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C.100-PROSTATIC CANCER AND HUMAN PAPILLOMAVIRUS (HPV): AUTO-IMMUNE THROMBOCYTOPENIA INDUCED BY GARDA

PROSTATIC CANCER AND HUMAN PAPILLOMAVIRUS (HPV): AUTO-IMMUNE THROMBOCYTOPENIA INDUCED BY GARDASIL AND CERVARIX VACCINE HPV L1 MIMICKING PLATELET GPV

Présentation 

ARTP 18 Nov 2015 Paris Porte Maillot

TRAN Guy Mong Ky

Retired, Public Health (Agence Régionale de Santé ARS Auvergne Rhône Alpes), Hospital Hôtel-Dieu, Clermont-Ferrand, FRANCE. Correspondence: 31 Avenue du Bois 92290 Chatenay Malabry. E-mail: Cette adresse email est protégée contre les robots des spammeurs, vous devez activer Javascript pour la voir. . Phone: +33 9 81 89 38 70.

BACKROUND Among the auto-immune complications occurring after anti-HPV vaccination (Gardasil and Cervarix), was reported thrombocytopenia (Pugnet G, 2009). Odds Ratio (OR) for Serious Autoimmune Adverse Events (SAAEs) reported by the Vaccine Adverse Event Reporting System (VAERS) from Jan 2006 through Dec 2012 is OR=1,3 (95% CI=0.48-3.5) (Geier DA, 2015) for thrombocytopenia. If severe, this thrombocytopenia can conduct to cerebral hemorrhage and eventually death.

METHODS Amino acid sequences comparison between HPV L1 and platelet gpV. We centered the alignment on the FP and related LP motifs (Leucine L replaces Proline P). Platelet alloantigen, P1T, on glycoprotein V is associated with neonatal alloimmune thrombocytopenia (Ertem M, 1994). Measles was investigated versus platelet gpIIbIIIa on the FP motif.

RESULTS   Platelet gpV was aligned with HPV (types -16,-18, -6, -11,-31,-33,-52,-58) L1 of Gardasil 9.

perfect molecular mimicry ALPDG was found between HPV-61,-72,-81 L1 and platelet gpV.

A common motif  LPDT was found between rubella virus nsp and HPV-18 L1. Rubella can induce thrombocytopenia (Okazaki N, 2011). There is a common motif ALPD between gpV, HPV-11 and HPV-6  L1. Anti-gpV specific antibodies are also particularly evident in Varicella virus thrombopenia (Mayer JL, 1996) and are cross-reactive with platelet (Wright JF,1994): Varicella ORF 24 and rubella nsp share the ALPDT motif.

There was a perfect molecular mimicry between Measles P protein strain Mvi/Victoria.AUS/12.99 (Bankamp B, 2008) and platelet gpIIb: 

   platelet gpIIb                                                                         782-RGNSFP-787

Measles P protein strain Mvi/Victoria.AUS/12.99                      199-RGNSFP-204

The other Measles virus strains have                                              RGNNFP

CONCLUSION  The perfect 100% molecular mimicry ALPDG, centered on a Proline, between HPV-61,-72,-81 L1 and platelet gpV raises the question of the etiology of the so-called "idiopathic" thrombocytopenic purpura. It is advocated to research HPV-61,-72,-81 as possible culprits, either by PCR or Metagenomics (Johansson H, 2013). HLA-DR3 may be a  risk factor. The alimentation must be strictly controlled, avoiding in particular aspirin and alliaceous. The obligatory vaccination by Measles Mumps Rubella vaccine, associated with Zoster-Varicella vaccine (Okazaki N, 2011) and 3 doses of Gardasil or Gardasil 9 or Cervarix, may enhance further the auto-immune response against platelet gpV and induce autoimmune thrombocytopenia. Gardasil 9 is particularly worrying.

BIBLIOGRAPHY Bankamp B. Genetic variability and mRNA editing frequencies of the phosphoprotein genes of wild-type measles viruses. Virus Res 2008, 135: 298-306. Ertem M. A new platelet alloantigen, P1T, on glycoprotein V associated with neonatal alloimmune thrombocytopenia. Pediatr Res 1994, 35: 160A. Geier DA. A case-control study of quadrivalent human papillomavirus vaccine-associated autoimmune adverse events. Clin Rheumatol 2015, 34: 1225-31. Johansson H. Metagenomic sequencing of "HPV-negative" condylomas detects novel putative HPV types. Virology 2013, 440: 1-7. Mayer JL. Varicella-associated thrombocytopenia: autoantibodies against platelet surface glycoprotein V. Pediatr Res 1996, 40: 615-9. Meenaghan M. Antibodies to platelet glycoprotein V in polytransfused patients with haematologic diseases. Vox Sang 1993, 64:167–70. Okazaki N. Detection of platelet-binding anti-measles and anti-rubella virus IgG antibodies in infants with vaccine-induced thrombocytopenic purpura. Vaccine 2011, 29: 4878–80. Pugnet G. Immune thrombocytopenic purpura following human papillomavirus vaccination. Vaccine 2009, 27: 3690. Wright JF. Virus-reactive antibodies cross-react with autologous platelets in a patient with varicella zoster virus (VZV)-associated idiopathic thrombocytopenic purpura (ITP). Blood 1994, 84 (suppl):185a

 


