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.
There is still HOPE of cure for all of us........
some news form the conferences ?
Sorry! No news about it yet.
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
thisis the program of conference in padova but no data for now or menthion about maf314 and this is extemely strange
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
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Authors: RM Mukherjee, P Balkumar Reddy, Jyothi Arava, et al
Published Date November 2010 Volume 2010:2 Pages 157 - 162
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.
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  and T-LIF release by T lymphocytes sensitized by HBsAg  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 . Also, Abdel-Ghaffar (1990) reported a significant decrease of both IL-2 levels and IL-2R among chronic HBV cases associated with schistosomiasis .
Saxena et al (1985) also reported similar observations . 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) . 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 . 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 .