Medical Forum / Diseases and Disorders / Hepatitis / March 2007
Iron levels and hepatitis transferance
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ironjustice@aol.com - 05 Mar 2007 03:53 GMT Do the sweat iron levels lower as body iron levels lower .. ? Would a vegetarians' sweat be less able to .. pass .. the hepatitis virus .. ? Do we have to lock them up .. ?
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WRESTLING WITH HEPATITIS B Reuters March 2, 2007 -- Findings from a study of Olympic wrestlers indicate that hepatitis B is found in the sweat of infected individuals, and so sweating might be a way that the virus could be passed between participants in contact sports.
Bleeding wounds and mucous membranes have been faulted in hepatitis B transmission during sports, but no study had looked to see if sweat carries the virus, according to the British Journal of Sports Medicine.
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The World's No.1 Science & Technology News Service
Body odour bugs starved to death
20:00 20 May 02
NewScientist.com news service
Starving the bacteria that cause body odour of the iron they need to grow may soon arm deodorants with an extra stink-stopping weapon.
Fresh sweat has no odour. But bacteria feed on our excretions, especially in the warm, damp armpits, and produce malodorous molecules as a byproduct. Standard underarm deodorants often use alcohol to kill the bacteria, but usually some bacteria survive and begin growing back.
Manufacturers sometimes add additional anti-bacterials, perfumes and antiperspirants to try to increase efficacy. But Andrew S Landa and colleagues at Unilever Research and Development, in Port Sunlight, north-west England, are trying a new approach - starving the bacteria of iron.
Sweat contains trace amounts of iron, and bacteria need it in order to multiply. So Landa and colleagues used a chemical called diethylenetriaminepentaacetic acid (DTPA), which binds iron and keeps the bacteria from using it.
Because some bacteria can also extract iron from iron-carrying proteins which are also present in sweat, the researchers also added butylated hydroxytoluene (BHT), which released the iron from the proteins, and allowed it to be captured by the DTPA.
Armpit assessors
American Society for Microbiology
According to a paper presented at the American Society for Microbiology meeting in Salt Lake City on Monday, a deodorant with DTPA and BHT added to alcohol kept bacteria populations lower after 24 hours than alcohol alone.
It controlled smell better, too, according to "expert assessors" at Unilever. These people have the unenviable job of applying the new deodorant and a control to the armpits of volunteers, and then assessing how the armpits smelled after five and again after 24 hours.
"I think we calculated for 8000 armpits," Landa says. The tests were double-blind, and again the iron-capturing formulation worked better than just alcohol.
Landa would not say whether Unilever is planning to market a deodorant that uses the new agents. But the company has already applied for patents on the technology in Europe and the US.
Kurt Kleiner
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ironjustice@aol.com - 05 Mar 2007 05:11 GMT On Mar 4, 7:53 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
> Do the sweat iron levels lower as body iron levels lower .. ? > Would a vegetarians' sweat be less able to .. pass .. the hepatitis [quoted text clipped - 98 lines] > > DEAD PEOPLE WALKING Sooo .. it is not ONLY the fault of those who .. carry .. the virus but the fault of the HOST / recipient .. DUE TO .. the susceptibility TO .. transferance / catching .. the virus ..
IF ones' lactoferrin were **empty** would it STOP the virus at the door .. ?
http://www.blackwell-synergy.com/links/doi/10.1034%2Fj.1600-0676.2000.020002125.x
Liver International Volume 20 Issue 2 Page 125 - April 2000
Iron enhances hepatitis C virus replication in cultured human hepatocytes
Abstract: Background: Iron overload in the presence of increasing concentrations of iron is one of the indicators of poor response to interferon therapy in chronic hepatitis C. In order to analyze the effect of iron on hepatitis C virus (HCV) replication, we measured replication in an HCV-infected cell line. Methods and Results: Cells from a non-neoplastic HCV-infected human hepatocyte line (PH5CH8) susceptible to HCV infection and supportive of HCV replication were used in this study. The replication of HCV RNA was measured by reverse transcription-nested polymerase chain reaction (RT-nested PCR). PH5CH8 cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyl tetrazolium bromide (MTT) assay. PH5CH8 cells were incubated with 0, 1, 10, 50, and 100 μM of FeSO4 at 37°C with 5% CO2. Forty- eight hours after iron supplementation, the quantity of HCV RNA in the cells incubated in 50 and 100 μM of FeSO4 was approximately ten times that of the cells with no iron supplementation. Similar changes were observed beginning at 12 h from supplementation with FeSO4 and continued for at least 72 h after supplementation. MTT assay indicated that iron did not have cytotoxic effects on the PH5CH8 cells. Conclusion: Iron enhances HCV replication in a hepatocyte cell line. The results suggest that iron deposition in hepatocytes could facilitate HCV infection in the liver.
