HIV May Be Slowed By a Gene
12 years ago
Infectious diseases like TB, HIV, and Hep C are difficult to combat. But the secret may lie in the same gene that keeps a person alive when they first begin to form in their mother’s womb. It is the same gene that tells our immune system when to turn on or off to fight a particular disease.
So what does this mean for the medical field? When it comes to diseases that overload the body’s immune system like HIV and many autoimmune disorders, this discovery can be a great step forward. Two doctors who headed the research just had their study published in November.
The gene that has been isolated has what may be considered the most important immune system task. It decides if a situations deserves an immune response or not. The wrong decision can have a seriously adverse effect on the body. Needless attacks result in autoimmune responses that injure the body. But failure to alert the immune system to legitimate threats can obviously result in great damage as well.
HIV and other diseases like it are so deadly because they have found ways to avoid the body’s immune response. This is a survival adaptation of the disease, but for the person infected it can be fatal. The idea behind the research done on this particular gene is that it can fight diseases with this type of amativeness.
The doctors are currently looking at the effect of turning this gene’s response on and off in the fight against certain disease. Seeing the results can help them to identify more fully the role that this gene plays in fighting disease as well as how to use it to overcome diseases that thus far have outwitted the human immune system.
The reason for all of the research is that this gene plays such a critical role. The doctors want to be certain of the effects a drug targeting its function would have on the body as a whole. If manipulating the gene fought one disease but compromised the immune system, it would still not help the patient in the long run. Because of this, any drugs involving the gene are still a number of years away. Despite this fact, it is still an exciting discovery.
Correlation Between HIV Treatment and Recurrent Malaria
12 years ago
According to the NIH, children with HIV who are receiving treatment are 40 percent less likely to suffer from recurring malaria. The study was done in Uganda using children age six and under. Some were just infants (over 170 of them, in fact). The study group was compared to a group of children receiving a different treatment.
The treatment that stopped malaria from recurring was a protease blocker. It slows the spread of HIV by blocking that particular enzyme. While the treatment seemed to make it less likely for malaria to reoccur, it did not prevent the children from getting the disease the first time.
The children were also receiving drugs to try and prevent them from getting malaria. When blood tests were done on the children, it was noticed that the ones receiving the protease treatment had more of the anti malaria medicine in their system.
This is not the first study that has been done on this particular HIV treatment. Previous research was conducted to prove the effectiveness of the drug combination in slowing the progress of HIV. However, it is not the first drug promoted by the WHO for HIV treatment in poor nations. Why not? For one thing, the treatment needs to be refrigerated. Because of this, medical facilities in many poor nations cannot afford the resources to keep a supply on hand. It also does not taste very good, which makes it more difficult to get children to take it.
Other variables in the study included the children being given a mosquito net to keep them from being infected in their sleep. These nets had mosquito repellent on them. All the children also received a regular supply of vitamins. Clean water was provided, so that water quality would not affect the outcome of the study.
Even with the best efforts of the individuals conducting the study, it was still noted that about two fifths of the children contracted malaria within half a year. The discrepancies, however, began to be noticed in those who survived the first round. Receiving the standard HIV treatment had the same two fifths chance of getting the disease again in the next four weeks. Of the children taking protease inhibitors, only 14 percent contracted the disease again. After two months, there was still a stark contrast in recurrent cases.
HSV-1 Infection Held Up in an Unsuspected Way
Research has suggested that one or two herpes viruses stop to attack skin cells before entering the body, leaving a window of opportunity to treat the disease before infection occurs during this early stage.
Proceedings of the National Academy of Sciences has published a report from researchers at Princeton University indicating that most viruses spread by throwing millions of particles at cells, but this is not the case with the HSV-1 (herpes simplex virus type 1). This virus (responsible for both genital legions and cold sores) just sends in one or two particles during the initial invasion of skin cells in order to form cold sores.
This was shocking to researchers since the disease is known to produce hundreds of particles within a cell according to Matthew Taylor who is the author of the study. What causes the hold up?
HSV-1 particles can remain dormant in a person for years after infection. The first stage of sore formation is when these cells awaken and infect nearby skin cells, beginning the process of forming a cold sore. Once this happens the virus replicates rapidly and we see the millions of copies as a visible cold sore. This is when the disease becomes transferable via skin to skin contact.
The fact that the cold sore is made up of just one or two particles initially means that when the disease is spread there is very little genetic diversity to it. This really should hurt the diseases’ ability to grow and spread since it lacks a variety of genomes. This is in sharp contrast with the way that HIV spreads with its many particles and distinct genomes. The result is that if any mutation weakens the HSV-1 virus, it becomes highly unlikely to be able to adapt and survive.
