Posts tagged HIV cure news
Antiretroviral therapies are efficient at lowering HIV levels in the blood. They suppress these levels enough that the virus can become virtually undetectable, making it hard to cure. While this provides the patient with a measure of health, and also slows disease progression, it is not enough to completely eradicate the virus from the body. Why is this the case? What is the key to eliminating the tenacious invader completely so as to have a cure?
Progress Towards a Cure
Study after study continues to show that antiretroviral therapy alone cannot completely rid the body of HIV. It is true that low viral levels within the blood can prove lifesaving, but HIV finds a way to hide, replicate, and even thrive. Attempting to kill off the virus in these areas is the key to completely wiping it out. Blood levels can be kept low because the drugs can effectively work within the vascular network. Researchers are finding that stores of HIV are located within the lymphatic system, specifically in lymph nodes and like tissues.
This presents challenges for healthcare. One, it is difficult for pharmaceuticals to reach the specific tissues where the virus replicates. It is rare for medications to filter into these lymph nodes. Also, there is the matter of viral mutation. As HIV patients increase in numbers, changes in the disease’s resistance to drugs begins to appear.
The good news is that usually it is the non-resistant form of the virus that hides and replicates. Once it releases into the blood, the drug therapies are still effective. Also, when researchers exposed the infected tissues to the drugs, the infection could be cleared. However, depending on the type and concentration of the drug therapy, the amount of drug-resistant HIV can fluctuate, making things complicated.
Further investigation is underway about how to infiltrate lymphatic tissue in order to remove stores of HIV. Researchers are convinced that once they gain a better understanding of how to reach these areas—combined with antiretroviral therapies—a cure for HIV will be at hand. Until then, daily treatment is the only way to keep the disease from progressing.
Treatment for HIV depends first on an HIV test. Curbing the growing number of patients with HIV requires the aid of healthcare institutions. The European guidelines for HIV testing are clear and ensure that each patient presenting with certain symptoms and diseases must be offered an HIV test. Patient screening is a good way to test and provide early treatment for those who are HIV positive.
To HIV Test or Not
Willingly most patients offered the test will take it. One study puts the acceptance rate at 99%. That is encouraging to health experts. However, when looking into the number of patients who were offered an HIV exam, European hospitals came up short. It was found that in Europe less than half of the patients who qualify were actually offered the test. Hospitals that had the lowest rates were in Northern Europe. Researchers are concerned that the number of those infected with HIV may be much higher than what is being reported.
Certain areas within the hospitals studied were more prone to recommend HIV testing. These wards are generally the ones regularly dealing with certain communicable ailments (like TB and Hepatitis). Therefore, HIV testing makes sense and is routinely offered. Another group of patients regularly asked are pregnant women, because careful testing can prove vital for the fetus as well. While very few fetuses actually test positive for HIV, the screening is offered and frequently accepted.
Why Is the Test so Frequently Not Offered?
One reason tests are sometimes not offered is medical staff discomfort in the area of HIV. Experts are researching other possible reasons for the sporadic or lack of effort to encourage testing in more patients – especially those in high risk categories. The correlation between the hospital ward and the amount of screening performed provides insight on the matter. Certain cases that present in different wards of the hospital may simply not relate to HIV in the minds of the healthcare providers. Changing this view, and encouraging these European hospitals to step up patient screening, could go a long way in helping to slow the scourge of HIV in Europe.
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.
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.
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.