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Written by Pierre Lance
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Thursday, 07 June 2018 18:31 |
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There are no translations available.
Article paru dans la revue Alternatif Bien-Être, rendu public. Il illustre la collusion avérée entre l'industrie pharmaceutique,les medias et les pouvoirs publics dans la politique sanitaire mondiale
Comme tous les gens bien informés le savent, le complexe pharmaco-industriel mondial (que j’ai surnommé dans mes ouvrages « le tyrannosaure ») est une véritable mafia qui a mis toute l’humanité en coupe réglée et qui fait la pluie et le beau temps au sein de toutes les «Autorités de santé» de dizaines de nations réputées indépendantes.
Or, en ce qui concerne la santé, ou plus exactement la maladie, aucun État n’est véritablement libre de ses choix, car la grande majorité de ses «experts» sont en conflit d’intérêts avec les grands laboratoires, dont ils sont salariés ou actionnaires. Aussi est-il de plus en plus urgent que les démocraties, à commencer par la France, veillent à ce que les décideurs des divers organismes de santé soient totalement indépendants de l’industrie pharmaceutique, faute de quoi il n’existera bientôt plus aucune liberté du citoyen en ce qui concerne sa santé et celle de sa famille. Sous prétexte de le «protéger», des décisions bafouant délibérément ses droits les plus élémentaires lui seront imposées.
Un prix Nobel face au tyrannosaure
L’une des plus grandes victoires (que j’espère provisoire) du « tyrannosaure » a été remportée récemment en France et en Italie par l’obligation de 11 vaccins infligés à nos bébés, alors que rien ne pouvait justifier une telle mesure, qui est une atteinte caractérisée à nos droits constitutionnels. Faut-il que le « tyrannosaure » soit puissant pour qu’il soit parvenu à circonvenir le Président Emmanuel Macron, qui fut pourtant élu dans le but de réformer et fortifier la démocratie française. Toutefois, la guerre des vaccins n’est pas terminée, et l’on voit de nombreux David saisir leur fronde afin de terrasser le monstrueux Goliath, empereur des seringues.
Le Pr Luc Montagnier lors d’un congrès à Lindau, en Allemagne
Parmi ces David figure désormais le Professeur Luc Montagnier, Prix Nobel de physiologie ou médecine, ancien professeur émérite à l’Institut Pasteur, directeur émérite de recherche au CNRS, ancien professeur à l’Université de New-York et membre des Académies des sciences et de médecine. Mais Luc Montagnier étant un esprit libre, qui a toujours refusé de se plier aux ukases des mandarins conformistes, il a poursuivi de nombreuses recherches personnelles en sortant des sentiers battus, ce qui lui a valu de féroces inimitiés. D’autant qu’il a pris fait et cause pour deux de mes « savants maudits », Mirko Beljanki et Jacques Benveniste.
Il a même annoncé en 2010 qu’il fuyait le «climat de terreur intellectuelle» qui sévit en France et il a pris la direction d’un institut de recherche à l’Université Jiaotong de Shangaï. Mais c’est en novembre 2017 qu’il a mis le comble à la fureur du « tyrannosaure » en alertant l’opinion sur les risques liés aux vaccins et en prenant nettement position, en compagnie du Pr Henri Joyeux, chirurgien cancérologue, contre la nouvelle loi infligeant aux nouveau-nés 11 vaccins obligatoires.
La presse complice
Dès lors, Luc Montagnier est devenu le nouvel « homme à abattre » et la mafia médico-pharmaceutique a mobilisé le ban et l’arrière-ban des mercenaires de la presse conformiste pour tenter de discréditer Luc Montagnier dans l’opinion publique. La dernière en date des attaques en règle contre ce grand scientifique est parue dans « Le Point » (N° 2386 - 24 mai 2018). J’avoue que, jusqu’ici, je considérais « Le Point » comme un journal sérieux. Depuis ce 24 mai, il a beaucoup baissé dans mon estime, car il a ouvert ses colonnes à un article qui déshonore les journalistes qui l’ont commis.