This results in two things. First, only the most fit particles survive. While that doesn’t sound positive, it also means that the disease can be targeted by specific treatment since it is not genetically diverse. Researchers in Tel Aviv are now working on drugs that can attack the disease at this vulnerable point.
Researchers are also looking into alpha-herpes viruses to see if they share the same weakness. Among these viruses are HSV-2 and the virus that causes chicken pox and shingles. Even West Nile virus and poliovirus are being looked into.
Scientists are excited to find that while the transmission of these diseases is very efficient, the means may also leave a window of opportunity for treatment.
The research was color coded in red, green, and blue using different viral genomes. Infected cells could thus be examined for particles in a particular color revealing the number of particles that had breached a cell. The method was developed in the math department in Princeton. The results showed an average of two or fewer viral genomes infecting cells.
The process was repeated with the pseudorabies virus, an alpha-herpes virus that is particular to animals. The results were the same.
Ribosomes Reveal New Target for Antiviral Therapies
12 years ago
by ADMIN
in HIV Therapy
It is tough to catch a target when you don’t know what its next move will be. It is even tougher when the target itself doesn’t know its next move. The unpredictability of RNA virus is what makes them resistant to antiviral drugs. Since every copy the viruses make of themselves is inaccurate, at least to some degree, the antiviral drugs do not know what to search for. It is like a police officer chasing someone based on a description, but the criminal dumps his coat in the trash and gives his hat to a stranger. For example, the only way to go after a disease like HIV is to pump a patient full of different types of drugs to try and wipe out hiding places, thus backing the disease into a corner.
So what do you do if you can’t fight an RNA virus? You could try attacking the host cells. The only problem with that is keeping the host safe while you do it. It’s not really a cure if it kills you. Ribosomes, however, may hold the key to cornering fatal viruses like rabies. Proceedings of the National Academy of Sciences published results on November 19th that are promising.
Ribosomes have always been believed to sort of be on autopilot just doing their thing, which happens to be making proteins. Amy Lee and Shawn Whelan are challenging that role and claim that ribosomes translate specific proteins which would connect them with virus replication. The study involved examining how mRNAs (messenger RNAs) are translated into proteins by host cells that are infected with RNA viruses. The pair discovered a particular protein on the surface of ribosomes that is crucial to virus RNA translation, but is irrelevant to most mRNAs. It is named rpL40. Targeting this protein could inhibit RNA virus reproduction without hurting host cell’s ability to produce good proteins.
At the present time, there is no treatment for the deadly virus, rabies. This is being presented as the first possible way to counteract that fatal virus. Initial screening using the vesicular stomatitis virus, a relative of rabies, showed that while the virus relied heavily on the rpL40 protein, only about 7 percent of mRNAs did. The class of virus that relies most heavily on this protein also includes the measles virus.
While there are no drugs yet to target rpL40, a number of research groups are now exploring this theory developed by Lee and Whelan.
HIV Defense from Cow Milk
12 years ago
by ADMIN
in HIV Prevention
Cow’s milk gets a bad rep today between lactose intolerance, allergies, and concerns over antibiotics given to the cows themselves. The fact is it still has a lot of nutrients for those who can stomach it, such as vitamin D and calcium. But scientists at Melbourne University in Australia have done something to make cow’s milk extra special. Researchers worked along with Immuron, Ltd. (an Australian biotechnology company) to give pregnant cows an HIV protein as a vaccination. The result: After giving birth, the cow’s milk initially contained antibodies that counteracted HIV.
But cows can’t even get HIV, right? While that is true, their bodies still produce antibodies to defend against the foreign protein, and these are then passed to the baby through milk right after birth. The colostrom (first milk) of a cow has been known to transmit necessary antibodies to keep calves from infection, and it has proved to be so in the case of HIV as well.
What was done with the milk in lab research? When tested, the antibodies combined with the HIV disease and counteracted its ability to enter human cells.
The research team is planning to use this discovery to develop a cream to prevent the spread of HIV. The idea would be for a woman to spread the cream on her vagina either before or immediately after sex (both for those who believe in ‘better safe than sorry’). Then, even if the partner was infected, the antibodies in the cream would prevent the HIV from being able to enter the woman’s cells. This isn’t the first company to come up with the idea of a microbicide to fight HIV infection. The hype is over the fact that this should be a cheaper and easier way to do it.
Of course, this is still a little ways off since first there will be animal testing and then human testing before the product can be marketed.