 
C.98-GARDASIL ANTI-PAPILLOMAVIRUS VACCINE: MOLECULAR MIMICRY OF HPV L1 WITH GONADOLIBERIN GNRH EXPLA


GARDASIL ANTI-PAPILLOMAVIRUS VACCINE: MOLECULAR MIMICRY OF HPV L1 WITH GONADOLIBERIN GNRH EXPLAINING PRECOCIOUS MENOPAUSE AND STERILITY

TRAN Guy Mong Ky

Retired, Public Health (Agence Régionale de Santé Auvergne Rhône Alpes), Hospital Hôtel Dieu, Clermont-Ferrand FRANCE. Correspondence: 31 Avenue du Bois 92290 Chatenay Malabry. E-mail: Cette adresse email est protégée contre les robots des spammeurs, vous devez activer Javascript pour la voir. . Phone: +33 9 81 89 38 70.

Association pour la Recherche sur les Tumeurs de la Prostate (ARTP)

18 Nov 2015 . Palais des Congrès, Porte Maillot, Paris

 
 

BACKGROUND

After Gardasil vaccination, a 16 years old Australian (Little DT, 2012) and a 18 years old French Jennifer Sellier (Carrère d'Encausse M, 2015) developped a premature menopause and sterility. Four more Australians were further reported (Little DT, 2014). In September 2015, the Vaccine Adverse Event Reporting System (VAERS) reported 95 irreversible cases among 104 early menopauses. This number did not reflect the reality, as only <1% to 10% are declared, owing to the fact that menopause is unknown from the general practionner as a Gardasil complication (NVIC). Therefore, in reality, there is 10 000 cases of sterility, a number which will grow continuously with time. The September 2015 French pharmacovigilance ANSM/CNAMTS report followed 14 auto-immune diseases, but did not include menopause/sterility among them, despite the fact that infertility can be induced by an immune mechanism, for example by woman antibodies against husband sperm, and fertility recovered by deletion of these antibodies. A FDA cohort began in Sweden with 3000 patients, this number fell to 1700 after 6 years, to 500 after 8 years, then the study was never terminated and simply burried. Gardasil was licensed in the market without any released data on the ovaries of the Sprague-Dawley female rats. Furthermore, Sprague-Dawley rats are prone to cancer, and are not the species of choice in the case of auto-imune disease. The data on male rats were stopped prematurely at the second injection. Tween 80 (polysorbate 80) containing ethylene glycol can provoke severe ovary deformities, degenerative follicles, sterility (Gajdova M, 1992) and anaphylactic shock. Some countries such as Japan, Denmark or Western European countries have yet a worrying decline of fertility. We investigated the auto-immune mechanism of sterility induced by Gardasil.

 

METHODS We compared the amino acid (AA) sequences of the Gardasil 9 vaccine HPV L1 and Gonadotropin Releasing Hormone GnRH, mumps virus (ovaritis, orchitis and sterility if during post-puberty). Mycoplasma and Enteroviruses [Coxsackie A6 (Foot Mouth Hand Disease or FMHD), Echovirus, Enterovirus E or Bovine Enterovirus (BEV)] were included, because Coxsackievirus A6 orchitis was reported in Finland; and in bull, orchitis, loss of libido, testicular degeneration, aspermatogenesis and sterility occurred after a BEV-1 infection (Weldon SL,1979). BEV has a large spectra and can infect humans.

RESULTS There is a molecular mimicry EHWS between HPV-57, -2, -27 L1 and the catfish, dogfish GnRH active site, Mycoplasma Salivarium (WP_024544007), extending to 6 AAs  EHWSKG and pEHWSHG (p=pyrrolidone).

 











We found a molecular mimicry between HPV-16, -18, -11, -6 L1 163-EHW and the GnRH active site  24-pEHW-26, prolonged upstream to 2 Cys 153-CMVGC-157 and 17-CVVGC-21.  GnRH (homo, teleost) 31-SPGGKRNAE-39 matches with HPV (-3, -34 chimera) 198-TPCGKQNAgE-207 (Span=28 AA).

Hypogonadotropic Hypogonadism 12 mutation R → C                              C

GnRH                            CV VGC SSpEHWS HGLSPGGKRNA E

PVH L1                         CMVGCapplgEHWGKGLSPCGKQNAgE

Mumps virus F                                   EQWS YPAKNC

Coxsakievirus A6        ALVFP         (Q,H)WINLRTNNCA

Enterovirus E VP2            LIYP          (Q,H)WINLRTNNS A

Mycoplasma Salivarium                  80-EHWSKG

Glutamine Q and Histidine H are cross-reactive, owing to their chemical similarities. A length of only 3 AAs is enough for a hypothalamic hormonal activity (i.e. TSH Releasing Factor pGln-His-Pro, Melanostatin Pro-Leu-Gly). The mutation R31C of GnRH 24-pEHWSYGLRPG-33 induces a Hypogonadotropic Hypogonadism 12 (HH12). C31 almost aligned with C171 of L1 163-EHWGKGKQC-171 and C324 of mumps virus F (Fusion) protein 315-EQWSYPAKNC-324. The most worrying is the discovery that Gardasil 9 contains 9 times the EHW motif, highly conserved in 71/75 (94,7%) studied HPV types.