Sous le titre « Mais qu’arrive-t-il au Pr Montagnier ?», deux folliculaires nommés Thomas Mahler et Violaine de Montclos, à l’évidence dûment chapitrés par le « tyrannosaure », et dont les connaissances médicales doivent être proches de zéro, se sont permis d’aligner un ramassis de moqueries, de rumeurs, de ragots assaisonnés par une pétition « anti-Montagnier » signée à l’aveuglette par les moutons de Panurge du corps médical. Les rédacteurs de ce galimatias nous disent, dès les premières lignes, avoir assisté à la conférence Montagnier/Joyeux, qu’ils nous présentent ainsi : « Sur la scène du Théâtre Michel, ce 7 novembre 2017, deux personnages donnent (...) une drôle de farce. »
Ainsi, d’entrée de jeu, le ton est donné : ces deux grands médecins sont des farceurs, tenez-vous le pour dit. Et ils poursuivent : « Devant un public nombreux qui leur est tout acquis, que prophétisent les deux compères (sic) opposés tous les deux à la vaccination obligatoire ? Un « empoisonnement » général de la population, une «tempête de cytokines» dans le cerveau de nos enfants... (Je précise que les cytokines sont des substances solubles de signalisation cellulaire agissant à distance pour réguler l’activité et la fonction d’autres cellules. Donc, Montagnier et Joyeux ont parfaitement raison : Il est logique et probable qu’une injection massive de plusieurs vaccins déclenche un « affolement » des cytokines aux conséquences imprévisibles.) ...et des « corrélations temporelles sérieuses » entre la mort subite du nourrisson et l’injection de vaccins avec adjuvants à base d’aluminium.»
Une interview truffée d’arrière-pensées...
Nos deux plumitifs ont tout de même été rendre visite à leur victime avant de la flinguer sans sommation et nous annoncent ainsi l’entrevue : «...Un Luc Montagnier on ne peut plus sûr de lui nous reçoit dans les bureaux fantomatiques de sa Fondation mondiale prévention et recherche sida, abritée par le siège parisien de l’Unesco.» J’ignorais que des bureaux pouvaient être « fantomatiques » et je constate que nos deux rédacteurs du « Point » ont une approche de la langue française pour le moins approximative.
Ils nous parlent ensuite d’une pétition signée par « plus d’une centaine de membres des Académies des sciences et de médecine » et qui proclame : « Nous ne pouvons accepter de l’un de nos confrères qu’il utilise son prix Nobel pour diffuser, hors du champ de ses compétences, des messages dangereux pour la santé, au mépris de l’éthique qui doit présider à la science et à la médecine. »
Or, je précise que l’Académie des sciences compte 262 membres et l’Académie de médecine 290 (sans compter les membres étrangers). Soit au total 552 membres, ce qui réduit les signataires de la pétition à la proportion de moins d’un cinquième des académiciens. Je présume que tous les autres, qui ont certainement été sollicités, ont refusé d’attaquer un de leurs pairs sans raison crédible. Mais en outre, le texte de cette pétition est totalement grotesque. D’abord parce qu’il est absurde de prétendre que Luc Montagnier « utilise » son prix Nobel dans quelque but que ce soit. Il est Prix Nobel, point barre, et ne peut avoir aucune influence sur toutes les personnes qui jugent bon d’en faire état. Quant aux ahuris qui ont signé ce torchon, on se demande de quel droit ils se permettent d’interférer dans l’action d’un de leurs confrères qui dit ce qu’il croit juste et qui parle en s’appuyant sur ses recherches et ses connaissances, auxquelles ses censeurs n’ont pas accès.
