Press Release
Source: Viral Genetics, Inc.

Viral Genetics, Inc. Unveils Potential Mechanism of Action in HIV/AIDS Research, Accepted to Present Findings at Prestigious IHV Meeting.

Team Welcomes Attendees to Poster Session to Discuss Findings, Which Could Lead to Inexpensive, Effective HIV Therapy, and May Be Applicable to Autoimmune Diseases.

AZUSA, Calif.--(BUSINESS WIRE) -- Aug 19, 2008 -- Viral Genetics, Inc. (Other OTC:VRAL - News), a biotechnology company that discovers and develops immune-based therapies, today unveiled a new theory regarding a potential mechanism of action, which could advance HIV/AIDS research and the development of an inexpensive, effective therapy for HIV. The study team says some of the study findings may also be applicable to autoimmune disease. Viral Genetics has been accepted by the Institute of Human Virology (IHV) to unveil and discuss its new model and findings at IHV’s 11th Annual International Meeting in an interactive poster session. The prestigious conference, founded by Dr. Robert C. Gallo, who co-discovered HIV as the cause of AIDS and developed the first HIV blood test, will take place September 11-13th in Baltimore, Maryland. For more information on the conference, visit www.ihv.org.

“IHV has created a collaborative environment where multidisciplinary research, education and clinical programs work to accelerate the development of pioneering therapies for HIV/AIDS. We are honored to have been accepted to discuss our data with IHV’s respected team and members of the research and medical communities,” said Haig Keledjian, CEO of Viral Genetics.

Strong Evidence of a Newly Discovered Mechanism of Action

Viral Genetics has and continues to use TNP-1, a mixture of peptides derived from thymic histones, to research HIV/AIDS. When used in six international human clinical trials, including a double blind placebo controlled study in South Africa, results indicated that 25-35% of the HIV-infected population exhibited significantly reduced viral load and clinical improvement. During in vitro research, the study group found that individual peptides in the TNP mixture can bind to antigen-presenting cells and may be able to redirect the immune response.

“Our work is unraveling a link between inflammatory events that characterize early stages of infection, the importance of inflammation on susceptibility to HIV, and a link to an individual’s MHC molecules,” commented Dr. M. Karen Newell, Ph.D., lead investigator of the study and a professor at the University of Colorado.

The study group has discovered, and will continue to search for, peptides that will bind with high affinity to the greatest number of molecules encoded by MHC alleles (genes) within the population. The MHC genes encode molecules that are expressed on antigen presenting cells. The group has finished preliminary studies, and is currently testing the candidate peptides in a number of in vitro and in vivo animal models that it believes will provide proof-of-concept studies for both HIV as well as other diseases.

To uncover the mechanism of action responsible for improvement in previous international clinical trials, the active components had to be identified and synthesized to purity. The purified peptides then had to be, and will continue to be, tested for activity, safety, and efficacy. As a result, Viral Genetics has uncovered evidence for a likely mechanism of action using its targeted peptide approach. The long-term goal of the study is to obtain an IND for testing the newly identified and synthesized peptides or “targeted peptides” that can appropriately redirect the immune response to HIV.

“Our findings suggest that, with the proper predictions, we can synthesize targeted peptides to treat people with different types of MHC alleles providing potentially an inexpensive, biologically active therapy for HIV,” added Newell.

The Immune Response to HIV: Friend or Foe?

“While the results in human clinical trials are promising, the challenge has been identifying the mechanism and the active component of the mixtures,” said Newell.

It has been shown by the group and others that Tregs, activated in response to non-specifically (accidentally) activated immune cells will kill the non-specific cells, and that Tregs can control a potentially adverse, non-specific response. Chronic problems occur when there is a failure (as a result of genetic defects, genetic predisposition or as a result of disease-dependent processes) to control and/or kill the non-specifically activated cells.

“It appears to be precisely when the non-specific cells don’t die on cue, that chronic pathologies begin,” added Newell.