 

 









CONCLUSION

Gardasil L1 mimics the GnRH active site pEHWxxG and is homologous to mumps virus F, Coxsackie A6 (FMHD) and Mycoplasma, all three responsible of sterility. This is coherent with an auto-immune disease directed against GnRH which is destroyed by anti-GnRH auto-antibodies cross-reactive with vaccine L1, in particular L1 of HPV-6 and -11, absent in Cervarix. Japan has suspended Gardasil in June 2013, India in 2010. As for mumps virus, pubescent adults are susceptible to have complications conducting to a definitve sterility, particularly in the feminine sex very prone to auto-immunity (they have a more reactive HLA system). One third of young women take oral contraceptives that can mask this complication during all the time they take the pill, so infertility may only develop when stopping contraception, about 15 years later, in the 2030s. The 3 intra-muscular injections provoke a powerful, durable and aggravating anamnestic response [induced by Aluminium-DNA complex (Lee SH, 2012)], which is 10 times more powerful than the natural infection. The Gardasil 4 HPV types possess the pEHWxxG motif, and more dramatically the Gardasil 9 have it 9 times. The obligatory Measles Mumps Rubella vaccine may enhance the auto-antibodies. Undetected enterovirus E infection on a background of selenium deficiency may aggravate the situation. Mycoplasma Salivarium contains also a GnRH epitope.

Plasmapheresis may be a possible solution to delete anti-GnRH auto-antibodies. Selenium levels must be determined and corrected. Selenium has an antiviral activity against enteroviruses.

BIBLIOGRAPHY

ANSM/CNAM report Sept 2015

Carrère d'Encausse M. Les médicaments sont-ils parfois dangereux pour notre santé? French TV 5, 10.2.2015.

Gajdova M. Food Chem Toxicol 1992, 31:180-90.

Lee SH. Detection of human papillomavirus L1 gene DNA fragments in postmortem blood and spleen after Gardasil® vaccination—A case report. Adv Biosc Biotech, 2012, 3: 1214-24

Little DT. Premature ovarian failure 3 years after menarche in a 16-year-old girl following human papilloma-virus vaccination. BMJ Case Rep 2012. 10.1136/bcr-2012-006879.

Little DT. Adolescent Premature Ovarian Insufficiency Following Human Papillomavirus Vaccination. A Case Series Seen in General Practice. J Investig Med High Impact Case Rep 2014, 2: 2324709614556129.

Little DT. Human papillomavirus vaccine and the ovary: the need for research. Paper presented at: Proceedings of the 18th World Congress on Controversies in Obstetrics, Gynecology and Infertility; October 24-27, 2013; Vienna, Austria.

NVIC.Org

SANEVAX

Weldon SL. Isolation of picornavirus from feces and semen from an infertile bull. J Am Vet Med Assoc 1979, 174:168-9.

 

 

Aknowlegments to Caprani A., President of Positifs Association, Positifs.org for financial support.

 
C.97bis -8 ° IAS 2015- Victory of pharmaceutical lobbies - life antiretroviral treatment for all!

The last conference of the International AIDS Society (IAS) on HIV Pathogenesis, its treatments and prevention was held in Vancouver (Canada) from 19 to 22 July 2015. It brought together over 6000 participants but became over the years a mercantile fair (sponsored by laboratories) whose almost exclusive promotion purposes with questionable arguments, always toxic treatments and broader populations to increasingly numerous to which the utility is far be demonstrated.
All the information presented in this conference can be found on the site
Abstracts: http://www.ias2015.org/WebContent/File/IAS_2015__MED2.pdf
An impressive amount of information at a fundamental level, clinical, prevention and social, has been provided. Unfortunately, nothing essential in terms of  what patients are waiting : efficient preventive or therapeutic vaccine , effective ways to eradicate or reduce reservoirs, non-toxic treatments, .... were made.
Let us recall that the long-term antiviral therapies may cause metabolic disorders (lipid abnormalities, diabetes), toxicities of liver , kidney, heart, bone disorders, peripheral neuropathy and even libido problems (erectile dysfunction) . These side effects of antiviral drugs can lead to serious illnesses and deaths, it is imperative that the patient be informed honestly so as not to undergo a medical and media hype and freely choose and accept treatment.

Pre-exposure prophylaxis (PrEP) was one of the main topics of discussion at the IAS 2015: How to take it, who should be able to take and when it will be available to you-Three studies presented show that for some people in some contexts, a less frequent use of PrEP, with doses determined according to sexual activity, was feasible and that a high number of sex remained protected by PrEP. This could offer people who want to use PrEP, and their physicians, additional options, allowing them to find a way to take PrEP that suits them best.
However our  association “Positifs” does not wish this prevention which  is very marginal, became the majority, except perhaps on groups at very high risk, such as prostitute (e) s. We maintain that the only prevention, safe, easy to implement and a very low cost (should be free) is the condom, which unfortunately does not sufficiently been campaigns by national health systems. PrEP will not serve if it requires only a majority fatten a little lobbies at the expense of the health of users who consume long-term toxic products and further despoiling a little more bloodless medical coverage systems.
One study, still serving the pharmaceutical lobbies, presented by Myron Cohen, revealed that the partner of a HIV patient, having an undetectable viral load avoids the transmission if he  uses a PrEP, while it is known for more than an HIV-positive 10 years with undetectable viral load is not contaminant !! PrEP in this case is unnecessary and criminal for all HIV-negative partners that condoms can be used for any occasion.
We believe that the best way to stop transmission is to test authoritarian way the entire population since over 50% of HIV positive are unaware of their status and thus is the major transmission vector, to make free condoms, and empower HIV-positive patients.