Mais voici que nos deux rédacteurs téléguidés adoptent un autre angle d’attaque et nous disent : « Dans les années 2000, déjà, il (Montagnier) repêche l’embarrassante théorie de la mémoire de l’eau popularisée par Jacques Benveniste, que le découvreur du sida voit comme un «Galilée des temps modernes». En 1988, cet immunologiste de l’Inserm publiait une découverte qui, d’après Le Monde, pouvait «bouleverser les fondements de la physique ». Après les annonces sensationnalistes, l’expérience, non reproductible, fait vite pschitt, et si les milieux complotistes et ésotériques les encensent, les travaux de Benveniste sont balayés par la communauté scientifique. » Là, j’avoue que je reste pantois devant l’ignorance crasse et la vanité redondante de nos deux gratte-papiers du «Point», qui, de toute évidence, n’ont pas la moindre idée de ce dont ils parlent et se contentent de faire chorus avec tous les pense-petit, les pisse-vinaigre et les va-d’la-gueule de la prétendue «communauté scientifique».
Avoir raison ne donne pas bonne presse
Personnellement, je connais très bien les travaux de Jacques Benveniste, dont les expériences étaient parfaitement reproductibles (à condition évidemment qu’on veuille bien se donner la peine d’essayer de les reproduire). Non seulement Benveniste parvint à établir que l’eau conservait la trace de tout ce qui la traversait, mais il réussit même à enregistrer ces traces et à les transmettre par Internet à très longue distance. Seulement voilà, comme ses travaux donnaient l’explication fondamentale de l’efficacité de l’homéopathie malgré la disparition de toute substance matérielle (et donc par un effet de « mémorisation »), il devenait aussitôt « l’homme à abattre » pour le cartel de la pharmaco-chimie dont l’allopathie demeure l’irremplaçable vache-à-lait. (Je rappelle que pas un médecin homéopathe n’est membre de l’Académie de médecine, et que lorsque celle-ci affecte de mépriser cette thérapie, dont l’efficacité a été mille fois prouvée, elle se permet de juger une discipline qu’elle n’a jamais étudiée et à laquelle ses membres ne connaissent rien).
Bref, Jacques Benveniste fut licencié de l’INSERM et privé de tout soutien et de toute ressource jusqu’à ce que mort s’ensuive. Aussi doit-on féliciter hautement Luc Montagnier d’avoir le courage de réhabiliter Jacques Benveniste, car il devient ainsi lui-même la cible privilégiée des mercenaires du « tyrannosaure ». Son nom vient donc allonger la liste des excommuniés de l’Eglise du caducée, qui compte déjà bien des scientifiques célèbres.
Nos deux frelons du «Point», se ridiculisant eux-mêmes sans s’en rendre compte, ne se privent d’ailleurs pas d’en égratigner quelques-uns au passage, faisant écho à une prétendue « maladie du Nobel » diagnostiquée par un pourfendeur américain des « pseudo-sciences » (les cloportes de la «communauté scientifique» nomment ainsi les sciences qu’ils ne comprennent pas), notamment Linus Pauling, dont ils n’ont évidemment pas lu le moindre texte, et qu’ils maltraitent sans vergogne par ces lignes assassines : «Ainsi Linus Pauling, légende de la physique quantique et double Nobel, qui se fourvoya dans des travaux sur la vitamine C...».
Or, non seulement Linus Pauling, génie incontestable, ne s’est nullement fourvoyé, mais c’est grâce à ses expériences que le monde entier connaît les vertus de la vitamine C (ou acide ascorbique), substance indispensable aux performances de notre système immunitaire. Toutefois, la vitamine C (présente dans tous les fruits et légumes et principalement dans les agrumes) est affligée d’un inconvénient majeur : elle ne coûte presque rien et ne peut permettre à aucun laboratoire de faire fortune. C’est pourquoi les spadassins de la mafia pharmaceutique entreprirent de ridiculiser Linus Pauling et y parvinrent pour une grande part, grâce à la complicité de journalistes bigleux dont l’esprit critique était tombé dans les chaussettes. (Toutefois, je suis obligé de me demander si quelques enveloppes rebondies ne circulent pas dans les salles de rédaction, afin d’encourager parfois la «bien-pensance».)
