HepC BC 
Therapeutic effects of glycyrrhizin in mice infected with LP-BM5 murine retrovirus and mechanisms involved in the prevention of disease progression
Biotherapy 1996;9(4):209-220
Watanbe H, Miyaji C, Makino M, Abo T
Department of Immunology, Niigata University School of Medicine, Japan.
Glycyrrhizin (GL), a plant extract, has been evaluated for its inhibitory effect on HIV replication in vitro and for its improvement of clinical symptoms in HIV-infected patients. In this study, we used GL in a murine AIDS model (MAIDS) to evaluate these effects. C57BL/6 mice were inoculated with LP-BM5 murine leukemia virus to cause MAIDS. Treatment with GL supplemented with glycine and cysteine (Stronger Neo-Minophagen C, SNMC) was then begun on day 0 or 4 wks after virus inoculation. SNMC was administered three times a week for up to 19 wks. Immunological abnormalities were monitored with respect to the surface phenotype identified by two-color staining for CD3 and IL-2 receptor beta-chain. All mice infected with the virus alone developed MAIDS and died by 14 wks after infection. The immunopathogenesis was estimated to be an abnormal expansion of intermediate CD3 cells (i.e., extrathymic T cells) as well as other types of lymphocytes. SNMC did not change the total mortality rate. However, some mice that began the treatment on day 0 or 4 wks after infection survived 3 wks longer. Splenomegaly and lymphadenopathy in such mice were suppressed. These mice showed normal phenotypic features and normal responses to Con A. These results suggest that SNMC is effective in some MAIDS mice in preventing the progression of disease. When lymphocytes isolated from the liver, spleen and lymph nodes of diseased mice were cultured in vitro, they showed a spontaneous proliferation. Interestingly, such proliferation was inhibited by addition of liver lymphocytes, but not splenic lymphocytes, obtained from normal or SNMC-treated mice. Since liver lymphocytes contains intermediate CD3 cells with autoreactivity, they may possibly suppress the progression of disease.
PMID: 9012540, MUID: 97164758
HepC BC
(Alt Med Rev 1997;2(2):87-93)
Echinacea: What Makes It Work?
Kerry Bone, B.Sc. (Hons), Dip. Phyto.
Extrapolations from pharmacological research have led some authors to suggest restrictions or contraindications for the use of Echinacea. This article examines the known chemistry and pharmacology of the various Echinacea species and products, and challenges some of these popular concepts. In particular, the hypotheses that Echinacea is a T cell activator and that it will accelerate pathology in HIV/AIDS, are found to be unsupported by careful analysis of known data. These misunderstandings have arisen mainly from enthusiastic extrapolations of in vitro data on polysaccharide components. The low levels of polysaccharides in most Echinacea products, particularly traditional extracts and tinctures, and their poor bioavailability suggest in most cases the therapeutic activity of Echinacea is due to other component fractions, including the alkylamides. The suggestion that Echinacea should not be prescribed for extended periods of time will be examined in a second article.
HepC BC Nippon Rinsho 1994 Jul;52(7):1823-1827
Okuno T, Arai K, Shindo M
Department of Internal Medicine, Akashi Municipal Hospital.
To assess the efficacy of interferon (IFN) combined with a large dose of glycyrrhizin (SNMC) therapy in patients with chronic hepatitis C who were resistant to interferon therapy alone, we studied 8 patients with chronic hepatitis C who did not respond to the initial interferon therapy. Initially all of 8 patients received 6 million units of alpha-IFN intramuscularly, three times a week, for 3 months and their serum alanine transaminase (ALT) did not decrease more than 50% at the end of therapy and returned to pretreatment levels after therapy. Six months later, all of these patients received alpha-IFN (6 MU) combined with 80 ml of SNMC intravenously, three times a week for 6 months. Prior to the initial IFN therapy alone, all of the patients were positive for anti-HCV and HCV RNA in the serum. With IFN therapy, serum HCV RNA became negative in 4 of 8 patients and HAI score decreased significantly although their ALT levels did not decrease more than 50%, while with IFN combined with SNMC therapy, ALT levels decreased approximately 70% in all patients (one became normal), serum HCV RNA became negative in 2 and HAI scores did not change significantly. There was no significant differences in decrease of HCV RNA titers and HAI scores between two therapy except the ALT levels. These findings suggest that IFN combined SNMC therapy does not appear to be more beneficial than IFN therapy alone.
