Aa
MAF 314 (probiotic gcmaf)
Dr. Cheney will show the results of 1 month trial of maf 314 on CFS/XMRV infected patients on the 22-25 september Ottawa conference (http://www.iacfsme.org/)
Prof. Ruggiero 27 e 29 sept a Padova http://www.siai2011.azuleon.org/
due to the extraordinary results professor ruggiero and the other scientists involved agreed to explain people on how to do maf314 in our home kitchens
we know that first weeks of maf 314 made a rise of cd4,cd8 and nk cells in aids and healthy subjects...much more potent than chemical gcmaf i am doing now
Prof. Ruggiero 27 e 29 sept a Padova http://www.siai2011.azuleon.org/
due to the extraordinary results professor ruggiero and the other scientists involved agreed to explain people on how to do maf314 in our home kitchens
we know that first weeks of maf 314 made a rise of cd4,cd8 and nk cells in aids and healthy subjects...much more potent than chemical gcmaf i am doing now
there is already political pressure to stop this...increadibel how can you stop courses to make a yogurt, ridiculous
anyway this emans we are on a right track and dr cheney clinic have already the courses full but if we see some effect of gcmaf on me or the data from the conferences are extraordinary, i do suggest to get hold of this maf314 and courses as soon as possible in case it gets blocked by politics
only 4 days left to see
Dr. Cheney will show the results on the 22-25 september Ottawa conference (http://www.iacfsme.org/)
Prof. Ruggiero 27 e 29 september at Padova http://www.siai2011.azuleon.org/
It makes me mad the more i investigate the more i realize how the world works... Humans beings are just batteries that fuel the rich people. The greatest maffia having all the legal industries. How the little man is worth nothing. Cancer can be cured and they know how. They just don t allow a 158 biljon dollar industrie going down the drain. hepatitis can be cured. the same with cancer.Why would they, there is no gain in it. Doctors hospitals what purpose do they have then? it just makes me so mad that i am powerless to do anything about it. Steffano and people like him are the only ones how can make a change for some of uss. We are humans we deserve a better world than this.
no news, cheney clinics said that they wont make trials on hiv/aids people and conferences are like silent for now, nothing about maf314.
i am afraid there has been a very big pressure on this beyond the worst we can think if all is silent, let's just hope it wont go all wasted
the only gcmaf study in US made several years ago had a simple "university student" to prepare gcmaf, so wired the student dyed in a car and the researcher team said they were not able to produce gcmaf as the student (what a coincidence).
i really hope US is not like this today
http://www.siai2011.azuleon.org/_docs/110919_Programma_finale.pdf
thisis the program of conference in padova but no data for now or menthion about maf314 and this is extemely strange
thisis the program of conference in padova but no data for now or menthion about maf314 and this is extemely strange
https://docs.google.com/viewer?a=v&pid=explorer&chrome=true&srcid=0B8E77QizhkLQYzU4MDEwNmUtMGIwYy00YzYwLWEyZTMtMGY2YTIzOGEwNjA5&hl=it
results of just 3-8 weeks, the potency of maf 314 is increadible compared to gcmaf alone, i also had the increase and normalization of some parameters but it took 18-20 weeks, we will compare at 24 weeks
results of just 3-8 weeks, the potency of maf 314 is increadible compared to gcmaf alone, i also had the increase and normalization of some parameters but it took 18-20 weeks, we will compare at 24 weeks
increase of cd8 t cells and NK t cells is the most important for hbv clearance, so maf may help us a lot
i noticed that at 1 month chemical gcmaf all my parameters where different than cronic hbv with norml cd4, abnormal very high cd8, low cd4/cd8 ratio
the only thing different from acute resolved hbv is both cd4 and cd8 are very high while at 1 month my cd4 were still not high enough, and also normal cd4/cd8 ratio
Relationship between serum HBsAg level, HBV DNA level, and peripheral immune cells in patients with chronic hepatitis B virus infection
Original Research
(1168) Views (503) Full article downloads
Authors: RM Mukherjee, P Balkumar Reddy, Jyothi Arava, et al
Published Date November 2010 Volume 2010:2 Pages 157 - 162
DOI: http://dx.doi.org/10.2147/HMER.S13796
RM Mukherjee1, P Balkumar Reddy1, Jyothi Arava1, PN Rao2, Sasikala Mitnala1, R Gupta2, DN Reddy2
1Asian Health Care Foundation, 2Asian Institute of Gastroenterology, Somajiguda, Hyderabad, India
Background: The chronicity of hepatitis B virus (HBV) infection is attributed to inappropriate functioning of cell-mediated immunity. Besides the importance of measuring serum HBV DNA and HBV surface antigen (HBsAg) as markers of viral replication and exposure, respectively, studies regarding their influence on immune cell status in chronic HBV infection are still scarce. Because such studies of chronic HBV patients have not been reported for India, we attempted to evaluate the relationship between serum concentrations of HBsAg, HBV DNA, and percentage of immune cells in peripheral blood of Indian subjects with chronic HBV infection.
