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Written by TRAN Guy Mong Ky   
Tuesday, 15 December 2015 17:36
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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: This e-mail address is being protected from spambots. You need JavaScript enabled to view it . Phone: +33 9 81 89 38 70.

BACKKROUND Endothelin (ET-1, 2, 3) (Yanagisawa M, 1989) is mitogenic for 3T3 fibroblasts (Takuwa N, 1989), induces osteoblast proliferation and is involved in osteoblastic bone metastases of Prostatic Cancer (PK) with translocation TMPRSS2:ERG gene fusion (Delliaux C, 2014). We found earlier by centering on the HQLL motif that:

HPV-18  E2           IQTLNHQVL

contains the osteoprotegerin active site           ET  SHQLL

as well as parathormone (PTH)                           IQ LMHNL

and  PTH-related Protein (PTHrP)                        S EHQLL

that could explain PK osteoclastic bone metastasis (Tran GMK, 2004). We search for an endothelin in HPV that could explain osteoblastic bone metastasis.

METHODS Amino acid sequences and three dimensional structure (3D) comparison between HPV and ET.

RESULTS By centering on the crucial tryptophan W21, which removal decreases ET potency by a factor > 1000 (Kimura S, 1988), we found that

HPV (cand 89), -150, -160 E6                  34-EL-35         48-LDIVW-52  is homologous to the

ET-1,-2,-3/sarafotoxin active site                5-DM-6          17-LDI IW-21

In 3D structure, HPV E6 has 2 separated functional sites, centered on the COOH-terminal tryptophane W 21 and on 5-DM-6 (of sarafotoxine). The homologous sequence LNVVW is found in HPV-3, -28, -29, -68 ME 180. In HPV-18 E6, W was replaced by Y. Burrowing asp Attractaspis engaddensis sarafotoxin, which induces a coronary spasm, differs slightly from ET:QDVIW (where Q replaced L).

Weak but highly selective ET-A Receptor antagonists were isolated from Streptomyces Misakiensis and sp n° 7338 (Miyata S, 1992). Highly potent and selective ET-A Receptor antagonist structures are pentapeptides:

cyclo (D-Asp-Pro-D-Val-Leu-D-Trp) (Ihara M, 1992) and

cyclo (D-Asp-Pro-D-Ile -Leu-D-Trp) (D=Dextrogyre) (Lippton, 1993).

CONCLUSION The molecular homology of HPV E6 with the active site of Endothelin, implicated in PK bone metastasis, supports further the HPV role in KP, not only in the primary tumor, but also specifically in osteoblastic bone metastasis. Interestingly, high doses of Vitamin C has an anti-Endothelin action (Dow C, 2015).

BIBLIOGRAPHY Delliaux C, Endothelin-1, a gene regulated by TMPRSS2:ERG fusion proteins in prostate cancer bone metastases. ARTP, Paris, Nov 19 2014. Ihara M. Biological profiles of highly potent novel endothelin antagonists selective for the ETA receptor. Life Sci 1992, 50: 247-55. Dow C.Vitamin C Supplementation Reduces ET-1 System Activity in Overweight and Obese Adults.14th Int Conf on Endothelin: Physiology, Pathophysiology and Therapeutics. Press release of the Am Physiol Soc, 4th September 2015, Kimura S. Structure-activity relationships of endothelin: importance of the C-terminal moiety. Bio Bio Res Com 1988, 156: 1182-6. Miyata S. WS-7338, new endothelin receptor antagonists isolated from Streptomyces sp. No. 7338. I. Taxonomy, fermentation, isolation, physico-chemical properties and biological activities. J Antibiot (Tokyo) 1992, 45: 74-82; 83-7; 698-703;788-91; 1029-40; 1041-6. Lippton. Am Heart Assoc, 66th Scientific Sessions, Georgia World Congress, Nov 8-11, 1993. Takuwa N. A novel vasoactive peptide endothelin stimulates mitogenesis through inositol lipid turnover in Swiss 3T3 fibroblasts. J Biol Chem 1989, 264: 7856-61. Tran GMK, Role of human papillomavirus type 18 in a subgroup of prostatic cancer with bone metastasis: Its protein E2 contains the osteoprotegerin active site EuroConf Cancer, Pasteur Inst. Jan 15-16 2004. Yanagisawa M. Molecular biology and biochemistry of the endothelins. Trends Pharmacol Sci 1989, 10: 374-8. Review.

Last Updated on Tuesday, 15 December 2015 17:55
Written by TRAN Guy Mong Ky   
Sunday, 13 December 2015 21:50
There are no translations available.


Présenté à

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: This e-mail address is being protected from spambots. You need JavaScript enabled to view it . Phone: +33 9 81 89 38 70.

