MICHIGAN STATE (US) — A new vaccine that combines the use of a disabled cold virus along with a gene that stimulates the immune system may offer protection against the parasite that causes malaria.
Researchers also have discovered another agent that stimulates the immune system—one that has been successful in improving immune responses in vaccines for diseases such as HIV—paradoxically made for a less effective malaria vaccine.
The findings, published in the journal PLoS One, will help develop more effective vaccine platforms in general, and specifically those for malaria vaccines, paving the way for human clinical trials, says Andrea Amalfitano, professor of microbiology, molecular genetics, and pediatrics at Michigan State University.
“Researchers across the globe are working on ways to prevent people from becoming infected with malaria,” says Amalfitano about the disease that kills up to a million people each year, mainly in sub-Saharan Africa. “Some vaccines are showing promise, but they are not as effective as they need to be for any mass distribution.”
Amalfitano and colleagues are focusing on one such vaccine platform, spearheaded by the U.S. Army, that targets a certain gene on the malaria parasite, a protein called Circumsporozoite Protein, or CSP.
The protein is thought to play a key role in creating an immune response to the malaria parasite. Past research shows people infected by malaria multiple times will begin creating an immune response to the protein, suggesting at some level it could be protective.
“What we are looking to do is improve the ability of the vaccine to induce immune responses to that protein,” Amalfitano says. “We are adding genes to the vaccine to try and stimulate the immune system.”
Those genetic agents, similar to chemical adjuvants, are stimulants that improve the ability of vaccines to induce beneficial immune responses in general.
In mouse models, researchers used two such “gene-adjuvants”: rEA and EAT-2, both of which aimed to illicit improved immune responses to the malaria CSP gene.
Surprisingly, the rEA agent—which was developed at Michigan State in part by the late Barnett Rosenberg—did not produce the desired result and in fact seemed to worsen the animal’s ability to generate an immune response to CSP.
However, the EAT-2 gene-adjuvant stimulated the immune system in a different way, and Amalfitano and his team were able to increase the ability of the immune system to respond to CSP to a level that surpassed currently available malaria vaccine systems.
“The results were surprising, but we were able to hit our goal eventually,” he says. “This research will help us as we create a viable vaccine. While the way that rEA is trying to stimulate the immune system may not be the best way for malaria, we did come up with an alternative adjuvant to effectively target the parasite.”
The next step is to see if malaria in animal models can be prevented using the EAT-2 gene-adjuvant. “Then we can take the lessons learned and really go forward and do what’s necessary to feel confident to begin human trials.”
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