The START study considers provide 'definitive' evidence on the benefits of early treatmentT?
Let us recall that the starting threshold of antiviral treatment was for 20 years, under pressure from the pharmaceutical lobbies, and experimenters of complacent trials systematically raised from 200, where the risk of opportunistic infections very minimal, 350, then 500 and now the announcement of seropositivity (with normal values ​​in the range 500-1000).
Emphasize again that the immediate start of treatment, requires that  possible non progressors patients , unidentified, suffer for years (5, 10 years sometimes more) toxic treatments of aggression with their train of 'side effects. For the majority of patients starting treatment at CD4 300-350, allows, with a negligible risk, to live many years without the constraint of a daily treatment and calmly await the arrival of less toxic and non-treatment day (which are today possible from the work of J.Leibowitch, father of HAART, but not shockingly implemented) or eradication therapy.
According to the results of the much awaited START study, the risk of disease or death are significantly lower among people who start antiretroviral therapy when their diagnosis when their CD4 count is still high, rather than waiting until 'that it falls below 350 cells / mm3. The latest results of the study were presented at the Congress of IAS 2015 and were published simultaneously in the early edition of the American Journal "New England Journal of Medicine" dated July 20, 2015.
“Positifs” does not share the beliefs of the authors of the study on the merits of early treatment. Indeed the START trial is a statistical study of 4685 patients followed for 3 years. Or recall to the uninitiated that more study is about the number the easier it is to demonstrate what we want. This multicenter trial conducted in 35 countries and funded by the American NIH with a huge budget and the results were taken and recommended, without critical analysis by WHO and UNAIDS show collusion NIH, pharmaceutical lobbies, WHO, UNAIDS.
Overall after 3 years, if we consider the non-serious and serious events related to HIV and the deaths were 1.8% of patients in the early group and 4.1% in the delayed group representing a 57% reduction. The most common events being tuberculosis and cancer. These high percentages of events for patients still having a well-preserved immunity seems to us suspect and casts doubt on the conclusions of the START study
If we honestly consider the START study, and which is taken up in detail the results of the test, we realize that there is no significant difference in the number of deaths (12 and 21 respectively) . Even if the reasons for these deaths are not explained, it seems surprising that apart from various accidents and suicides, today we can still die of HIV given the existing therapeutic arsenal. These deaths rather bad sign monitoring patients and poor therapeutic strategies.
Concerning tumoral pathologies were observed 0.20 cases / 100 patients / year in the early group and 0.56 event / 100patients / year in the delayed group, but the difference is significant after one year. For Kaposi's sarcoma were 11 cases in the delayed group and 1 in the early group. These figures seem overstated us in relation to all the data already published for HIV + patients still having a well-preserved immunity (CD4> 350).
Regarding serious cardiovascular events there is no significant difference between the 2 groups (14 and 12 cases).
In summary, even assuming that this study has not been tampered with, only the well-informed patient is entitled to decide whether or not to start antiviral treatment as soon as he knows his HIV status when he had CD4 high and normal (600-1000) and low viral load, taking a risk of 5.6 / 1000par year instead of 2/1000 per year of contracting a tumor pathology.
Note that the only interest to the community of early treatment is the lack of contamination of the partners as soon as viral load falls below 1000copies while condom use has the same effect but with a very low cost and without toxicity. Moreover, it seems to us wanting indecent to treat patients who do not really need, so that we do not have the financial means to deal with tens of millions of HIV around the world that we really need!
For eradication, Asier Sáez-Cirion presented the case of a girl who was infected at birth and was immediately treated with antiretroviral therapy when she was a child. She has not taken antiretroviral therapy for twelve years, since the age of six years, with a viral load well below the limits of detectability of standard tests. People in this type of unusual situation (also called post-processing controllers), represent a functional model of healing, one of the objectives of the research on treatment. It appears indecent that such  case be presented as a useful model in the search for healing, whereas healing not only functional but real exists.This revolutionary  cure has be presented by Dr Prakask in off, at Institut Pasteur in Paris since more than two years  (see on this site C.92- Revolution hidden in the eradication of the virus HIV-treatment of Dr Prakash), with  some patients cured since 5 years. This work which is known by  our scientific authorities (F.Barré-Sinoussi, Luc Montagnier, C.Katlama, JF Delfraissy ...), are beautifully obscured. It is lamentable and criminal Dr. Prakask was not the guest of honor at the conference!