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Virus Res. 2000 Jan;66(1):51-63. Links Characterization of antiviral activity of lactoferrin against hepatitis C virus infection in human cultured cells.Ikeda M, Nozaki A, Sugiyama K, Tanaka T, Naganuma A, Tanaka K, Sekihara H, Shimotohno K, Saito M, Kato N. Virology and Glycobiology Division, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo, Japan.
We recently found that bovine lactoferrin (bLF), a milk glycoprotein belonging to the iron transporter family, prevented hepatitis C virus (HCV) infection in human hepatocyte PH5CH8 cells, that are susceptible to HCV infection, and demonstrated that the anti-HCV activity of bLF was due to the interaction of bLF and HCV. In this study we further characterized the anti-HCV activity of bLF and the mechanism by which bLF prevents HCV infection. We found that bLF inhibited viral entry to the cells by interacting directly with HCV immediately after mixing of bLF and HCV inoculum. The anti-HCV activity of bLF was lost by heating at 65 degrees C, and other milk proteins (mucin, beta-lactoglobulin and casein) did not prevent HCV infection, indicating that bLF prevented HCV infection in a rather specific manner. Furthermore, we found that bovine lactoferricin, a basic N-terminal loop of bLF that is an important region for antibacterial activity, did not exhibit any anti-HCV activity, suggesting that some other region is involved in anti-HCV activity. We confirmed that prevention of HCV infection by bLF was a general phenomenon, because bLF inhibited HCV infection with all five inocula examined, and bLF inhibited HCV infection in human MT-2C T-cells, that were susceptible to HCV infection. In addition, infection with hepatitis G virus, which is distantly related to HCV, was prevented also by bLF. In conclusion, lactoferrin is a natural glycoprotein which effectively protects against HCV infection in hepatocytes and lymphocytes by neutralizing the virus.
PMID: 10653917 [PubMed - indexed for MEDLINE] ----------------------------------------------------------------------------------
Jpn J Cancer Res. 1999 Apr;90(4):367-71. Links Lactoferrin inhibits hepatitis C virus viremia in patients with chronic hepatitis C: a pilot study.Tanaka K, Ikeda M, Nozaki A, Kato N, Tsuda H, Saito S, Sekihara H. Third Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama. tanaka97@med.yokohama-cu.ac.jp
Hepatitis C virus (HCV) is associated with the development of cirrhosis and hepatocellular carcinoma. We recently found that bovine lactoferrin, a milk protein belonging to the iron transporter family, effectively prevented HCV infection in cultured human hepatocytes (PH5CH8). We tested the hypothesis that lactoferrin inhibits HCV viremia in patients with chronic hepatitis C. Eleven patients with chronic hepatitis C received an 8-week course of bovine lactoferrin (1.8 or 3.6 g/day). At the end of lactoferrin treatment, a decrease in serum alanine transaminase and HCV RNA concentrations was apparent in 3 (75%) of 4 patients with low pretreatment serum concentrations of HCV RNA. However, 7 patients with high pretreatment concentrations showed no significant changes in these indices. This pilot study suggests that lactoferrin is one potential candidate as an anti-HCV reagent that may be effective for the treatment of patients with chronic hepatitis.
