Hepatitis C (HCV) is a chronic affliction caused by a lipid-enveloped virus with a high mutation rate. All pathogenic viruses with high mutation rates are major threats to humanity because they are more likely to act as they never had before. HCV's wide genetic spectrum and mutational thrust are responsible for its expanding prevalence base and its growing worldwide distribution. By some estimates, hepatitis C world prevalence will reach a quarter billion in a few years.

Hepatitis C preferentially invades the liver, but it can also affect other organ systems, including the bone marrow and the kidneys. Progressive liver destruction may lead to cirrhosis and liver cancer. Indeed, after 20 years, about 25% of hepatitis C patients develop cirrhosis, and another 5% liver cancer. Up to 20% of patients, however, conquer the disease, presumably due to the adaptability and creativity of their immune systems (Liang 2000).

The hepatitis C virus is spread by body fluid transmission. Like many other viruses, its life cycle shows fluctuations of relative dormancy alternating with viremic episodes when blood is virally flooded. It is estimated that in any one viremic hepatitis C episode, up to 10 billion viral particles may be generated daily. The immune system in hepatitis C is thus perennially challenged.

Clinically, in the first few years, hepatitis C is often manifested by vague symptoms of fatigue, headache, and gastrointestinal malaise. Later on, the extent of organ damage determines the severity of its symptom profile.

Medications for hepatitis C include interferons, which are natural cellular products that activate neutrophils, macrophages, and natural killer (NK) cells, and drugs that inhibit enzymes responsible for viral replication (e.g., ribavirin). Success rate is variable and relapses are common. Frequently, these drug cocktails are poorly tolerated leading to discontinuation (Dieperink 2000).

Blood ozonation may initially sound like a toxic process. It is not. Decades ago, German clinicians thought that ozonation could clear blood of pathogens, much as it does water. They devised methods of interfacing ozone with blood so that its cellular elements (e.g., red and white blood cells, platelets) retained their integrity. Immune models have surpassed this early notion of ozone's direct viral clearance. In the miniscule doses in which ozone is administered to blood, it is now firmly documented that blood ozonation stimulates immune system components to produce natural interferons and cytokines capable of initiating viral kill (Paulesu 1991, Larini 2001, Bocci 2005).

Additionally, it may appear surprising--or even preposterous--to suggest that our own bodies rely on endogenously-generated reactive oxygen molecules, one of which is ozone, to oxidize constantly invading pathogens. A greatly underappreciated study from the Scripps Institute found that ozone is indeed created by our own neutrophils and macrophages to serve as a natural virucidal agent (Wentworth 2002).

The prevalence of hepatitis C is variable in different regions of the world. In the U.S., about 1% of the population is affected, an estimated 4 million carriers. Certain groups, for a variety of reasons, are preferentially afflicted. Veterans, for example, have a prevalence rate significantly higher than that of the general population (Roselle 1997).

In Egypt, the prevalence rate is the highest in the world. Fully 20% of the population is afflicted by hepatitis C, or approximately 12 million individuals. This phenomenon is partially explained by a vaccination program gone awry. Regardless of its causation, this huge hepatitis infection rate represents a national public health emergency (Frank 2000, Strickland 2002, Mohamed 2006).

The National Research Centre (NRC) in Cairo contacted me after noting my articles (e.g., Sunnen 1988). In view of the Egyptian hepatitis C emergency, health authorities were interested in new therapeutic approaches for hepatitis C, namely innovative technologies of oxygen/ozone administration. Indeed, contemporary conventional drug therapies were--and are--prohibitively onerous for a target population of 12 million. In addition, they are inordinately prone to failure and to serious side effects.

NRC representatives came to New York where a meeting was held in August 2000 with Medizone International, Inc.--of which I was President and Director of Research. Protocols were agreed upon and a contractual agreement was signed by all parties. The study was officially named:

The study was to involve 66 patients. The main objectives of the study were to measure and evaluate:

1. Hepatitis C viral load reduction with blood ozonation
2. Liver enzyme recovery
3. Clinical improvement, as measured by scales of health and well-being

Officially, the investigators for this study were:

The study was well under way as regard the selection of participating patients and the readying of NRC personnel and laboratory facilities.

In 2001 and into 2002, however, through various actions, and for reasons that can, as of now, only be speculated, the New York State Department of Health (NYSDOH) stopped this world-first U.S. - Egyptian collaborative medical study. As a result, Medizone International, Inc., to this day, remains severely crippled. Millions of patients thus lost a unique opportunity for better health care.

Lamentably, this destructive action continues to convey negative messages, not only to the Egyptian medical research community and to Egyptian patients hopeful for treatment breakthroughs for hepatitis C, but also, by way of extension, to the medical community in the greater Middle East. It also embodies a transgression against essential research that was envisioned to benefit our own citizens. Indeed, hepatitis C is an important determinant for death via liver failure and liver cancer, and is the leading cause for liver transplantation.