Methods: Thirty-one HbsAg-positive subjects were evaluated for serum HBe antigen (HBeAg), anti-Hbe, and alanine transferase status by standard enzyme-linked immunosorbent assay (ELISA) and biochemical procedures. Serum HBV DNA level was determined by real-time TaqMan® polymerase chain reaction assay. Serum HBsAg level was measured by a third-generation sandwich ELISA kit. Peripheral immune cell profiling was done by multifluorometric flow cytometry analysis, for which 21 healthy subjects were included as controls.
Results: The majority (93.5%) of the study subjects were HBeAg-negative and anti-HBeAg-positive. Mean viral load, HBsAg, and alanine transferase levels were 4.20 ± 1.96 log copies/mL, 5.98 ± 4.62 log IU/mL, and 74.5 ± 110 IU/mL, respectively. In comparison with controls, total T cell and cytotoxic T cell populations were significantly (P < 0.05) reduced in HBV-infected subjects, while the status of B cells, natural killer cells, T helper cells, and ratio of T helper to cytotoxic cells remained unaltered.
Conclusion: Suppression of the peripheral cytotoxic T cell population in chronic HBeAg-negative chronic HBV infection is influenced by increased viral load. Serum HBsAg concentration appeared independent of serum HBV DNA level and immune cell status. Nonelevation of natural killer cell and T helper cell numbers in subjects harboring lower to moderate HBV loads is further indicative of noninduction of innate as well as a coordinated adaptive immune response favoring chronicity of the disease.
articles about cd counts, NK counts and hbv infection outcome
DECLINE OF INTRAHEPATIC CCCDNA AND INCREASE OF IMMUNE CELL REACTIVITY AT WEEK 12 OF ANTIVIRAL TREATMENT WERE ASSOCIATED WITH HBEAG LOSS
Q. Zheng, Y.-Y. Zhu, J.-J. Jiang*, J. Chen
Liver Diseases Research Center, the First Affiliated Hospital of Fujian Medical University, Fujian Medical University, Fuzhou, China. ****@****
Background: Early viraemia clearance facilitates the recovery of antiviral T cell responses. The dynamic changes of intrahepatic viraemia clearance and immune cells reactivity during early phase of nucleos(t)ide therapy and the impact of these changes on HBeAg seroconversion are unknown.
Methods: Eight HBeAg(+) chronic hepatitis B patients were treated with adefovir dipivoxil for 48 weeks. Paired liver biopsies before and at week 12 of treatment were analyzed for intrahepatic HBVDNA and cccDNA by the real-time fluorescent PCR. In situ expressions of CD4,CD8 T cells, and NK cells were also analyzed by immunohistochemistry.
Results: After 48 weeks of ADV therapy, HBeAg loss was observed in 3 of the 8(37%) HBeAg(+)patients.After 12 weeks treatment, median intrahepatic total HBV-DNA and cccDNA had decreased by 1.52 log10 and 1.92 log10 copies/ug, respectively.About 98% intrahepatic HBVDNA were cleared in the early phase of the anti-viral treatment. Lower baseline levels of intracellular HBV DNA and cccDNA were found in the patients with HBeAg loss than in those who remained HBeAg+. Patients with HBeAg loss had lower cccDNA levels at week 12 than patients who remained HBeAg+. In parallel to the decline in viral load, the numbers of intrahepatic CD8+T-lymphocytes and NK cell increased in patients with HBeAg loss compared with their baseline values. Only one patient without HBeAg loss has similar result.