Je vous ferai grâce de toutes les autres balivernes qui émaillent ces trois pages du «Point», dont le seul but est de jeter le discrédit sur l’un de nos plus brillants chercheurs. On nous dit, et je trouve ça très amusant, que certaines hypothèses médicales de Luc Montagnier sont « très controversées ». Parbleu ! Comme si les travaux de tous les pionniers qui s’aventurent dans les forêts vierges de la connaissance en traçant leur propre chemin pouvaient ne pas être « controversés » par la piétaille des conformistes et des médiocres qui ne savent circuler que sur les autoroutes bien balisées du «scientifiquement correct». Quoiqu’il en soit, Luc Montagnier et Henri Joyeux viennent d’adresser une requête au Président Macron pour demander que soit inscrit dans la Constitution le principe de précaution en matière de santé. Si cette requête était satisfaite, l’obligation vaccinale généralisée aurait du plomb dans l’aile, car le moins qu’on puisse dire est qu’elle foule aux pieds toute précaution envers les enfants fragiles et nos libertés essentielles du même coup.
Cela dit, je ne veux pas mettre en doute la bonne foi de M. Mahler et de Mme de Montclos, même s’ils se sont laissés trop aisément manipuler par quelques mandarins. Mais je me vois contraint de leur faire un reproche majeur : Leur conscience professionnelle de journalistes aurait dû les inciter, au minimum, à prendre connaissance de tous les arguments scientifiques et médicaux qui ont été développés par les médecins contestataires de l’obligation vaccinale, et notamment ceux du Dr Dominique Rueff, diplômé universitaire de cancérologie, publiée le 15 juillet 2017 (https://www.lettre-docteur- rueff.fr/vaccinations- obligatoires-jai-choisi-camp/) .
Enfin je me permettrai d’inciter M. Sébastien Le Fol, directeur de la rédaction du «Point» et M. Etienne Gernelle, directeur de publication, dont j’apprécie grandement les éditoriaux, de bien vouloir rappeler à leurs rédacteurs qu’ils ont un devoir d’objectivité et de loyauté et que leur travail ne consiste pas à «servir la soupe» à quelque coterie que ce soit ni à être des «snipers» médiatiques à la solde des ennemis déclarés de l’un des plus éminents esprits libres de la science française.
Pierre Lance
Pierre Lance est l’auteur d’une vingtaine d’ouvrages et notamment de la série Savants maudits, chercheurs exclus (4 tomes, 2002 à 2010 - Guy Trédaniel Editeur) qui regroupe les biographies résumées de 48 chercheurs de génie qui furent méconnus, occultés, voire persécutés par la « nomenklatura » scientifique et médicale.
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Last Updated on Saturday, 09 June 2018 18:41 |
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Written by Hyeyoung Min
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Saturday, 23 December 2017 16:42 |
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There are no translations available.
La médecine occidentale, en raison de son arrogance de supériorité, ignore et dénigre les apports des médecines traditionnelles. Nous publions ci dessous l'intérêt du ginseng rouge coréen pour lequel il a été établi une activité antivirale contre le HIV , mais également contre de nombreux virus, auquels le seropositif est sensible(infections opportunistes). Enfin, le ginseng rouge retarde l'absence de mutations du virus qui peuvent conduire à la resistance aux antiviraux. Nous avions déjà signalé (http://www.positifs.org/fr/publications/our-publications/128-c39-interet-de-lutilisation-dantimutagenes.html) le caractère anti-mutagène du ginseng rouge.
J Ginseng Res. 2016 Oct; 40(4): 309–314.
Ginseng, the natural effectual antiviral: Protective effects of Korean Red Ginseng against viral infection
Abstract
Korean Red Ginseng (KRG) is a heat-processed ginseng developed by the repeated steaming and air-drying of fresh ginseng. Compared with fresh ginseng, KRG has been shown to possess greater pharmacological activities and stability because of changes that occur in its chemical constituents during the steaming process. In addition to anticancer, anti-inflammatory, and immune-modulatory activities, KRG and its purified components have also been shown to possess protective effects against microbial infections. Here, we summarize the current knowledge on the properties of KRG and its components on infections with human pathogenic viruses such as respiratory syncytial virus, rhinovirus, influenza virus, human immunodeficiency virus, human herpes virus, hepatitis virus, norovirus, rotavirus, enterovirus, and coxsackievirus. Additionally, the therapeutic potential of KRG as an antiviral and vaccine adjuvant is discussed.
