus’s ability to lie dormant in the immune system of a host’s body, and scientists started believing a cure for the virus was impossible. Many decided, with this idea, to only focus their research on stopping the replication process of the virus cells and maintaining a healthy state of those infected. Some, though, still try novel ways to eliminate this difficult virus, as it can stay undetectable for years and suddenly resurface and eradicate the infected person’s immune system. In fact, one group of researchers has made some wonderful discoveries about which cells in the body the virus hides, once again paving a potential route to a cure for HIV. Most have concluded that the cells HIV usually hides in are our CD4 cells – also known as helper T cells – and since these are integral for our immune system to do its job, there was little we could do to eliminate the virus from those cells and the body as a whole. Surprisingly, this group of researchers has found another type of cell in which the virus may hide, one that is much more vulnerable to medical treatment and manipulation.
The research was lead by the Yerkes National Primate Research Center, in Emory University, as it involved monkeys that were infected by Simian Immunodeficiency Virus (SIV), which is essentially a sister virus to HIV that affects primates. Researchers examined these primates before and after infection, and in some they removed the helper T cells that many believe is the main focus for HIV’s attack. When they were removed, the virus cells attacked immune system cells called macrophages, which naturally have a much shorter lifespan than helper T cells. This is significant because the three-day lifespan of the macrophages is much less than an average helper T cell, meaning it would be difficult for the HIV cells to lie dormant for their required few weeks (minimum) to continue their replication process. This possible route to a cure for HIV means that we can now think of different methods to eradicate HIV, and no longer be bound to only the antiretroviral medications currently used to keep it at bay.
Stopping the Spread of HIV Through Social Media
The trends of social media have changed how, and how quickly, information becomes publicly known. Social media can now tell us things like where the next fashion, music, and entertainment movements will occur, along with which regions of the United States are more likely to love something that other regions will hate. One application of the information now available through social media is to map out the spread of diseases such as influenza and strands of the common cold. This application could lead to more sophisticated ways of stopping the spread of HIV, by using social media to track and possibly halt further infection.
Sean Young, at the Center for Digital Behavior at the University of California, Los Angeles, published an article this past October dealing with a possible future, where social media can predict and even change biomedical outcomes. This translates into being able to chart, predict, and maybe even ebb the transmission of preventable infectious diseases, like HIV. Social media information, such as Twitter tweets and Facebook posts, which shows the recent – or eminent – drug and sexual related activities associated with the risk of infection, can be collected and cross-referenced with known information on HIV. In addition to education of what activities and what areas are at the highest risk of infection, this cross-referencing can help medical researchers find focal points to make testing more available. It can also help researchers make the availability of treatment an easier possibility for those getting tested and learning they’re HIV positive. Surveys are also showing that those who post about this topic, or who read about HIV through their online communities, are more likely to get themselves tested.
A cautionary tale for many is that the collection of this data is done the same way corporations are currently taking information in an attempt to raise profits. This type of marketing has created a major backlash from those who fear for their privacy. Sean Young has an answer to this caution: “Since people are already getting used to the fact that corporations are doing this, we should at least support public health researchers in using these same methods to try and improve our health and well-being.” He further added, “We’re already seeing increased support from patients and public health departments.” Young hopes that a more general acceptance of this type of data collection by medical researchers will follow suit. He, like many, believes that social media and other modern technologies are the key to stopping the spread of HIV in the future.
Are You More Immune to HIV Than You Thought?
9 years ago
by ADMIN
in HIV Management
For the past several decades, doctors and scientists could not understand why some people quickly get sick – and can die – when infected with HIV, while others seem to naturally resist the virus for several years with less damage done to their immune systems. Researchers at the University of Minnesota’s College of Biological Sciences and Medical School looked at the virus’s rapid-mutation ability, along with how it attacks the human immune system to replicate, and hypothesized that this distinct difference in how the virus differently affects infected individuals is somehow caused by the genetics of the infected host. In trying to understand why some are more immune to HIV than others, these researchers discovered a new crack in the HIV cell’s armor which helps explain this phenomenon.
