Hepatitis C Treatment Advance

Newer Hepatitis C Treatment Article

Rather then attempting to kill Hepatitis C virus cells, Japanese researchers have created a treatment that occludes its ability to reproduce. Though still unsure how Hepatitis C duplicates once inside human cells, its researchers were able to prevent the mechanism by which the virus combines with necessary cellular elements for multiplication.

The method deals with cells infected with the hepatits virus, not the virus itself, meaning that drugs could be developed to stop the multiplication process while preventing the virus from becoming resistant.

It is still unknown how exactly the hepatitis-C virus (HCV) multiplies once inside human cells. But researchers know that once the virus enters the cell, it develops a platform for multiplication by combining itself with a certain lipid, an organic compound.

The team at Chugai Pharmaceutical Co., led by Masayuki Sudo, determined a point inside cells where the HCV combines itself with the lipid.

Without the platform, the HCV is unable to duplicate itself, the researchers said.

Using human liver cells, the team added a substance to the lipid that prevented it from combining with the HCV. Thus, the platform for multiplication could not synthesize, the researchers said.

"If we can target the mechanism of virus-infected cells, it could prompt the development of more effective drugs," Sudo said.

An estimated 1 million to 2 million are infected with hepatitis C in Japan.

"HCV is troublesome because of its many mutations," said Takaji Wakita, a senior researcher at the Tokyo Metropolitan Institute for Neuroscience. "If we can target something that is contained in the cells, we may be able to come up with drugs that would prevent the virus from developing resistance. We need to make sure of the side effects, including the possibility that the treatment could affect other cells."

A reply to a the previous Hepatitis C article

A good reply I found on a Hepatits Newsgroup about the Hepatitis C treatment article..

"It is generally accepted..."

I read this all the time. It usually means that original, on point experiments establishing the claim were never done, or were terribly flawed, as is the case for "essential fatty acids," for example. British scientist Harold Hillman wrote an entire book on a few examples of this. Hep C. is a fabrication. Iron probably plays a major role, along with lipid peroxidation and exposure to some (if not many)
"pathogenic organisms." The same nonsense is true of "HIV/AIDS," where the "virus" was never found (even though the technology is available - has been for a long time - and is not especially expensive), but instead protein fragments which are just cellular debris have been declared "markers" of infection. Listen to these people and you are in deep trouble, as I almost was. I was told to take anti-acid medication, but determined by my own research that I needed to take stamach acid and pepsin supplements, which I still do to this day, several years later, with no signs of the original "disease," no thanks to "modern medicine." Interestingly, I purchased an old Cycopedia of Medicine from circa 1920 and that was the only refernce for using stomach acid supplementation. These "experts" have "gone backwards,"
though the technology has advanced, and creates an image of "great achievements," depsite the incredible failures of the "war on cancer," the "AIDS vaccine" (which is an impossiblity), etc.

Dietary iron restriction improves aminotransferase levels in chronic

Third Department of Internal Medicine, Mie University School of Medicine, Edobashi 2-174, Tsu City, Mie 514-8507, Japan. motoh@clin.medic.mie-u.ac.jp

BACKGROUND/AIMS: It is generally accepted that iron overload plays an important role in the pathogenesis of liver cell injury in chronic hepatitis C. The present study was undertaken to evaluate whether low-iron diet improves liver function tests in patients with chronic hepatitis C. METHODOLOGY: Seventeen patients with chronic hepatitis C (13 men and 4 women, 54 +/- 14 years old) that did not respond to, or were unsuitable for interferon therapy, were enrolled in this study. All patients had been pretreated with ursodeoxycholic acid for more than 12 months before the beginning of the study. Dietary iron intake was restricted to less than 7 mg/day, and the patients were followed up for 18 months.

RESULTS: Mean daily iron intakes, calculated from food records, were 5.9 and 6.4 mg after 6 and 12 months, respectively. The mean serum ferritin decreased significantly from 362 ng/mL at entry to 179 ng/mL after 18 months. The serum unsaturated iron binding capacity level increased significantly from 163 micrograms/dL at entry to 203 micrograms/dL after 18 months. The serum aspartate aminotransferase decreased significantly from 62 IU/L at entry to 47 IU/L after 18 months, and serum alanine aminotransferase from 68 IU/L at entry to 53
IU/L after 18 months. Serum iron, hepatitis C virus-RNA titer and platelet count remained unchanged throughout the study.

CONCLUSIONS: These results suggest that iron-restricted diet may be an important therapeutic modality for improving liver injury in patients with chronic hepatitis C.