Among the many works presented include:
-the association Long-term non-progressors and alteration in the metabolism of cholesterol (MOPEA013 G.Rappocciolo et al)
-the antibodies against 3S motif of gp41 protects the fall in CD4 (MOPEA014-V. Old Man et al). Indicate that the therapeutic vaccine VAC-3S, which is one of C.Katlama responsible! Is based on this result. - IPROTECT1 MULTICENTRE EUROPEAN TEST VACCINE 6 therapeutically VAC-3S tested on patients with undetectable viral load after 12 weeks it shows an increase in the CD4 / CD8 0,48au starting at 0.49 or 0.57 depending on the dose injected.
- Zinc Deficiency in HIV + and inflammatory reaction. Inverse correlation between CRP and Zn concentration. Interest  of supplementation (KC MOPEB184- Poudel et al)
-Interest of supplementation of  lactobacillus casei (TUPEB295- H. Ichimura et al). The effect of lactobacillus casei, Shirota strain, was tested on 60 children, 31 on HAART and 29 without HAART for 8 weeks and 20 HIV-. CXCR3CCR6-CD4 and CD4 + significantly increases and the percentage of CD4 in the 3 groups . The activation of CD8 + greatly decreases in HIV + without HAART, weakly in HIV-. Viral load decreases slightly but significantly in the group without HAART .The concentration of lactobacillus and bifidobacterium increases significantly in the stool. It might be recommended to supplement with Lactobacillus casei for HIV for which CD4 capped at an insufficient level, but also to accelerate the fall of viral load.

-the doravine, a new NNRTI is as effective as efavirenz but with fewer side effects


 
C.97-8° IAS 2015- Victoire des lobbys pharmaceutiques-le traitement antiretroviral à vie pour tous!
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La dernière conférence de l’international AIDS Society(IAS), sur la pathogénèse du HIV, ses traitements et sa prévention s’est tenue à Vancouver (Canada)  du 19 au 22 Juillet 2015. Elle    a réuni plus de 6000 participants mais est devenue au fil des années une foire mercantile( sponsorisée par les laboratoires) ayant pour but quasiment exclusif  la promotion, avec des arguments contestables, de traitements toujours  toxiques et de plus étendus  à des populations de plus en plus nombreuses pour qui l’utilité est loin d’être démontrée.

L’ensemble des informations présentées dans cette conférence se trouvent sur le site

Abstracts : http://www.ias2015.org/WebContent/File/IAS_2015__MED2.pdf

Une quantité impressionnante d’informations au niveau fondamental, clinique, prévention et social, ont été fournies. Malheureusement, rien   d’essentiel au niveau de l’attente des patients : vaccin préventifs ou thérapeutiques validés, voies efficaces  d’éradication ou de réduction des réservoirs, traitements non toxiques,…. n’a  été apporté.

Rappelons pour mémoire que la prise d’antiviraux à long terme peut  provoquer des désordres métaboliques(anomalies lipidiques, diabète), des  toxicités hépatique, rénale, cardiaque, induire des problèmes osseux, des neuropathies périphériques et même des problèmes de libido (troubles érectiles). Ces effets indésirables des antiviraux pouvant conduire à des pathologies graves et à des décès, le patient doit en être informé honnêtement et ne pas subir un matraquage médiatique afin de  choisir et accepter librement un traitement.

La prophylaxie pré-exposition (PrEP) a été l’un des principaux sujets de discussion à l’ IAS 2015: Comment la prendre, qui devrait pouvoir la prendre et quand sera-t’elle disponible?Trois études présentées  montrent que pour certaines personnes, dans certains contextes, une utilisation moins fréquente de la PrEP, avec des doses déterminées en fonction de l’activité sexuelle, était réalisable, et qu’un nombre élevé de rapports sexuels restaient protégés par la PrEP. Ceci pourrait offrir aux individus qui veulent utiliser la PrEP, et à leurs médecins, des options supplémentaires, leur permettant ainsi de trouver une façon de prendre la PrEP qui leur convienne mieux.

Cependant notre association «  Positifs » ne souhaite pas que cette prévention qui est très marginale, devienne majoritaire, sauf peut-être sur des groupes à très fort risque, tels les prostitué(e)s. Nous maintenons que la seule prévention, sure, facile  à mettre en œuvre et d’un coût dérisoire( qui devrait être gratuite)est le préservatif, qui malheureusement ne fait pas suffisamment l’objet de campagnes de promotion par les systèmes de santé nationaux. La PrEP ne servira si elle s’impose à une majorité qu’à engraisser un peu plus les lobbys au détriment de la santé des utilisateurs qui consommeront à long terme  des produits toxiques et en spoliant encore un peu plus les systèmes de couverture médicale exsangue.

Une étude,encore au service des lobbys pharmaceutiques, présentée par Myron Cohen, a montré que  le partenaire d’un patient séropositif, ayant une charge virale indétectable évite la transmission s’il utilise une PrEP, alors que l’on sait depuis plus de 10 ans qu’un séropositif ayant une charge virale indétectable n’est pas contaminant !!La PrEP dans ce cas est inutile et criminelle pour les partenaires séronégatifs d’autant que le préservatif peut être utilisé en toute occasion.

Nous considérons que la meilleure manière de stopper la transmission est de tester de manière autoritaire l’ensemble de la population puisque plus de 50% des séropositifs ignorent leur statut et constituent ainsi le vecteur majeur de transmission, de rendre le préservatif gratuit, et de responsabiliser les séropositifs.

L’étude START considère apporter des preuves « définitives » sur les avantages du traitement précoce ?

Rappelons pour mémoire que le seuil de démarrage d’un traitement antiviral a été depuis 20 ans, sous la pression des lobbys pharmaceutiques, et d’expérimentateurs d’essais complaisants,  systématiquement relevé, passant de 200, où les risques d’infections opportunistes sont très minimes, à 350, puis 500 et aujourd’hui   à l’annonce de la séropositivité(avec des valeurs normales dans la gamme 500-1000).