Hypothesis - Targeted Peptides as a Therapeutic Strategy for HIV

Viral Genetics’ working hypothesis is that treatment with custom-designed and predicted “targeted peptides,” which will bind to the surface of the right white cells (antigen presenting cells) could, in turn, activate specific Tregs (a special category of T cells widely reported to dampen chronic inflammation). Dampening inflammation may be required to decrease the number of activated CD4 T cells that can become virally infected. The hypothesis is supported by recent findings showing that there is a correlation between the presence and numbers of Tregs and the length of time between initial infection with HIV and full-blown AIDS (Baker et al. 2007. “Peripheral CD4 loss of regulatory T cells is associated with persistent viremia in chronic HIV infection.” Clin. Exp. Immunol. 147 (3): 533-539 and Eggena, M. P. 2005. “Depletion of Regulatory T cells is associated with immune activation.” J. Immunol. 174:4407-4414). As Treg numbers decline, there is a simultaneous rise in viral load. This may suggest that by activating Tregs with targeted peptides, the consequence could be a delay in the rise in viral titer associated especially with late-stage HIV disease.

The result of linking inflammation, cellular activation and MHC has been the development of targeted peptides that may interfere with, and re-direct, the activation of cells critical to the pathology of the disease. With HIV, the ability of the virus to infect its target requires that the CD4 T cell being infected be activated and that, at least in part, activation may result from an inflammatory response.

By understanding the requirements for activating the Treg, Viral Genetics could potentially prevent the inflammation-dependent activation of CD4 T cells that is required for the cell to become infected by the virus. The team aims to further, and rigorously, test these possibilities.

As a result of its findings, Viral Genetics is currently focused on increasing its number of expert collaborators, including clinical scientists and physicians, best-suited to accelerate the rigorous testing of its model. For more information on Viral Genetics’ mechanism of action and findings, the study team will post materials on the company’s website at the conclusion of the IHV Meeting.

“We are very excited after many years of research to finally have discovered what appears to be the promising mechanism of action that could optimize our treatment to its fullest potential. This also opens the door to a paradigm shift in thinking around HIV/AIDS therapies,” said Monica Ord, SVP of corp. development and communications for Viral Genetics.

About Viral Genetics

Viral Genetics, Inc. is a biotechnology company that discovers and develops immune-based therapies for HIV and AIDS using its thymus nuclear protein compound (TNP). The company recently entered into an Exclusive License Agreement with the University of Colorado and V-Clip Pharmaceuticals (a subsidiary of the Company) to license technology developed by M. Karen Newell, PhD that appears to explain TNP and provide a means to optimize therapies based on TNP for future clinical trials. TNP may have other potential applications for other infectious, autoimmune, and immunological deficiency diseases that the company intends to study in the future. Viral Genetics believes that its investigational HIV/AIDS drug based on TNP, called VGV-1, represents a unique approach to treating HIV due to the apparently novel mechanism, low toxicity profile, simple dosing regimen, and short-course of treatment. As a type of immune-based therapy, it focuses on boosting the immune system to allow the body to fight HIV more efficiently. VGV-1 has been studied in five human clinical trials for the treatment of HIV/AIDS. Online at www.viralgenetics.com.

This news release contains forward-looking statements that involve risks and uncertainties associated with financial projections, budgets, milestone timelines, clinical development, regulatory approvals, and other risks described by Viral Genetics, Inc. from time to time in its periodic reports filed with the SEC. VGV-1 is not approved by the US Food and Drug Administration or by any comparable regulatory agencies elsewhere in the world. While Viral Genetics believes that the forward-looking statements and underlying assumptions contained therein are reasonable, any of the assumptions could be inaccurate, including, but not limited to, the ability of Viral Genetics to establish the efficacy of VGV-1 in the treatment of any disease or health condition, the development of studies and strategies leading to commercialization of VGV-1 in the United States, the obtaining of funding required to carry out the development plan, the completion of studies and tests on time or at all, and the successful outcome of such studies or tests. Therefore, there can be no assurance that the forward-looking statements included in this release will prove to be accurate. In light of the significant uncertainties inherent in the forward-looking statements included herein, the forward-looking statements should not be regarded as a representation by Viral Genetics or any other person that the objectives and plans of Viral Genetics will be achieved.

Contact:
For additional information, please contact:
Viral Genetics
Haig Keledjian, CEO, 626-334-5310

Source: Viral Genetics, Inc.

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