Keywords: antiviral, ginsenosides, hepatitis virus, influenza virus, Korean Red Ginseng
1. Introduction
Viruses are infective obligate parasites that can replicate only in the living cells of animals, plants, fungi, or bacteria. Although extremely small in size and simple in structure, viruses cause numerous diseases such as cancer, autoimmune disease, and immunodeficiency as well as organ-specific infectious diseases including the common cold, influenza, diarrhea, hepatitis, etc. [1], [2], [3], [4].
Recent progress in the formulation of antiviral therapies and vaccines has helped to prevent, shorten the duration, or decrease the severity of viral infection [5], [6], [7]. Most antiviral agents are designed to target viral components, but mutations in the viral genome often result in drug resistance and immune evasion, creating a major hurdle for antiviral therapies and vaccine development [8]. In addition, the continuous emergence of new infectious agents such as the Ebola virus and Middle East respiratory syndrome coronavirus (MERS-CoV) necessitate the advancement of novel therapeutic approaches. Accordingly, great attention has recently been drawn to the development of antivirals with broad-spectrum efficacy and immunomodulators which improve host resilience by increasing host resistance to the viral infection [9].
Korean ginseng (the root of Panax ginseng Meyer) is one of the most popular medicinal plants used in traditional medicine in East Asian countries including Korea [10]. Ginseng contains various pharmacologically active substances such as ginsenosides, polysaccharides, polyacetylenes, phytosterols, and essential oils, and among those, ginsenosides are considered the major bioactive compounds [11]. Korean Red Ginseng (KRG) is a heat-processed ginseng which is prepared by the repeated process of steaming and air-drying fresh ginseng [12]. KRG has been shown to possess enhanced pharmacological activities and stability compared with fresh ginseng because of changes in its chemical constituents such as ginsenosides Rg2, Rg3 Rh1, and Rh2, which occur during the steaming process [13].
Currently, numerous studies have reported the beneficial effects of KRG on diverse diseases such as cancer, immune system disorder, neuronal disease, and cardiovascular disease [14], [15], [16], [17]. In addition, KRG and its purified components have also been shown to possess protective activities against microbial infections [18]. In this review, we summarize the current knowledge on the effects of KRG and its components on infections with human pathogenic viruses and discuss the therapeutic potential of KRG as an antiviral and vaccine adjuvant.
2. Respiratory syncytial virus
Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection. This viral infection shows mild and indistinguishable symptoms from common colds in adults and healthy children but can also cause severe lower respiratory tract diseases such as pneumonia and bronchiolitis in premature babies and infants with underlying health conditions and immunocompromised patients. No effective antiviral therapy or preventive vaccine in early life is currently available, but maternal vaccination is considered a possible strategy to provide RSV antibody protection to young infants [1].
The Kang Laboratory (Georgia State University, GA) has published several studies on the immunomodulatory and antiviral effects of KRG extract (RGE) on RSV [19], [20], [21]. Although a formalin-inactivated RSV (FI-RSV) vaccine was developed in the 1960s, immunization with FI-RSV was halted because vaccinated children experienced severe respiratory disease during the natural RSV infection. The severe form of the disease caused by the FI-RSV has been attributed to the strong T-helper type 2 (Th2) immune response, and RGE has been shown to mitigate such Th2 responses by enhancing the T-helper type 1 (Th1) response in F1-RSV immunized mice which have Th2-dominant immune response intrinsically [19]. Thus, RGE-treated mice that were immunized with FI-RSV showed improved clinical outcomes via an increase in the immunoglobulin G2a (IgG2a) antibodies level and interferon (IFN)-γ production accompanied by a decrease in IL-4 production and weight loss after RSV infection [19]. The data indicate that RGE possesses an immunomodulatory effect by balancing Th1 and Th2 immune responses, and protects the host from severe pulmonary inflammation upon FI-RSV immunization and RSV infection.
