Human immunodeficiency virus or HIV damages the immune system to prevent the body from fighting off disease and infection. If left untreated, HIV can lead to acquired immunodeficiency syndrome (AIDS) and weaken the immune system enough where a common cold can become fatal. HIV is a sexually transmitted infection (STI) and is spread through unprotected sexual contact. It can also be spread through contact with blood such as the use of shared needles. Untreated HIV patients can also spread the disease to their children during pregnancy, childbirth, or breastfeeding. Symptoms of HIV include fever, headache, joint pain, rash, sore throat, swollen lymph nodes, weight loss, cough, and others. Unfortunately, a patient with HIV does not always have symptoms and may not realize they are carriers of the viral infection. As a result, asymptomatic patients are not treated, and the virus progresses to AIDS. However, once HIV is detected, it can be treated with little risk of progressing. Although treatment for HIV is improving, there still is not a cure. Many scientists are currently on enhancing HIV treatment as well as preventative care.
A recent article in Science Immunology, by Dr. Darrell Irvine and others, demonstrated that a series of HIV vaccines can overcome HIV mutation in patients. Irvine recently became Professor of Immunology & Microbiology at the Scripps Research Institute. Prior to moving to Scripps, he was Professor of Biomedical Engineering at the Ragon Institute at Massachusetts Institute of Technology (MIT) and a Howard Hughes Medical Institute investigator. His work focuses on vaccine development for HIV and cancer with tools to develop new vaccine structures and drug delivery systems. His recent published work is a big step toward HIV treatment because it addresses HIV mutation – a major obstacle that limits efficacy in HIV vaccines. Irvine and his team discovered that a strong immune response is generated with two vaccinations one week apart.
The development of this vaccine resulted from computational modeling and mouse experiments that generated a vaccine made of an HIV envelop protein with nanoparticles that elicit an immune response. Previous work found that more vaccinations generated increased neutralizing antibodies. Irvine and others wanted to determine if a similar response could be achieved with fewer doses. Remarkably, researchers discovered that injecting 20% of the vaccine during the first immunization and 80% of the vaccine during the second immunization resulted in an optimal response similar to a seven-dose regimen.
The team investigated the mechanism behind the two-dose vaccine and why it worked as well as the seven-dose vaccine. Researchers found that during the first vaccination, more of the protein is chopped-up before reaching the lymph nodes to elicit an immune response. The lack of intact protein led to few immune cells generating antibodies. However, those few activated cells primed the immune system to then receive the higher dose the second time. In this second immunization the proteins injected are bound to the antibodies before they can be chopped-up and broken down. This leads to increased immune cell activation and the mass production of broad neutralizing antibodies.
The successful optimization of HIV vaccine output by tweaking the dose has previously never been accomplished. This work provides new information that advances vaccine technology and provides patients with optimal results and fewer immunizations. Although more work needs to be done, Irvine and others hope to bring this two-dose regimen to the clinic. Irivine and his team for the first time, optimized vaccine dose that overcomes HIV mutation and reduces vaccination events. This work will not only make vaccine protection more feasible but provide improved treatment for HIV patients.