PMID: 8078202, MUID: 94359046
HepC BC VIMRx BEGINS PHASE I/II HEPATITIS C TRIAL
Oral VIMRxyn(r) to be Evaluated for Treatment of Hepatitis C
WILMINGTON, DE, January 8, 1997-VIMRx Pharmaceuticals Inc. (NASDAQ: VMRX) announced that it has begun a Phase I/II clinical trial to determine the antiviral effectiveness of VIMRxyn(r), chemically synthesized hypericin, in reducing the viral load of patients suffering from infectious chronic hepatitis C. The trial is being directed by Jeffrey Jacobson, M.D., Chief of Infectious Diseases at the Bronx VA Medical Center and Associate Professor of Medicine at Mt. Sinai School of Medicine in New York. The trial is designed for twenty-four patients to be orally dosed with VIMRxyn(r) once daily for a period of two months. Results from the trial should be available within nine months.
In the United States, about 150,000 people each year are newly infected with the hepatitis C virus (HCV) and it is estimated that 4 million people in total are infected. There is no known cure and interferon alpha -2b is the only drug approved by the FDA for treatment of hepatitis C in the U.S. The long-term consequences of chronic HCV infection include cirrhosis of the liver and liver cancer.
"VIMRx is moving forward on yet another therapeutic front. Hepatitis C is a major worldwide health problem," said Richard Dunning, President and Chief Executive Officer of VIMRx, "and we're committed to thoroughly investigating VIMRxyn(r)'s effectiveness in fighting the disease, just as we are to defining our drug's capabilities in a variety of other areas, including AIDS and cancer. We're also enthusiastic about working with a medical researcher of Dr. Jacobson's capability."
VIMRx, based in Wilmington, DE, is currently developing two technology platforms: chemically synthesized hypericin, VIMRxyn(r), and through its majority-owned affiliate, Innovir Laboratories, catalytically active Oligozymes. VIMRxyn(r) is currently in clinical development for the treatment of HIV, brain cancer and hepatitis C, and is in pre-clinical development for the sterilization of blood. Innovir's Oligozyme technology seeks to control disease-triggering flaws in individuals' genetic chemistry. In addition to its potential use as a therapeutic in attacking diseases at the genetic level, the Oligozyme technology is being developed as a pharmaceutical research tool, to aid in drug target identification and validation. VIMRx also intends to be active in identifying and acquiring additional technologies and products.
Copyright (c) 1996-97, VIMRx Pharmaceuticals, All Rights Reserved.
HepC BC Israeli Doctor's Studies into Hypericum for HCV: Address and phone numbers
Dr Hazan's address (and tel #s) in Israel:
Dr. Sadik Hazan
12 Havradim Street
Ganei-Yehuda, Israel
Tel: 972-3-5343312
Fax 972-3-5353493
Dr. Hazan has the world's most carefully standardized Hypericin extract.
HepC BC Am-J-Epidemiol. 1995 Dec 1. 142(11). P 1136-46.
Corrao-G. Ferrari-P-A. Galatola-G
The analysis of the combined effects of nutritional factors with other putative disease determinants in log-linear or logistic models is methodologically complicated by the strong multicollinearity between nutritional factors, resulting in poor precision in estimating the parameters. Furthermore, the generally used multiplicative structure is not always the most appropriate for describing the resulting joint effect of two or more factors on the disease risk. The authors addressed such problems in a case-control study assessing the interactions between alcohol intake, chronic hepatitis C virus (HCV) infection, and nutrient intake on the risk of liver cirrhosis. During the period from November 1989 to May 1990, 282 patients admitted to the medical departments of the hospitals of the Province of L'Aquila (central Italy) were enrolled: 115 cirrhotic patients aged 24-82 years (78 of whom were males) hospitalized because of liver decompensation, and 167 control patients aged 25-84 years (100 of whom were males) admitted tothe same hospitals for acute diseases unrelated to alcohol intake, infection with hepatotropic viruses, and nutrition. No dose-effect relation was found between the intake of any nutrient and the risk of cirrhosis using classical methods. The analysis of principal components showed, however, that a pattern of higher lipid but lower protein and carbohydrate intakes was significantly associated with the risk of cirrhosis. The Breslow and Storer parametric family of relative risk functions showed that a multiplicative structure was the most adequate to describe the joint effect of nutritional pattern with alcohol intake and/or chronic HCV infection, whereas an additive structure best described the joint effect of chronic HCV infection and alcohol intake. In conclusion, the analysis of principal components and the Breslow and Storer family are useful tools to explore the role of diet on disease risk when precise pathogenic knowledge is not available. As an original finding, the authors suggest that a higher lipid intake, combined with lower protein and carbohydrate intakes, modifies multiplicatively the risk of cirrhosis associated with alcohol intake and/or chronic HCV infection.
HepC BC