Furthermore, the fruits of this research would have extrapolated far beyond the treatment of hepatitis C. Immune function enhancement is a bonus for a host of diseases. In addition, it appears that lipid-enveloped viruses have increased vulnerability to ozone exposure. Ozone-based therapeutics, administered via innovative technologies, could thus well complement current treatment options for viruses such as hepatitis B, HIV, and influenza, among others.

This article embodies an appeal to the international medical community for the support of this vital research initiative.

• Abdel-Hamid M, El-Daly M, Molnegren V et al. Genetic diversity in hepatitis C virus in Egypt and possible association with hepatocellular carcinoma. J Gen Virology 2007 May 1; 88(5): 1526-1531
• Amato G, Sacchetta A, Borreli E, Bocci V. Ruollo dell'ozonoterapia mediante grande autoemotrasfusione nel trattamento delle epatiti croniche post-epatite virale (II parte). In: Proceedings: I Congresso IMOS, Italia, Siena, 2-4 Nov 2000
• Askari FK. Hepatitis C: The silent epidemic. Harper Collins, 2001
• Bartenschlager R. Candidate targets for hepatitis C virus-specific antiviral therapy. Intervirology 1997; 40: 378-393
• Bocci V. Ozone: A New Medical Drug. Springer, 2005
• Bocci V. Oxygen-Ozone Therapy: A critical evaluation. Kluwer Academic Press, Dordrecht, 2002
• Bolton DC, Zee YC, Osebold JW. The biological effects of ozone on representative members of five groups of animal viruses. Environmental Research 1982; 27: 476-48
• Buckley RD, Hackney JD, Clarck K, Posin C. Ozone and human blood. Archives of Environmental Health 1975; 30: 40-43
• Cardile V, et al. Effects of ozone on some biological activities of cells in vitro. Cell Biology and Toxicology 1995 Feb; 11(1): 11-21
• Carpendale MT, Freeberg JK. Ozone inactivates HIV at noncytotoxic concentrations. Antiviral Research 1991; 16: 281-292
• Dailey JF. Blood. Medical Consulting Group, Arlington MA, 1998
• Di Bisceglie AM, Bacon BR. The unmet challenge of hepatitis C. Scientific American 1999; 281:58-63
• Dienstag JL. Sexual and perinatal transmission of hepatitis C. Hepatology 1997; 26: 66S-70S
• Dieperink E, Willenbring M, Ho SB. Neuropsychiatric symptoms associated with hepatitis and interferon alpha: A review. Am J Psychiatry 2000 June; 157(6): 867-876
• Evans AS, Kaslow RA (Eds). Viral Infections in Humans: Epidemiology and Control, Fourth Edition, Plenum, New York, 1997
• Feitelson MA. Hepatitis C Virus: From Laboratory to Clinic. Cambridge University Press. Cambridge UK, 2002
• Frank C, Mohamed MK, Strickland GT, et al. The role of parenteral antischistosomal therapy in the spread of hepatitis C virus in Egypt. Lancet 2000; 355:887-891
• Gonzalez-Peralta RP, Qian K, She JY, et al. Clinical implications of viral quasispecies heterogeneity in chronic hepatitis C. J Med Virology 1996; 49: 242-24
• Harrison TJ, Zuckerman AJ (Eds). The Molecular Medicine of Viral Hepatitis. Molecular Medical Science Series. John Wiley & Sons, New York, 1997
• Hurst CJ. Viral Ecology. Academic Press, New York, 2000
• Knipe DM, Howley PM. Fundamental Virology, Fourth Edition. Lippincott Williams& Wilkins, Philadelphia, 2001
• Konrad H. Ozone therapy for viral diseases. In: Proceedings 10th Ozone World Congress 19-21 Mar 1991, Monaco. Zurich: International Ozone Association 1991: 75-83
• Kourie JI. Interaction of reactive oxygen species with ion transport mechanisms. Am J Physiol 1998; 275: 1-24
• Larini A, Aldinucci C et al. Ozone as a modulator of the immune system. In: Proceedings of the 15th Ozone World Congress, London, UK, 11th-15th Sept 2001. Speedprint MacMedia Ltd, Ealing, London, UK, p 1-10
• Liang TJ, Hoofnagle JH, (Eds). Hepatitis C. Academic Press, San Diego, 2000
• Maggi F, Fornai C, Morrica A, et al. Divergent evolution of hepatitis C virus in liver and peripheral blood mononuclear cells of infected patients. J Med Virology 1999; 57: 57-63