Soulignons de plus que le démarrage immédiat d’un traitement, impose à des patients qui pourraient être non progresseurs, mais non identifiés, de  subir pendant de longues années(5, 10 ans parfois plus) l’agression de traitements toxiques avec leur cortège d’effets indésirables. Pour la majorité des patients, le démarrage d’un traitement à 300-350 CD4, permet avec un risque négligeable de vivre plusieurs années sans  la contrainte d’un traitement journalier  et d’attendre sereinement l’arrivée de traitements moins toxiques et non journaliers( qui sont possible aujourdhui depuis les travaux du J.Leibowitch, père des trithérapies, mais ne sont pas scandaleusement  mis en oeuvre ) ou d’un traitement d’éradication.

Selon les résultats très attendus de l’étude START, les risques de maladies ou de décès sont notablement moins élevés chez les personnes qui commencent le traitement antirétroviral dès leur diagnostic, lorsque leur taux de cellules CD4 est encore élevé, plutôt que d’attendre jusqu’à ce qu’il chute en dessous de 350 cellules/mm3. Les derniers résultats de l’étude ont été présentés au congrès de l’IAS 2015 et ont été publiés en même temps dans le tirage précoce du Journal américain « New England Journal of Medicine » daté du 20 Juillet 2015.

Positifs ne partage pas les convictions des auteurs de l’étude sur le bien fondé d’un traitement précoce. En effet l’essai START est une étude statistique portant sur 4685 patients pour un suivi de 3 ans. Or rappelons pour les non initiés que plus une étude porte sur le grand nombre plus il est facile de démontrer ce que l’on souhaite . Cet essai multicentrique réalisé dans 35 pays et financé par le NIH americain avec un budget colossal dont les résultats ont été repris et recommandés, sans analyse critique par l’OMS et l’ONUSIDA, montrent la collusion NIH, lobbys pharmaceutiques, OMS, ONUSIDA.

Globalement au bout de 3 ans, si l’on considère les évenements non serieux et serieux liés au HIV ainsi que les décès on a 1,8% des patients dans le groupe précoce et 4,1% dans le groupe différé ce qui représente une réduction de 57%. Les évènements les plus fréquents étant la tuberculose et les cancers. Ces forts pourcentages d’évènements pour des patients ayant encore une immunité bien conservée, nous parait suspect et jette le doute sur les conclusions de l’étude START

Si l’on considère honnête l’étude START et que l’on reprend dans le détail les résultats de l’essai, on s’aperçoit qu’il n’y a pas de différence significative sur le nombre de décès(12 et 21 respectivement).Même si les raisons de ces décès ne sont pas explicités, il nous semble surprenant qu’en dehors des suicides et accidents divers, on puisse encore décéder aujourd’hui du HIV compte tenu de l’arsenal thérapeutique existant. Ces décès signent plutôt un mauvais suivi des patients et de mauvaises stratégies thérapeutiques.

Concernant les pathologies tumorales on a observé 0,20 cas/100 patients/an dans le groupe précoce et  0,56 cas/ 100patients/an dans le groupe différé, mais la différence n’est significative qu’après un an. Pour le sarcome de Kaposi on a 11 cas dans le groupe différé et 1 dans le groupe précoce. Ces chiffres nous paraissent surestimés par rapport à l’ensemble des données déjà publiées pour des patients HIV+ ayant encore une immunité bien conservée( CD4>350).

Concernant les accidents cardiovasculaires sérieux il n’existe pas de différence significative entre les 2 groupes(14 et 12 cas).

En résumé, même en supposant que cette étude n’ait pas été trafiquée, seul le patient bien informé est habilité à décider s’il souhaite ou non  démarrer un traitement antiviral dès qu’il connait sa séropositivité, alors qu’il a des CD4 élevés et normaux (600-1000) et une faible charge virale, en prenant un  risque  de 5,6/1000par an au lieu de 2/1000 par an de contracter une pathologie tumorale.

Soulignons que le seul intérêt pour la collectivité d’un traitement précoce est  l’absence de contamination des partenaires,  dès que la charge virale devient inférieure à 1000copies alors que l’utilisation du préservatif a le même effet mais avec un coût dérisoire et sans toxicité. Par ailleurs, il nous parait indécent de vouloir traiter des patients qui n’ont pas vraiment besoin, alors que l’on ne dispose pas des moyens financiers pour traiter les dizaines de millions de séropositifs de par le monde qui on en vraiment besoin !

Concernant l’éradication,  Asier Saez-Cirion a présenté le cas d’une jeune fille qui avait été infectée à la naissance et qui avait été immédiatement traitée avec un traitement antirétroviral quand elle était enfant. Elle n’a pas pris de traitement antirétroviral pendant douze ans, depuis l’âge de six ans, avec une charge virale bien en dessous des limites de détectabilité des tests de norme. Les personnes dans ce type de situation inhabituelle (également appelés contrôleurs post-traitement), représentent un modèle de guérison fonctionnelle, un des objectifs de la recherche sur le traitement. Il nous apparait indécent qu’un tel cas soit présenté comme un modèle utile dans la recherche de la guérison, alors que la guérison non seulement fonctionnelle mais réelle existe déjà. Elle   à été apportée il y a déjà deux ans par le Dr Prakask(  voir sur ce site C.92- Révolution occultée dans l’éradication du virus HIV- le traitement du Dr Prakash) qui a  un recul de 5 ans sur certains  patients.  Ces travaux connus par nos autorités scientifiques( F.Barré-Sinoussi, Luc Montagnier, C.Katlama, JF Delfraissy…), sont superbement occultées. Il est lamentable et criminel que le Dr  Prakask n’ait pas été l’invité d’honneur de cette conférence !