Conclusion: The increased numbers of intrahepatic CD8+T-lymphocytes and NK cell is associated with the lower levels of cccDNA in the early phase of anti-viral treatment, which would promote the recovery of anti-viral immunity and facilitate the HBeAg loss.
http://www.emro.who.int/publications/emhj/0302/17.htm
Cellular immune response in acute hepatitis B leading to chronic carrier state
Immunological findings: phenotypic analysis of T-cells and subsets
In the current study, the frequencies of T-helper and T-suppressor subsets in reference to the total T cell population were monitored using specifically labelled monoclonal antibodies in an indirect immunofluorescent technique. The analysis revealed a nonsignificant decrease (P > 0.05) in total T-lymphocytes (CD3+) among the acute, and chronic HBV cases compared to the controls. Also CD4+ and CD8+ populations were nonsignificantly different among the acute cases as compared to the control subjects. However, a highly significant (P < 0.001) decrease in the CD4+ in chronic cases compared to the acute cases and controls was observed. The frequencies of CD8+ cells in such patients were subsequently elevated. The decreased T-helper subset and the increased T-suppressor subset observed in the chronic cases resulted in a diminished T-helper to T-suppressor ratio of 1:1 compared with 2:1 observed in the acute and control groups (Table 4).
In accordance with our study, Abdel-Ghaffar (1990) and Ahmed (1990) in similar studies reported significant increase in the frequency of T-suppressor subsets in their studied cases [14,15]. Evidence that specific T-suppressor cells present in the circulation of patients with HBsAg positive chronic hepatitis prevent both anti-HBs antibody production in vitro [16] and T-LIF release by T lymphocytes sensitized by HBsAg [17] were reported. Whether these T suppressor cells appeared early in the course of the infection and contributed to the development of the HBV chronic carrier state or were secondary to the HBsAg overload present in chronically infected subjects was unknown.
Cytokines findings, IL-2 and IL-2R
When our patients' lymphocytes were stimulated in vitro with PHA, the IL-2 levels in culture supernatants and the frequency of IL-2R-bearing cells revealed low values among the chronic group as compared to the control and acute cases and the decrease was highly significant (P < 0.001). In contrast the frequency of IL-2R-bearing cells displayed a nonsignificant increase (P < 0.05) among the acute cases as compared to the controls. However, induced IL2 levels in the former population were significantly (P < 0.05) increased (Table 5). Our data were in accordance with Ozeki et al (1990) who reported highly significant (P < 0.001) low IL-2 values among their studied chronic HBV patients [18]. Also, Abdel-Ghaffar (1990) reported a significant decrease of both IL-2 levels and IL-2R among chronic HBV cases associated with schistosomiasis [14].
Saxena et al (1985) also reported similar observations [19]. They attributed the decrease to a central defect in the response to IL-1 resulting in an insufficient expression of IL-2 receptors. This was evident by the still consistently impaired proliferative response when exogenous IL-2 was included in the in-vitro cultures. Furthermore and although IL-2 production was decreased, exogenous IL-2 or IL-1 was unable to correct the low proliferative response, evidenced by Anastasskos et al (1987) [20]. In the present study, we failed to demonstrate a correlation between IL-2 levels in the culture supernatants and the frequency of IL-2 receptor (Tac antigen)-bearing cells of the same cultured cells among all HBV cases studied, acute and chronic. Abdel-Ghaffar (1990) reported similar observations [14]. This might be due to the fact that IL-2 receptors are of two types, high affinity and low affinity receptors. Both react and are monitored with the Tac monoclonal antibody following different experimental manipulations for each receptor type. An adequate number of high affinity receptors are mandatory for the mitogenic action of IL-2 [21].
Cellular immune response in acute hepatitis B leading to chronic carrier state
Immunological findings: phenotypic analysis of T-cells and subsets
In the current study, the frequencies of T-helper and T-suppressor subsets in reference to the total T cell population were monitored using specifically labelled monoclonal antibodies in an indirect immunofluorescent technique. The analysis revealed a nonsignificant decrease (P > 0.05) in total T-lymphocytes (CD3+) among the acute, and chronic HBV cases compared to the controls. Also CD4+ and CD8+ populations were nonsignificantly different among the acute cases as compared to the control subjects. However, a highly significant (P < 0.001) decrease in the CD4+ in chronic cases compared to the acute cases and controls was observed. The frequencies of CD8+ cells in such patients were subsequently elevated. The decreased T-helper subset and the increased T-suppressor subset observed in the chronic cases resulted in a diminished T-helper to T-suppressor ratio of 1:1 compared with 2:1 observed in the acute and control groups (Table 4).
