The BioMedicine plasmids, which were originally developed for the treatment of malaria and other viral infections, are now being tested in HIV-infected patients with a new type of vaccine that’s easier to make and can be administered by mouth.
The first clinical trials for the newly developed vaccine, which will be administered through mouth, were published in the journal Nature Medicine.
The drug will target a gene called MC2R, which is critical for the growth of HIV.
“This gene is the most important gene in controlling HIV infection,” said study lead author J. Scott Waddell, a researcher at the University of Southern California, in a statement.
“If you have a disease like malaria or another viral infection, and you have MC2Rs down, then it’s difficult to make a vaccine that will target it.”
The researchers have already tested the vaccine in HIV patients with MC2r deficiency, but they’ve now moved forward to see if it works in the more common and prevalent type of MC2 deficiency that affects HIV-positive people.
This type of mutation leads to a condition called MC1R deficiency, in which the MC1 receptor, which normally works in an immune-suppressing manner, does not function properly.
“There are a lot of people in the U.S. who have MC1Rs and they’re not getting enough drugs to fight HIV,” Waddel said.
“So we’ve now shown that this new vaccine can be used in people who are having MC1r deficiency and have the gene that controls MC2 and that’s the type of people we want to see the vaccine work best in.”
The vaccine, called the MC2RIV (mimics MC2 protein) vaccine, is a protein called MC3R that’s made by the MC3 gene.
Researchers at the Broad Institute and Sanofi-Aventis have developed a way to make MC3r from a natural form of MC3 protein.
The protein is also present in other viral genomes, including HIV.
To make the protein, researchers use a protein that’s similar to the proteins that make MC2, and then make a polymer that’s not as strong as the one that makes MC2.
When the polymer gets coated with a specific antibody, the protein binds to the antibody, and the antibodies are then able to bind to and activate a protein in the virus.
When they do this, the virus is able to use the polymer as a way of binding to other proteins in the immune system, like the MC5 receptor.
These antibodies can then act like a receptor to turn on the MC4 protein, which helps the immune cells to kill the virus and keep it from spreading.
The researchers also have created a version of the protein that also has a different amino acid sequence.
They think this will allow the new vaccine to be more effective at targeting MC1 and MC2 receptors.
MC2-deficient MC1 patients can have a lower level of antibodies than normal, and MC1-deficiency MC2 patients have higher levels of antibodies.
This could be because the immune systems are more sensitive to the MC protein.
It also could be that MC2 is more prevalent in MC1 than MC2 as well.
In other words, MC1 might be more sensitive than MC1 to MC2 proteins.
This makes sense, because MC1 is more often found in the body, and therefore MC1 antibodies can more easily cross over from one person to another.
This is especially true in people with MC1 deficiency, which could be one reason why they’re more likely to develop the disease.
Researchers are also testing whether the new gene will be more useful in people without MC1 or MC2 antibodies, and if it can prevent the virus from replicating in the first place.
“The key to understanding this is the mechanism by which MC2s are able to stop replication of HIV,” said lead author Eric D. Condon, a research scientist at the UC San Diego Center for Regenerative Medicine, in the statement.
MC3 receptors can only be activated by MC2 if they’re present in the same place in the blood.
The team says this is because MC3s are expressed in different places in different cells, which means MC3 is able “to detect different places that the MC proteins are being activated by different signals.”
The team is also interested in seeing whether MC3-activating antibodies in the vaccine will also be able to protect against viral replication.
The study was funded by a National Institutes of Health (NIH) Office of Research Infrastructure grant.