Producing a Cure for HIV Through the
Use of Monoclonal
Understanding our commitment to curing the human
immunodeficiency virus (HIV) starts with an overview of
the challenge this virus presents to the human immune system.
Here’s how we’re committed to curing HIV:
When bacteria, viruses or chemicals enter our body, our immune system goes to war. Bacterial or viral invaders, called antigens, are first met by ‘helper’ T cells. Once called into action, the helper T cells stimulate B cells. These B cells create customized antibodies (or immunoglobulins) that attach or bind to the antigen. The antibody ‘scouts’ have a critical role, since they ‘mark’ specific antigens as enemies to the system. Now the immune system’s ‘killer’ T cells know how to recognize the antigens that must be attacked and destroyed. This process helps our body eliminate the invaders and return to peaceful, normal function.
HIV targets and kills the ‘helper’ T cells, cutting the connection to B cells and stalling the critical process of antibody production. The result? The immune system is unable to identify antigens, ‘killer’ T cells can’t find invaders, and the immune system’s ability to protect is compromised. No cure exists today, but we’re committed to curing HIV.
Since HIV disrupts this cell ‘special-ops team’s’ production of antibody ‘markers’, we have set out a way to introduce antibodies into the immune system with the power to target, and even neutralize the HIV virus.
Monoclonal Antibodies Opened the Door
More than 40 years ago, biomedical researchers found a way to fuse a B cell that was creating customized antibodies with an immortal B cell — one that would continue to divide and grow — resulting in a cell that could target a specific invader and have a long cell life. Their discovery, monoclonal antibodies, has fueled disease research, including ours.
The first monoclonal antibodies were created with animal cells, making them less compatible with human immune systems. Our solution had to be fully humanized to be more effective in patients and to avoid patient rejection. And since HIV can also compromise the effectiveness of vital ‘killer’ T cells, we sought an antibody capable of stopping the HIV virus cells from reproducing.
Curing HIV — The BioClonetics Commitment
Through years of effort, our research team has created a cell line that produces a fully human monoclonal antibody, the Clone 3 antibody that binds to the HIV virus. Importantly, tests in the international research institutes of Harvard Medical School, Duke University, University of California San Francisco, University of South Florida and Polymun Scientific show that Clone 3 neutralizes over 95% of primary HIV isolates tested.
More significantly, however, is the fact that the target site on the HIV virus to which our antibody binds is immutable – in other words, the binding site is always present from virus strain to virus strain. Today, there are more than 5000 strains of the HIV virus worldwide and if an antibody target a site that mutates, it fails to have a sustained ability to defeat the virus. In our case, the Clone 3 antibody target a site that exists in 98% of the 500 strains currently known.
Our antibody also surpasses the capability of other monoclonal antibodies now being tested and considered. While it is widely accepted today that monoclonal antibodies will play a critical role in a cure for HIV, massive programs, such as that sponsored by the Vaccine Research Corporation (VCR) and the NIH, have supported monoclonal antibodies which have not targeted the Achilles heel of the virus. For example, in recent trials, Vaccine Research Corporation’s VRC01 antibody, an antibody targeting HIV's CD4 binding site, was only able to modestly delay the return of viral replication following interruption of antiretroviral therapy (ART). This situation is referred to as “virus escape” and when it occurs, the protection required is not provided. This result was reported in a study presented at the recent Conference on Retroviruses and Opportunistic Infections (CROI 2016) in Boston. In other words, VRC01 did not maintain viral suppression on its own. (http://www.aidsmap.com/VRC01-antibody-delays-but-does-not-prevent-HIV-rebound-after-antiretroviral-treatment-interruption/page/3047632/).
In contrast, our Clone 3 antibody binds to an immutable site and expectedly will not face virus escape.
With these promising results, we are quickly moving forward to complete additional testing and seeking support to launch preclinical trials this year. More than 36 million people worldwide are living with HIV with almost 2 million new cases in 2016. About half are receiving treatment.
One million people died — 120,000 of the deaths were children.
We must do better — and now, we can. BioClonetics Immunotherapeutics is one step closer to ending the search for the HIV cure.