In accordance with our study, Abdel-Ghaffar (1990) and Ahmed (1990) in similar studies reported significant increase in the frequency of T-suppressor subsets in their studied cases [14,15]. Evidence that specific T-suppressor cells present in the circulation of patients with HBsAg positive chronic hepatitis prevent both anti-HBs antibody production in vitro [16] and T-LIF release by T lymphocytes sensitized by HBsAg [17] were reported. Whether these T suppressor cells appeared early in the course of the infection and contributed to the development of the HBV chronic carrier state or were secondary to the HBsAg overload present in chronically infected subjects was unknown.
Cytokines findings, IL-2 and IL-2R
When our patients' lymphocytes were stimulated in vitro with PHA, the IL-2 levels in culture supernatants and the frequency of IL-2R-bearing cells revealed low values among the chronic group as compared to the control and acute cases and the decrease was highly significant (P < 0.001). In contrast the frequency of IL-2R-bearing cells displayed a nonsignificant increase (P < 0.05) among the acute cases as compared to the controls. However, induced IL2 levels in the former population were significantly (P < 0.05) increased (Table 5). Our data were in accordance with Ozeki et al (1990) who reported highly significant (P < 0.001) low IL-2 values among their studied chronic HBV patients [18]. Also, Abdel-Ghaffar (1990) reported a significant decrease of both IL-2 levels and IL-2R among chronic HBV cases associated with schistosomiasis [14].
Saxena et al (1985) also reported similar observations [19]. They attributed the decrease to a central defect in the response to IL-1 resulting in an insufficient expression of IL-2 receptors. This was evident by the still consistently impaired proliferative response when exogenous IL-2 was included in the in-vitro cultures. Furthermore and although IL-2 production was decreased, exogenous IL-2 or IL-1 was unable to correct the low proliferative response, evidenced by Anastasskos et al (1987) [20]. In the present study, we failed to demonstrate a correlation between IL-2 levels in the culture supernatants and the frequency of IL-2 receptor (Tac antigen)-bearing cells of the same cultured cells among all HBV cases studied, acute and chronic. Abdel-Ghaffar (1990) reported similar observations [14]. This might be due to the fact that IL-2 receptors are of two types, high affinity and low affinity receptors. Both react and are monitored with the Tac monoclonal antibody following different experimental manipulations for each receptor type. An adequate number of high affinity receptors are mandatory for the mitogenic action of IL-2 [21].
Interferon-g findings
The data on IFN-g production by PHA stimulated peripheral blood mononuclear cells from the studied patients revealed a highly significant (P < 0.001) increase among the acute HBV group as compared to the healthy subjects and chronic cases (Table 6). However, IFN-g production among the chronic cases revealed a highly significant decrease (P 0.05) when compared to the controls (Table 6). The results published by Kakumu et al (1989) [22], Inowa et al (1989) [23], Fuji et al (1987) [24], Ikeda et al (1986) [25] and Abb et al (1985) [26] were in accordance with the present data. The findings of defective IFN production in patients with chronic HBV infection reported in our study and by other investigators had led to the hypothesis that this might be a primary defect which could have been instrumental in the early stages of infection in permitting continued viral infection. These have led to the speculation that a defect in the ability to produce sufficient IFN during acute viral hepatitis may lead to chronic infection. Our data enabled us to suggest that IFN levels were statistically highly correlated (P < 0.001) to IL-2 levels. Both cytokines increased in acute HBV cases and control subjects, and both decreased in the chronic cases (data not presented).
The release of IL-2 by Th1 cells seemed to be the main stimulus for the sequential synthesis of IFN-g . When exogenous IL-2 was added to peripheral blood lymphocytes (PBL) in culture, there was a significant increase in the amount of IFN-g [23]. When both cytokines were correlated to Th subsets they were statistically insignificant. This was explained by the fact that measurement of Th subset in the present study did not specifically identify Th1, the main inducer of IFN-g and IL-2.