PMID: 10363572 [PubMed - indexed for MEDLINE] --------------------------------------------------------------------------------
Lactoferrin is a globular protein found in milk and many mucosal secretions such as tears. Its molecular atomic mass is 80,000 u (80 kD). This protein belongs to the transferrin family proteins (transferrin, melanotransferrin, ovotransferin, etc.) showing a high affinity by iron (ferric state). Lactoferrin is a multifunctional protein with antimicrobial activity (bacteriocide, fungicide) and is part of the innate defense proteins mainly at mucoses. ... en.wikipedia.org/wiki/Lactoferrin
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ironjustice@aol.com - 05 Mar 2007 06:34 GMT On Mar 4, 9:11 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
> On Mar 4, 7:53 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote: > [quoted text clipped - 223 lines] > > - Show quoted text - <<snip>> Individuals with a serum ferritin level greater than 300 ng ml(-1) failed to respond to IFN in 93% of the cases studied. <<snip>>
Published by the University of Chicago Press
6565 View: Overview Glossary HistCite Guide Author(s) Bayraktar Y; Koseoglu T; Temizer A; Kayhan B; VanThiel DH; Uzunalimoglu B Title Relationship between the serum alanine aminotransferase level at the end of interferon treatment and histologic changes in wild-type and precore mutant hepatitis B virus infections Source JOURNAL OF VIRAL HEPATITIS 3 (3): 137-142 Date 1996 MAY Type Journal : Article LCR: 7 NCR: 22 LCS: 0 GCS: 2 Comment Address HACETTEPE UNIV,FAC PHARM,DEPT ANALYT CHEM,ANKARA,TURKEY. HACETTEPE UNIV,SCH MED,DEPT GASTROENTEROL,ANKARA,TURKEY. HACETTEPE UNIV,SCH MED,DEPT PATHOL,ANKARA,TURKEY. Reprint Bayraktar, Y, OKLAHOMA MED RES FDN,LIVER DIS PROGRAM,BELL BLDG, 825 NE 13TH,OKLAHOMA CITY,OK 73104. Abstract Unravelling the role of interferon (IFN) in the treatment of chronic hepatitis B is complicated by many factors, Several mutant forms of hepatitis B virus (HBV) have recently been discovered; the most common of these is the precore mutant, characterized by hepatitis Be antigen (HBeAg) negativity and hepatitis Be antibody (HBeAb) positivity in an individual with an active HBV infection, The aim of this study was to compare the response rate to IFN therapy in patients with wild-type HBV infection and in individuals infected with the precore mutant, A second aim was to evaluate the role of an increased serum ferritin in terms of the IFN response rate in these two different types of HBV infection, IFN therapy was administered at a dose of 5 MU subcutaneously three times weekly for 6 months to 41 individuals with a chronic wild-type hepatitis B infection and 16 individuals with a precore mutant chronic HBV infection, An IFN response was defined as normalization of the serum alanine aminotransferase (ALT) level and an HBeAg to HBeAb seroconversion (in wild-type hepatitis infection), and a normalization of the serum ALT in individuals infected with a precore mutant infection, At entry, the two groups were matched for age, gender, serum ALT, serum iron, total iron binding capacity (TIBC), serum ferritin and liver histology. Forty-six per cent of the subjects with wild-type disease responded to IFN therapy. By contrast, only four of the 16 cases (25%) of the precore mutant cases responded (P < 0,05), Ferritin levels correlated well with the type of IFN response; as the serum ferritin level increased, the response rate to IFN declined, Hapatic infection caused by a precore HBV mutant is more resistant to IFN therapy than wild- type infection, The serum ferritin level appears to influence the type of IFN response achieved, Individuals with a serum ferritin level greater than 300 ng ml(-1) failed to respond to IFN in 93% of the cases studied. --------------------------------------------------------------------------------
Title Inhibition of Human Immunodeficiency Virus Type 1 Replication in Human Mononuclear Blood Cells by the Iron Chelators Deferoxamine, Deferiprone, and Bleomycin Author(s) Niki A. Georgiou, Tjomme van der Bruggen, Maroeska Oudshoorn, Hans S. L. M. Nottet, Joannes J. M. Marx, and B. Sweder van Asbeck1 Identifiers The Journal of Infectious Diseases, volume 181 (2000), pages 484–490 DOI: 10.1086/315223 PubMed ID: 10669330
Availability This site: PS | HTML | PDF (136.6k) Copyright © 2000, the Infectious Diseases Society of America. Abstract Replication of human immunodeficiency virus type 1 (HIV-1) can be influenced by iron. Hence, decreasing the availability of iron may inhibit HIV-1 replication. Deferoxamine and deferiprone, both forming catalytically inactive iron-chelator complexes, and bleomycin, by use of which iron catalyzes oxidative nucleic acid destruction, were investigated. Expression of p24 antigen in human monocyte-derived macrophages and peripheral blood lymphocytes (PBL) was reduced by all 3 iron chelators. In PBL, p24 reduction was mirrored by a decrease in proliferation after incubation with deferoxamine or deferiprone, suggesting that viral inhibition is closely linked to a decrease in cellular proliferation. In contrast, clinically relevant bleomycin concentrations reduced p24 levels by 50% without affecting proliferation. When deferoxamine and the nucleoside analogue dideoxyinosine were used in combination, they acted synergistically in inhibiting HIV-1 replication. These observations suggest that iron chelators with different mechanisms of action could be of additional benefit in antiretroviral combination therapy.
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