In addition, RGE protected human epithelial cells from RSV-induced cell death and viral replication and inhibited the production of proinflammatory cytokines in vitro upon RSV infection [20], [21]. Moreover, RGE treatment improved clinical outcomes by preventing weight loss and increasing viral clearance and IFN-γ production in bronchoalveolar lavage cells in mice [20], [21]. RGE also increased the numbers of CD11c+ dendritic cells, IFN-γ-secreting CD8+ T cells, and CD4+ T cells in bronchoalveolar lavage fluids [20], [21]. Taken together, these studies demonstrate that ginseng has immunomodulatory and antiviral effects against RSV infection through multiple mechanisms, and further studies are required to elucidate the underlying immunoregulatory and antiviral mechanisms at the molecular level.
3. Rhinovirus
Rhinovirus is the major cause of the common cold. Rhinovirus is transmitted from person-to-person via contact or aerosol and causes upper respiratory illness [22]. Although generally mild and self-limiting, rhinovirus infection may cause asthma or chronic obstructive pulmonary disease in chronic infection and lead to severe complications for asthmatics, elderly people, and immunocompromised patients [23], [24]. Currently there is no cure or prevention for rhinovirus infection, and treatment mainly relies on symptom alleviation using nonsteroidal anti-inflammatory drugs (NSAIDs), nasal decongestants, and antihistamines. Nonetheless, consistent effort has been made to identify effective preventions and antiviral medication for rhinovirus [25].
In an attempt to investigate the effects of ginsenosides on rhinovirus infection, Song et al [26] examined the antiviral activities of protopanaxatriol (PT)-type ginsenosides (Re, Rf, and Rg2), and protopanaxadiol (PD)-type ginsenosides (Rb1, Rb2, Rc, and Rd). The results showed that PT-type ginsenosides protected HeLa cells from human rhinovirus 3 (HRV3)-induced cell death as determined by sulforhodamine B staining of viable cells and morphological assessment [26]. However, PD-type ginsenosides did not show any protective effects and even stimulated the HRV3-induced cell death significantly, implying a structure-dependent effect of ginsenosides on HRV3. The selective antiviral activities of panaxatriol-type ginsenosides were also found in the case of coxsackievirus, as described below. Future studies are needed to elucidate the relationship between the antiviral activities and structural differences among panaxadiol- and panaxatriol-type ginsenosides.
4. Influenza virus
Influenza virus is the most common human respiratory pathogen that causes annual endemic and periodic pandemic infection. There are three types of influenza viruses: A, B, and C. Human influenza A and B viruses cause seasonal disease nearly every winter, whereas the influenza C virus causes mild respiratory disease. Influenza A viruses are the most virulent human pathogens, and their serotypes are further classified and termed based on the viral surface proteins hemagglutinin (H) and neuraminidase (N). Novel mutant strains continuously emerge causing influenza pandemic outbreaks, and there were some historically renowned lethal strains such as “Spanish influenza (H1N1)”, “Asian influenza (H2N2)”, “Russian influenza (H1N1)”, “Hong Kong influenza (H5N1)”, and swine-origin H1N1 influenza recently found in Mexico [27], [28].