• Major ME, Feinstone SM. The molecular virology of hepatitis C. Hepatology 1997; 25: 1527-1538
• Maertens G, Stuyver L. Genotypes and genetic variation of hepatitis C virus. In: The Molecular Medicine of Viral Hepatitis. John Wiley $ Sons Ltd., London, 1997: 225-227
• Maillard JY. Virus susceptibility to biocides: an understanding. Reviews in Medical Microbiology 2001 Ap; 12(2): 63-74
• Mawsouf N, Tanbouli T, El-Tayar W. Ozonetherapy in HCV infection. In: OzonHandbuch, Grunlagen Pravention, therapie (Viebahn-Hansler, Knoch HG, Eds) Landsberg, in press
• Max J. Antibodies kill by producing ozone. Science 15 Nov 2002; 298: 1319
• Mohamed MK, Bakr I, El-Hoseiny M et al. HCV-related morbidity in a rural community of Egypt. J Med Virology 2006 Sept; 78(9): 1185-1189
• Mohamed MK, Abdel-Hamid M, Mikhail N et al. Intrafamilial transmission of hepatitis C in Egypt. Hepatology 2005; 42(3): 683-687
• Monjardino J. Molecular Biology of Hepatitis Viruses, Imperial College Press, London, 1998
• Olinescu R, Smith TL. Free Radicals in Medicine. Nova Science Publishers, Huntington, 2002
• Par A, et al. Hepatitis C virus infection: pathogenesis, diagnosis and treatment. Scandinavian Journal of Gastroenterology. 1998 Suppl; 228: 107-114
• Paulesu L, Luzzi L, Bocci V. Studies on the biological effects of ozone: Induction of tumor necrosis factor (TNF-alpha) on human leucocytes. Lymphokine Cytokine Research 1991; 5: 409-412
• Pawlotsky J. Hepatitis C virus resistance to antiviral therapy. Hepatology Nov. 5, 2000; 32: 889-89
• Ray SC, Arthur RR, Carella A et al. Genetic epidemiology of hepatitis C virus throughout Egypt. J Inf Diseases 2000 Sept; 182(3): 698-707
• Razumovskii SD, Zaikov GE. Ozone and its reactions with organic compounds. Elsevier, New York, 1984
• Roselle G, Danko LH, Mendenhall CL. A four-year review of patients with hepatitis C antibody in Department of Veterans Affairs Facilities. Military Medicine 1997;162: 711-714
• Roy D, Wong PK, Engelbrecht RS, Chian ES. Mechanism of enteroviral inactivation by ozone. Applied Environmental Microbiology 1981; 41: 728-733
• Sarara AI. Chronic hepatitis C. South Med J. 1997; 90: 872-877
• Seeff LB. Natural history of hepatitis C. Hepatology 1997; 26: 21S-28S
• Simmonds P. Genetic diversity and evolution of hepatitis C virus - 15 years on. J Gen Virology 2004; 85: 3173-3188
• Strickland GT, Elhefni H, Salman T et al. Role of hepatitis C infection in chronic liver disease in Egypt. Am J Tropical Medicine and Hygiene 2002; 67(4): 436-442
• Sunnen GV. Ozone in Medicine. Journal of Advancement in Medicine. 1988 Fall; 1(3): 159-174
• Trivedi M. Newly diagnosed hepatitis C: Lack of symptoms doesn't mean lack of progression. Postgraduate Medicine 1997; 102: 95-98
• Valentine GS, Foote CS, Greenberg A, Liebman JF (Eds). Active Oxygen in Biochemistry. Blackie Academic and Professional, London, 1995
• Vaughn JM, Chen YS, Novotsky JF. Effects of ozone treatment on the infectivity of hepatitis virus. Can J Microbiol 1990; 36: 557-560
• Vaughn JM, Chen Y, Linburg K, Morales D. Inactivation of human and simian rotaviruses by ozone. Applied Environmental Microbiology 1987; 48: 2218-2221
• Viebahn R. The Use of Ozone in Medicine. Odrei Publishers, Iffezheim, 1999
• Wells KH, Latino J, Gavalchin J, Poiesz BJ. Inactivation of human immunodeficiency virus Type 1 by ozone in vitro. Blood 1991 Oct; 78(7): 1882-1890
• Wentworth P, McDunn JE, Wentworth AD, et al., Evidence for antibody-catalysed ozone formation in bacterial killing and inflammation. Science 13 Dec 2002; 298: 2195-2199
• Wright JW (Ed). The New York Times Almanach. Egypt - population, Penguin 2007, p 569
• Yamamoto M, et al. The effects of ozone on treatment of 4 patients suffering from hepatitis C. Bulletin of Japan Research for the Medical Use of Ozone 1996; 3: 1-2
• Younossi ZM, Ong JP, O'Shea R. Contemporary Diagnosis and Management of Hepatitis C. Handbooks in Health Care, 2003