BACKROUND HPV are found in Prostatic Cancer (PK) by PCR only when the primer is E (=Early) and not L (=Late) (Tran GMK, 2004). This particularity may be explained by L loss during integration (Johansson H, 2013). Cripto-1 (Teratocarcinoma-Derived Growth Factor-1), a member of Epidermal Growth Factor (EGF) family, is involved in PK progression (Terry S, 2013, 2015). It is a co-receptor of TGF-β, induces E-Cadherin loss (Zhong XY, 2008) in Epithelial to Mesenchymal Transition (Thiery JP, 2002) and stimulates the PI3K/Akt pathway. E-Cadherin down regulation can also be induced by HPV E6 (Matthews K, 2003). As HPV contains many oncogenes implicated specifically in PK [HPV-11 E2 = EGF-HRG-TGFα mitogens chimera (Tran MKG, 1997) with a common MHIESL hexapeptide, Osteoprotegerin in bone metastases (Tran GMK, 2004), Nucleophosmin 1 (NPM1) in androgeno-regulation (Tran GMK, 2014)], we search for a molecular homology between Cripto-1 and HPV.

METHODS Amino acid sequences comparison of HPV with Cripto-1 EGF motif        



HPV-18 E2                                   113-CFkKGGqTV 45-YFdGNK D 127-DGNKDNC

Cripto-1                                         83-CL


A      S                                           D W T      323-PPNN   L  KCWR  Q RC    122-VQVYF

matches with Cripto-1                        120-D(W,T)L      124-LPKKcsLcKCWHgQlRC    142-PQAFL

CONCLUSION The discovery of Cripto-1 being a viral HPV-18 E2 oncogene, whereas EGF is a HPV-11 E2, confirms the HPV role in PK, and E-cadherin loss as a factor of metastasis. A safe and efficient vaccine is warranted, as Gardasil and Gardasil 9 based on L1 may be followed by menopause/sterility and  multiple sclerosis, and Cervarix by thrombocytopenia. A BT PHARMA vaccine based on a HPV-16 and -18 oncogene E7, instead of L1 as in Gardasil and Cervarix, is in phase II trial at the Pasteur Institute (Paris). E7 is much smaller than L1 and has less worrying epitopes.

BIBLIOGRAPHY Matthews K. Depletion of Langerhans cells in human papillomavirus type 16-infected skin is associated with E6-mediated down regulation of E-cadherin. J Virol 2003, 77: 8378-85. Terry S. Involvement of CRIPTO-1 in progression of prostate tumors. Eurocancer, Paris, June 25-26, 2013. Terry S. CRIPTO overexpression promotes mesenchymal differentiation in prostate carcinoma cells through parallel regulation of AKT and FGFR activities. Oncotarget 2015, 6: 11994-2008. Thiery JP.  Epithelial-mesenchymal transitions in tumour progression. Nat Rev Cancer 2002, 2: 442-54. Tran MKG. Human Papillomavirus (HPV) E2 protein contains a chimera of epidermal growth factor (EGF) and EGF family mitogens: Heregulin and Tumor Growth Factor. 6th Eur HIV Conf, Hamburg 1997, P474. Tran GMK. Role of human papillomavirus type 18 in a subgroup of prostatic cancer with bone metastasis: Its protein E2 contains the osteoprotegerin active site. EuroConf Cancer, Pasteur Inst. Jan 15-16 2004. Tran GMK. Prostatic cancer of viral origin: Homology of human oncogenic papillomavirus (HPV) L1 with nucleophosmin (NPM1), a controller of androgen receptor transcription. ARTP, Nov 19, 2014, Paris. Zhong XY. Positive association of up-regulated Cripto-1 and down-regulated E-cadherin with tumour progression and poor prognosis in gastric cancer. Histopathology. 2008, 52: 560-8.


Last Updated on Tuesday, 29 December 2015 19:52
Written by TRAN Guy Mong Ky   
Sunday, 13 December 2015 21:11
There are no translations available.



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: This e-mail address is being protected from spambots. You need JavaScript enabled to view it . 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


Last Updated on Sunday, 13 December 2015 21:12
Written by TRAN Guy Mong Ky   
Saturday, 21 November 2015 16:56
There are no translations available.


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: This e-mail address is being protected from spambots. You need JavaScript enabled to view it . 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


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.




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.


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.



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, for financial support.

Last Updated on Saturday, 21 November 2015 17:02
C.97bis -8 ° IAS 2015- Victory of pharmaceutical lobbies - life antiretroviral treatment for all! PDF print email
Written by Dr Adrien Caprani   
Wednesday, 09 September 2015 16:11
There are no translations available.

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
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 to us that such indecent case is presented as a useful model in the search for healing, while healing not only functional but real exists. It has been paid there are already two years by Dr. Prakask (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

Last Updated on Saturday, 12 September 2015 11:48

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