So, not only the phenotypic analysis of Th subsets was a must but also their functional differences should be studied to confirm the hypothesis proposed that defective Th1 was the main element underlying viral persistence in chronic HBV infections.
The data on IFN-g production by PHA stimulated peripheral blood mononuclear cells from the studied patients revealed a highly significant (P < 0.001) increase among the acute HBV group as compared to the healthy subjects and chronic cases (Table 6). However, IFN-g production among the chronic cases revealed a highly significant decrease (P 0.05) when compared to the controls (Table 6). The results published by Kakumu et al (1989) [22], Inowa et al (1989) [23], Fuji et al (1987) [24], Ikeda et al (1986) [25] and Abb et al (1985) [26] were in accordance with the present data. The findings of defective IFN production in patients with chronic HBV infection reported in our study and by other investigators had led to the hypothesis that this might be a primary defect which could have been instrumental in the early stages of infection in permitting continued viral infection. These have led to the speculation that a defect in the ability to produce sufficient IFN during acute viral hepatitis may lead to chronic infection. Our data enabled us to suggest that IFN levels were statistically highly correlated (P < 0.001) to IL-2 levels. Both cytokines increased in acute HBV cases and control subjects, and both decreased in the chronic cases (data not presented).
The release of IL-2 by Th1 cells seemed to be the main stimulus for the sequential synthesis of IFN-g . When exogenous IL-2 was added to peripheral blood lymphocytes (PBL) in culture, there was a significant increase in the amount of IFN-g [23]. When both cytokines were correlated to Th subsets they were statistically insignificant. This was explained by the fact that measurement of Th subset in the present study did not specifically identify Th1, the main inducer of IFN-g and IL-2.
So, not only the phenotypic analysis of Th subsets was a must but also their functional differences should be studied to confirm the hypothesis proposed that defective Th1 was the main element underlying viral persistence in chronic HBV infections.
i just posted the most interesting parts of this last study because if we use gcmaf or maf 314 we can use cd counts and cytokine tests to see if maf or gcmaf are having an effect
for example in my case cd4/cd8 ratio was 0.4 while they say acute are usually 2:1 ratio.so with my gcmaf therapy i need to increase cd4 at least more than double
redlabs.com have also cytokine tests, this way we may have a clue of wht we do with gcmaf to immune system
Thanks for the info. I honestly do not understand many things but anyway I'll follow this post as this is also one of the hopes of cure for us.....
there is no prof it has an effect on hbv at all so i suggest not to use this for hbv now
maf314 can be bought in austria (dr Uta Santos-König vienna) and germany kassel (dont have the name of clinic now)
Yes they are blocking cures.. For HBV for sure. Till 2017 they will continue to feed us antivirals..
Things are really bad, the system wants to get rid of very sick people and make money while they are at it. But do it slowly. I walked that road. Still do. In America it is the worst of ALL industrialized nations how they treat us. The Doctors, the hospitals and of course the health insurance companies that still continue to not provide health insurance coverage for very sick people. You have HBV you have to pay 3 or 4 times as much as a healthy person or you get no health coverage at all. Or they put you into a high risk insurance pool (Obama care) that has 75,000 yearly benefit cap. And then what? When one day in the Hospital here just the bed costs $10,000 So that is why many good doctors that really like to bill health insurance really don't want to deal with people like us. $75,000 for these business guys is nothing.
Here is another example.. There is GS9620.. Imiquimod that works, very very promising drug. So they are doing "clinical trials" makes sense..
But they are very selective of who they take. I live within driving distance of San Diego. And just because I take Baraclude I cannot try this drug. Have to be on Tenofovir fro 3 months or more.. Does that make sence to you?
What is the difference? Both are the same group of drugs. Both do the same thing, both are toxic, and really dangerous drugs if you talk with HIV treating people - off the record. But it is still better to be on them, then not.. I am just saying..
So one can ask what kind of a research this is anyway? And what kind of research they are doing in the Antiviral Center there is SD if they test Corporate sponsored medication, according to the guide lines that Gelead has set up. This is not research, this type of research they over at Gelead could do them selves. When one think of research you would think doctors there would try pioneering treatments on patients that are willing, without any conditions attached.