Parmi les très nombreux travaux présentés citons :

–l’association des long terme non progresseurs et l’alteration du métabolisme du cholesterol(MOPEA013 G.Rappocciolo et al)

-les anticorps contre le motif 3S de la gp41 protège de la chute des CD4(MOPEA014-V. Vieillard et al). Indiquons que le vaccin thérapeutique VAC-3S, dont C.Katlama est l’une des responsables !, est basé sur ce résultat. - IPROTECT1 ESSAI MULTICENTRIQUE EUROPEEN 6 VACCIN THERAPEUTIQUE-  VAC-3S Testé sur des patients ayant une charge virale indétectable, il montre après 12 semaines   une augmentation du rapport CD4/CD8 de 0,48au départ à 0,49 ou 0,57 selon la dose injectée.

-Déficit en Zn et HIV– Déficit en Zn chez HIV+ et réaction inflammatoire. Corrélation inverse entre CRP et concentration en Zn. Intérêt d’une supplémentation( MOPEB184-  K.C Poudel et al)

-intérêt d’une supplémentation en lactobacillus casei (TUPEB295- H. Ichimura et al). L’effet   de lactobacillus casei, souche Shirota a été testé sur 60 enfants : 31 sans HAART et 29 sous HAART pendant 8 semaines ainsi que 20HIV-. CD4 et CXCR3CCR6-CD4+ augmente de manière significative ainsi que le pourcentage de CD4 dans les 3 groupes .L’activation desCD8+ décroit très fortement chez les HIV+ sans HAART et faiblement chez les HIV-. La charge virale  décroit faiblement mais de manière significative dans le groupe sans HAART .La concentration de lactobacillus et de bifidobacterium augmente de manière significative dans les selles. Il pourrait être recommandé de supplémenter en lactobacillus casei pour les séropositifs pour lesquels les CD4 plafonnent à un niveau insuffisant, mais également pour accélerer  la chute de la charge virale.

-La doravirine, un nouvel INNTI est aussi efficace que l'efavirenz mais avec moins d'effets secondaires

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C.96-PROSTATE CANCER AND CADMIUM : A SILENT INODORE TOXIC PENETRATING BY INHALATION.
Poster présenté à 

Association de la Recherche contre les Tumeurs de la Prostate ARTP 2014, 19 November, Paris Palais des Congrès

 

                                                                                                                   Results

Most important, as Cadmium half-life is as long as 30 years (Leblanc JC, 2006), it is not eliminated spontaneously and accumulates in the prostate with time, which corresponds to an increased PK risk with age. Cadmium vapours, even in the solid state, penetrate insidiously, are odorless and tasteless. Molluscs (mussels, oysters), crustaceans organism. Tobacco contains Cadmium, [but also dioxine TCDD (→ Ha-Ras mutations), nitrosamines (→ Ki-Ras mutations)]. The Hazard Ratio for PK specific mortality is 1.82 if the patient smokes (Kenfield SA, 2011). Occupational studies show a correlation with the professional work in contact with Cadmium (Kjellstrom T, 1979, in Sweden).

                                                                                                              C-Myc oncogen

Cadmium increases the oncogene c-Myc in renal (Tang N, 1991) and RWPE-1 prostatic cells (Achanzar WE, 2000). C-Myc stimulates telomerase promoter  (high levels in PK). C-Myc up-regulates the androgen receptor messenger RNA (Grad J, 1999). Myc confers androgen-independent prostate cancer cell growth (Bernard D, 2003; Kokontis J, 1994).  C-myc transgenic mice develop prostatic intra-epithelial neoplasia (Zhang X, 2000).

Loss Of Heterozygosity (LOH) of Bin-1(Bridging integrator 1) located at chromosome 2q14, an anti-Myc tumor suppressor is found in 42% of KP, in metastatic tumors and androgen-independent tumor cell lines (Ge K, 2000; Sakamuro D, 1996; Schmidt EV ). Subjects with Bin-1 LOH are likely to be more vulnerable to Cadmium oncogenicity.
                                                                                                            Conclusion

Cadmium is a risk factor in a PK subgroup; 3 high-quality studies of toenail selenium and PK risk indicated a reduction in PK risk (Relative Risk = 0.29) with a toenail selenium concentration 0.85-0.94 μg/g (Hurst R, 2012).

TheUS Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed that a long term supranutritional supplemental dose of selenomethionine (200 μg/d) in a selenium-replete population did not significantly reduce the risk of developing prostate cancer. However no data on the cadmium level were presented (Lippman SM, 2009).

ALA, thioctic acid) are Cadmium chelators (El-Maraghy SA,2011). Some soils are rich in Cadmium: in the surrounding area of discharges, gold mines (Orbiel valley, where snails have a Cadmium level 30 times the normal value), dams funds (Sauviat); professionally, workers at risk are those of Cadmium-Nickel battery (Sahmoun AE, 2005), anti-corrosion coating, plastic paints, luminescent materials, metalworking (INRS toxicological card, 1992).