HIV attacks the immune system in order to replicate within the infected host’s cells. It seeks out the immune system cells called T lymphocytes (T cells), and uses the cell’s molecular machinery to replicate within them, killing the cells when it is done with each cell. This infection eventually depletes the system of necessary T cells, leaving the infected host helpless to other invading viruses and bacteria. The T cells do have a defense against this, as they have an anti-virus protein in their arsenal – called APOBEC3 – which has the ability to block the HIV cell’s replication process. If they are successful, they can effectively stop the virus from replicating and eventually clear it from the system as the virus cells die off. Unfortunately, HIV has developed a counter-attack to this protein, a protein of their own – called Vif – which attach themselves to the APOBEC3 cells and trick the T cells into destroying their own protein, leaving them defenseless to the virus’s replication and destructive abilities. To learn why some seem to be able to naturally fend off the virus – at least for a lot longer than others – researchers looked closer at these proteins. They found strong clues as to why some immune systems work better against the virus than others.
Some people have a greater ability to create a version of the APOBEC3 protein, which is known as APOBEC3H. This particular form of the protein is boosted whenever someone is infected with HIV, which made the researchers believe this plays an important role in the immune system’s defense against HIV. What they found was a confirmation of this assumption, as people with a more stable accumulation of the APOBEC3H protein seem to be more naturally immune to HIV than those with a more unstable accumulation of this protein. Whenever the infecting HIV cells had a weaker version of their Vif protein (as constant mutations cause the virus to be varied in its strengths and weaknesses), the infected individual with a stable APOBEC3H protein in their T cells had a better time limiting the HIV cells from replicating. This was not the case if the infecting virus cells were equipped with a stronger Vif protein. This discovery helps scientists and doctors with a new path towards attacking HIV, with a possible road to a cure. The more we can suppress the virus’s Vif protein, the more our natural immune system has a chance to combat against the infection. Coupled with a strong antiretroviral regimen, this could help stop the virus from replicating, and possibly killing it outright.
Heroin Withdrawal Quickens the Spread of HIV, Researchers Say
9 years ago
by ADMIN
in HIV Management
With the hypothesis that heroin use contributes to a faster spread of the HIV cells in an infected person’s body, researchers out of Yale University conducted a study to look at the link between opiate use and HIV. They teamed up with scientists from Boston University and in Russia, studying participants’ CD4 count to determine their results. These results were quite different than they imagined, as the participants who claimed heavy heroin abuse had higher levels of CD4 than those who claimed only intermittent usage. With this information, the team has concluded that heroin withdrawal quickens the spread of HIV in an infected person’s body, as opposed to a steady use of the narcotic. CD4, which refers to a cluster of differentiation 4, is a specific form of protein that is typically found on immune system cells such as T helper cells and macrophages. This combination of the protein and immune cell, commonly known as white blood cells, are necessary for a healthy immune system to work properly, or at all. Because of this, the amount of CD4 protein found in a person’s body is a good indicator of how well their immune system is working, as lower amounts of these CD4 cells means a weaker or compromised immune system. Fewer CD4 cells in an HIV infected person’s body means the virus has destroyed more of the T helper cells where this glycoprotein is found.
Using this method of determining how much HIV has spread throughout an infected person’s body, the international research team looked at seventy seven participants, all from Russia, all heavy alcohol consumers, and none whom were then on antiretroviral medication. Those who self-reported no usage of heroin had a standard depletion rate of CD4 cells. This came as no surprise to the teams. What was surprising was the fact that those who reported heavy opiate usage had a slower rate of CD4 depletion than those who only occasionally used the drug. This ruled out the notion that heroin speeds up the spread of HIV cells in an infected person’s body, and opened new questions to the teams. Their conclusion is that it isn’t heroin use that speeds up the replication process of HIV – as previously believed – but that heroin withdrawal is the factor that quickens the spread of HIV. Though they cannot yet determine why this is, they do know that heroin withdrawal is one of the worst known to mankind, and like alcohol and benzodiazepines it is one of the only three categories of withdrawals which can actually kill a person. Jennifer Elelman, the lead author of the study and assistant professor at Yale School of Medicine, said, “We expected that HIV-positive patients who abused heroin on an ongoing basis would have the greatest decreases in their CD4 count,” adding that the international research team is now looking at the withdrawal process in relation to the spread of HIV. Not to leave all of their previous assumptions behind as they look at this process, Dr. Edelman continued, “We will also evaluate the effects of heroin and other opioids on other aspects of immune function.”
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.