So face 2 will be 2014 for GS9620.. and face 3.. yes you guessed right, right up there in 2016 :)
Yet everybody "wants to help" so they say.. BUT they won't give the medication to people that need it unless thy take an antiviral that from a specific drug maker that also happens to sponsor these trials of their product. This is what this is. Product testing, and not really about helping people.. But they think we are stupid, from low income, and can be told some bs line and be quiet.
Here is what I was told about GS9620 off the record btw.. that they have data, that people Loose HBsAG.. on it over 3 months of this stuff. They just can't guarantee that it wont come back at some later point. I say this is very important, I think it should be available for people that want to try it so we can report it here and spread the awareness. This is the way to fight HBV for real.
The reason guys all the stuff is happening is because we are being quiet about it. That health care for profit hides cures from people. That medicine became an industry - somebody profits while others suffer.
Things are really bad, the system wants to get rid of very sick people and make money while they are at it. But do it slowly. I walked that road. Still do. In America it is the worst of ALL industrialized nations how they treat us. The Doctors, the hospitals and of course the health insurance companies that still continue to not provide health insurance coverage for very sick people. You have HBV you have to pay 3 or 4 times as much as a healthy person or you get no health coverage at all. Or they put you into a high risk insurance pool (Obama care) that has 75,000 yearly benefit cap. And then what? When one day in the Hospital here just the bed costs $10,000 So that is why many good doctors that really like to bill health insurance really don't want to deal with people like us. $75,000 for these business guys is nothing.
Here is another example.. There is GS9620.. Imiquimod that works, very very promising drug. So they are doing "clinical trials" makes sense..
But they are very selective of who they take. I live within driving distance of San Diego. And just because I take Baraclude I cannot try this drug. Have to be on Tenofovir fro 3 months or more.. Does that make sence to you?
What is the difference? Both are the same group of drugs. Both do the same thing, both are toxic, and really dangerous drugs if you talk with HIV treating people - off the record. But it is still better to be on them, then not.. I am just saying..
So one can ask what kind of a research this is anyway? And what kind of research they are doing in the Antiviral Center there is SD if they test Corporate sponsored medication, according to the guide lines that Gelead has set up. This is not research, this type of research they over at Gelead could do them selves. When one think of research you would think doctors there would try pioneering treatments on patients that are willing, without any conditions attached.
So face 2 will be 2014 for GS9620.. and face 3.. yes you guessed right, right up there in 2016 :)
Yet everybody "wants to help" so they say.. BUT they won't give the medication to people that need it unless thy take an antiviral that from a specific drug maker that also happens to sponsor these trials of their product. This is what this is. Product testing, and not really about helping people.. But they think we are stupid, from low income, and can be told some bs line and be quiet.
Here is what I was told about GS9620 off the record btw.. that they have data, that people Loose HBsAG.. on it over 3 months of this stuff. They just can't guarantee that it wont come back at some later point. I say this is very important, I think it should be available for people that want to try it so we can report it here and spread the awareness. This is the way to fight HBV for real.
The reason guys all the stuff is happening is because we are being quiet about it. That health care for profit hides cures from people. That medicine became an industry - somebody profits while others suffer.
Nice preach VeteranB ..
the light side that the GS9260 can remove HBsAg in 3 months .. great ..
the component that you mentioned it .. Imiquimod .. is it availble by any means .. tablet .. syrup .. capsules .. injection ..
do u have any idea about the toxity of gs9260?
is there any known person .. that take gs9260 in the trials phase?
the light side that the GS9260 can remove HBsAg in 3 months .. great ..
the component that you mentioned it .. Imiquimod .. is it availble by any means .. tablet .. syrup .. capsules .. injection ..
do u have any idea about the toxity of gs9260?
is there any known person .. that take gs9260 in the trials phase?
Hi stef
What about the injectable GCMAF? Do you think it works for hep B?
Also have you tried alinia with simvastatin? Is there any interaction? I am not familiar with alinia. I have to import it from progressiveRX as you suggested and check it purity.
What about the injectable GCMAF? Do you think it works for hep B?
Also have you tried alinia with simvastatin? Is there any interaction? I am not familiar with alinia. I have to import it from progressiveRX as you suggested and check it purity.
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