Posts tagged HIV cure

How HIV Affects the Mind as a Person Ages

Year after year, advancements made in the treatment of HIV are helping many to lead longer and healthier lives. As individuals enter their later years, it is important to know what to expect when living with HIV, and how it affects the mind.

Current Standards for Testing

For example, at least one-third of HIV-positive patients will develop what is termed HIV-associated neurocognitive disorder. The medical community knows of this disorder, and very often tests older adults who are HIV-positive. New information on the cognitive functions of those living with an HIV infection may change how physicians test for the disorder.

Normally, doctors will administer a standard neuropsychology exam. If a patient scores well on this test, he is usually deemed cognitively normal. This standard test seemed to be doing the job—until the matter was further investigated. Researchers examined a group of patients who had passed this test, but then subjected them to different types of testing. The surprising results exposed the need for further probing when looking to diagnose HIV-associate neurocognitive disorder.

What the Research Revealed

Older, HIV-positive adults were asked to perform certain mental tasks on cue. At times, the tasks were changed from one to another. This is where physicians began to notice a lag between healthy participants and those with HIV. This response to switching tasks was significantly slower in the HIV group.

To delve a bit deeper, brain scans were ordered. The scans revealed that the dorsal anterior cingulate cortex was reacting differently in the control group than the HIV-positive one. This area of the human brain is linked to both executive and apathetic deficits. These cognitive impairments may come in under the radar with standard testing.

The Latest Developments on How HIV Affects the Mind

At this time, we have no way to treat the disorder. Efficient testing, however, is still vital to patients, as well as their families and caregivers. Understanding that some functions might come a little slower to HIV-positive individuals during their later years is important for those who interact with them daily. Effective testing and education are the keys to finding out how HIV affects the mind.

These studies are recent. More study and research are underway.

New Drug Make Awaken Dormant HIV Cells for Complete Eradication

Current treatments for HIV infections have come a long way over the past decade. Still research continues to try and find a cure for this tenacious viral invasion. While antiretroviral therapies may control the infection, treatment does not eliminate it completely from the body. There are some cells that have been infected with HIV that remain dormant and undetected by the immune system. Should a patient cease treatment, these cells could reactivate. However, recent research teams have noted a new class of drug that may be the key to purging these dormant cells. That could mean an HIV cure.

Cells that contain the HIV gene are difficult to find because they are wrapped up in the DNA. Certain drugs that are used to unravel this gene to treat other conditions still have a tough time finding the virus. Also, it is not easy to wake the virus as many of these types of drugs have not been successful in doing so. Here is where the new drug comes in. Smac mimetics, as it is called, works by acting as an alarm. This alarm acts quickly and is effective at awakening latent HIV-infected cells. It can do this without the risk of also activating the immune system which, if drastic enough, could prove fatal. But, the awakening of these cells can lead to detection by the immune system and eradication. All of this is accomplished because the drug uses the so-called back-door of the cell when it enters. Thus, a complete purge of the virus from the host occurs. If used together with the gene unraveling drugs, it is believed that Smac mimetics will prove successful.

With so much new information and so many trials underway, sometimes promising results do not make it into therapy for quite a while. This brings us to the other benefit of Smac mimetics – it is already being used for clinical trials in cancer treatments. The trials already conducted have gone very well. So while HIV-1 specific testing and formulating needs to be done, it is possible to see the drug being used for HIV in a much more reasonable timeframe than if it was a new development for an HIV cure.

The Body’s Immune Cells Actually Cause HIV Patients to Develop AIDS

That AIDS is brought about through an HIV infection is not new knowledge. Results from a recent investigation on the process from HIV infection to AIDS, however, sheds light on the topic. Actually, the findings show that it is the body’s own cells that cause AIDS, rather than the virus directly. This new concept could change how to proceed with treatment and HIV cure.

The virus, upon entering the host, infects a healthy immune system cell (CD4 T cells). The cell in turn can infect other healthy cells. Therefore, infection is spread either from the free-floating HIV itself or via the infected cells. While this has been common knowledge for some time, it was unknown that the latter is much more destructive when it comes to disease progression. Not only is cell to cell transfer much more efficient and effective, but it can also be deadly.