A systematic study of toenail Cadmium levels by graphite-furnace atomic absorption spectrometer is advocated in PK. For this subgroup, Cadmium chelation by Selenium (+ vitamine E) and ALA is logical. Heavy metal detoxification by parsley, coriander, garlic (allium ursinum) may be useful (Willem JP, 2014).


                                                                                                                          Bibliography

Achanzar WE et al. Cadmium induces c-myc, p53, and c-jun expression in normal human prostate epithelial cells as a prelude to apoptosis. Toxicol Appl Pharmacol 2000, 164: 291-300. Bernard D et al. Myc confers androgen-independent prostate cancer cell growth. J Clin Invest 2003, 112: 1724-31. Bryś M et al. Zinc and cadmium analysis in human prostate neoplasms. Biol Trace Elem Res 1997, 59:145-52. Ekman P. Genetic and environmental factors in prostate cancer genesis: identifying high-risk cohorts. Eur Urol 1999, 35: 362-9. El-Maraghy SA, Nassar NN. Modulatory effects of lipoic acid and selenium against cadmium-induced biochemical alterations in testicular steroidogenesis. J Biochem Mol Toxicol 2011, 25: 15-25.     Ge K et al. Loss of heterozygosity and tumor suppressor activity of Bin1 in prostate carcinoma. Int J Cancer 2000, 86: 155-61.  Goyer RA, Liu J, Waalkes MP. Cadmium and cancer of prostate and testis. Biometals 2004,17: 555-8.   Grad JM et al. Multiple androgen response elements and a Myc consensus site in the androgen receptor (AR) coding region are involved in androgen-mediated up-regulation of AR messenger RNA. Mol Endocrinol 1999, 13: 1896-911. Hurst R et al. Selenium and prostate cancer: systematic review and meta-analysis. Am J Clin Nutr 2012, 96:111-22.      Julin B et al. Dietary cadmium exposure and prostate cancer incidence: a population-based prospective cohort study. Br J Cancer 2012, 107: 895-900. INRS toxicological card, 1992   Kenfield SA et al. Smoking and prostate cancer survival and recurrence. JAMA 2011, 305: 2548-55.     Kjellström T et al. Mortality and cancer morbidity among cadmium-exposed workers. Environ Health Perspect 1979, 28:199-204.  Kokontis J. Increased androgen receptor activity and altered c-myc expression in prostate cancer cells after long term androgen deprivation. Cancer Res 1994, 54: 1566–73           Leblanc JC et al. CALIPSO. Etude des consommations alimentaires de produits de la mer et imprégnation aux éléments traces, polluants et oméga 3 . Rapport d'étude Afssa, Ministère de l'Agriculture et de la Pêche, INRA . 2006 Oct, 106 p. Lippman SM. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009, 301:39-51.    Morganti G et al. [Clinico-statistical and genetic research on neoplasms of the prostate]. Acta Genet Stat Med 1956-1957, 6: 304-5. French.   Ogunlewe JO, Osegbe DN. Zinc and cadmium concentrations in indigenous blacks with normal, hypertrophic, and malignant prostate. Cancer 1989, 63:1388-92.    Sahmoun AE et al. Cadmium and prostate cancer: a critical epidemiologic analysis. Cancer Invest 2005, 23: 256-63. Sakamuro D et al. BIN1 is a novel MYC-interacting protein with features of a tumour suppressor. Nat Genet 1996,14: 69-77.    Sanchez Garcia A et al. Geochemical prospection of cadmium in a high incidence area of prostate cancer, Sierra de Gata, Salamanca, Spain. Sci Total Environ 1992,116: 243-51.    Schmidt EV.  MYC family ties. Nat Genet 1996, 14: 8-10. Schöpfer J. Selenium and cadmium levels and ratios in prostates, livers, and kidneys of nonsmokers and smokers. Biol Trace Elem Res. 2010,134:180-7.    Tang N, Enger MD. Cadmium induces hypertrophy accompanied by increased myc mRNA accumulation in NRK-49F cells. Cell Biol Toxicol 1991, 7: 401-11.     Tang N, Clapper JA, Enger MD. Cd++ inhibits EGF induced DNA synthesis but not EGF induced myc mRNA accumulation in serum starved NRK-49F cells. Cell Biol Toxicol 1991, 7: 35-47.    Vinceti M et al. Case-control study of toenail cadmium and prostate cancer risk in Italy. Sci Total Environ 2007, 373: 77-81.     Waalkes MP et al. Carcinogenic effects of cadmium in the noble (NBL/Cr) rat: induction of pituitary, testicular, and injection site tumors and intraepithelial proliferative lesions of the dorsolateral prostate. Toxicol Sci 1999, 52: 154-61.   West DW et al. Adult dietary intake and prostate cancer risk in Utah: a case-control study with special emphasis on aggressive tumors. Cancer Causes Control 1991, 2: 85-94. Willem Jean-Pierre. Les dégâts des métaux lourds. Sept 2014  (Guy Trédaniel Ed.) 268 pages.     Yoshizawa K. Study of prediagnostic selenium level in toenails and the risk of advanced prostate cancer. J Natl Cancer Inst 1998, 90: 1219-24.   Zhang X et al. Prostatic neoplasia in transgenic mice with prostate-directed overexpression of the c-myc oncoprotein. Prostate 2000, 43: 278-85

 


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