Once a healthy immune cell has been infiltrated, HIV DNA fragments begin to accumulate within the cell. At first it goes undetected, but the cleaning up of these fragments becomes too much for the cell, and it is eventually detected. This overload signals the cell’s defense system. This, in turn, triggers a molecular response. The chain of events that follows is fatal, cell suicide, if you will. Once the enzyme caspase-1 is activated, what usually follows is cell death (pyroptosis). This preprogrammed response in immune cells is a type of self-defense. Cell to cell infection is so successful because mass cell ‘suicides’ are what can eventually lead to disease progression, a wiped out immune system, and AIDS.

Upon this discovery, a number of experiments were performed to confirm the findings. The results supported what had been uncovered. Scientists are sure that it is due to the efficiency in which the infection transfers from cell to cell that leads to mass cell death. In turn, treatment of HIV and preventative measures against AIDS may now focus on inhibiting cell to cell transfer rather than just on the unattached virus itself. Turning attention to CD4 T cells and coming up with solutions that will prevent infection transfers should assist in halting not just the spread of infection, but also disease progression into AIDS and thus promise of an HIV cure.

Multiple Variants Hurt Outcome for HIV Patients

Not all trials are conclusive or yield the results that scientists expect but everyday brings us closer to an HIV cure. Indeed, they still provide insight into matters not yet fully understood. That was certainly the case in a study recently conducted. The study took the results taken from two separate HIV vaccine trials and examined them together. The findings helped researchers determine what factors could lead to poorer patient outcomes on a clinical level. Both trial outcomes were compared to see how initial infection and viral characteristics could possibly be used to foresee the success of a patient’s treatment. While the study failed to be definitive, it has led scientists to look at matters in a different light.

The Results of the Study

HIV-1 on its own would establish, early on in the infection, its viral population. Once set, it generally remains constant. The patient is tested for viral load. Within a short time from the time of infection, this viral load can become relatively stable. This leads to a good prognosis for those pursuing treatment therapies. Outcomes begin to vary, however, as the viral population varies. When there is more than one viral variant, the colony becomes complex. This makes it unstable. Those who present with HIV infection but have multiple viral variants, usually have higher viral loads. It is easier for clinicians to predict a homogeneous population of the virus when compared to the alternative. These one-variant communities follow the step-by-step progression of the disease in a way that makes treatment more effective.

On the other hand, the unpredictability of variant viral populations can be tricky to treat. By comparing previous studies, it is hoped that what determines the variants, and how the host and virus interact in the initial phases of infection, will come to the fore. Being able to have a clearer picture of viral population workings and how it relates to the host’s response (especially during the early stages) could prove invaluable. Researchers expect that, upon learning the answers to these questions, a better strategy against the viral infection can be formulated, hopefully in vaccine form and later into an HIV cure.

How the Immune System Can Detect HIV

New HIV research has been revealing the workings of the human immune system. The hidden inner workings hold keys to solving some of the most formidable infections facing humankind. One such unlocked mystery is the discovery that one of the immune system’s sensor cells – cGAS – can detect HIV-1.

The cellular molecule, cGAS, is what sounds the alarm when there is an invasion of foreign matter. It has been believed, up until now, that cGAS could not detect retroviruses (such as HIV-1) because of the structural design of its DNA. Human DNA has two strands connected by molecular rungs. Retroviruses have just one strand. Researchers, therefore, concluded that this was one reason the body has trouble ridding itself of the intruder.

The HIV1 can, however, join together. They do this by twisting around each other to form a double strand. While these are more likely to be detected, the strand is often too short and passes through the cGAS radar. Here, however, is where the next piece in this chess game comes into play. The molecular building blocks of these DNA strands, called guanosines, can be detected by cGAS. It does not matter whether the HIV-1 is in its single-strand mode or not. Actually, it hardly mattered at all. What triggered the greatest immune response was the amount of guanosines. When more was added, the cellular defense response increased significantly. This strong reaction declined when the amount was lessened and all but stopped when it was removed altogether.

When HIV-1 infects a body, it imposes its DNA onto the healthy cell’s DNA. The result is a DNA that is curiously lacking in guanosines. It could be a reason as to why HIV-1 is particularly adept at cloaking – being virtually undetected by its host. However, some patients present with such a high number of HIV DNA that the guanosines that do remain still alert the cells, and the defense systems are activated. In these instances, the virus can remain suppressed indefinitely. This strong immune response is believed to be because of the detection of these all-important guanosines and the sensitive radar that detects it, cGAS.

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