Ample studies have been conducted to demonstrate the antiviral activities of RGE and purified compounds present in ginseng on influenza virus A infection in vitro and in vivo. RGE treatment improved the viability of human alveolar epithelial A549 cells upon H1N1 infection accompanied by a decrease in virus-induced cytokine secretion and reactive oxygen species (ROS) formation [29]. Protopanaxatriol-type ginsenoside Re has been shown to protect human umbilical vein endothelial cells (HUVECs) from avian H9N2/G1 influenza-induced apoptosis by inhibiting virus-induced interferon-inducible protein-10 (IP-10) production [30]. The inhibitory effects of RGE on viral replication were also tested in Madin–Darby canine kidney (MDCK) cells using the 2009 pandemic H1N1 virus [31]. In in vivo studies, RGE, ginseng polysaccharide (GP), or ginseng saponin was orally administered to mice or ferrets prior to viral infection, and their protective effects were evaluated by measuring body weight, survival rate, lung viral titers, cytokine production, histopathology, etc. The antiviral effects on the H1N1 strain have been most widely tested, and those on H3N2, H9N2/G1 (avian influenza), and H5N1 were also examined. In detail, RGE has been reported to have antiviral effects on H1N1, H3N2, and H5N1 [31], [32]; GP has effects on H1N1 and H3N2 [33]; and saponin has an effect on H1N1 [34]. The antiviral activities of RGE, GP, and ginseng saponin fraction have also been compared using the H1N1 strain. Yin et al [34] showed that GP was the most effective in improving the symptoms of influenza virus infection, followed by RGE and saponin in that order.
In addition to antiviral activity, RGE also plays a role as a mucosal adjuvant against influenza virus A/PR8 during viral infection [35]. When administered with inactivated virus and RGE intranasally, immunized mice produced increased levels of influenza virus-specific antibodies with improved neutralizing activities in blood and mucosal secretions, notably the IgA antibody in the lung. RGE plus virus immunization also resulted in the enhanced secretion of Th1 and Th2-type cytokines in splenocytes upon challenge infection, although a Th2 type response was more remarkable. This adjuvant effect of RGE was comparable to that of conventional adjuvants such as aluminum hydroxide and cholera toxin. Additionally, immunization of mice with inactivated H3N2 influenza antigen and ginsenoside Re resulted in increased immune responses by elevating both Th1 and Th2 cell activities [2]. The secretion of serum-specific IgG1 and IgG2a and hemagglutination inhibition titers were all increased, and in vitro stimulation of splenocytes produced higher levels of Th1 and Th2 cytokines in ginsenoside Re-administered mice. Furthermore, dietary intake of RGE and Korean Red Ginseng saponin (KRGS) has also been shown to improve H1N1 vaccine efficacy by increasing anti-influenza virus A-specific IgG titers and survival rates [36]. In addition, GP induced cross-protective vaccine efficacy. When mice were vaccinated with influenza virus-like particles (VLPs) originating from H1N1 together with GP, the immunized mice developed heterosubtypic protection and survived a lethal challenge with the H3N2 virus. Taken together, the data suggest the use of RGE, KRGS, ginsenoside Re, and GP as adjuvant or dietary supplements to enhance the vaccine-induced immune response and improve protection against influenza virus infection.
5. Human immunodeficiency virus
Human immunodeficiency virus (HIV) belongs to the genus Lentivirus in the family Retroviridae, and two types of HIV have been characterized: HIV-1 and HIV-2 [37]. HIV-1 is the major type of HIV accounting for 95% of infections worldwide and is more virulent and infectious than HIV-2 [38]. HIV-2 is mainly seen in West Africa and has lower infectivity [39], [40]. There are well-defined stages of HIV disease progression from acute infection, clinical latency, and acquired immunodeficiency syndrome AIDS, and an HIV-positive patient is diagnosed with AIDS when his/her CD4+ cell count falls < 200 cells/mm3. HIV treatment or highly active antiretroviral therapy (HAART) involves the combination of multiple drugs with different mechanisms of action. HAART can effectively suspend or prevent disease progression from one stage to the next and prolong the lives of HIV-positive patients dramatically by lowering the viral load, maintaining immune system function, and preventing opportunistic infections [7], [41]
When combined with zidovudine monotherapy or HAART, RGE has been shown to exert antiviral effects by maintaining CD4+ T cell counts [42], [43], [44], [45] and delaying the occurrence of resistance mutation [42], [43], [46] in HIV-1 patients. RGE treatment alone even showed significant antiHIV effects [44], [47], [48], [49], implying that RGE intake may become an alternative form of treatment for HIV-1 patients. Negative factor (Nef) is a virulence factor required for achieving high virus load and the progression to AIDS [50]. The 5′ long terminal repeat (LTR) acts as a promoter of the entire viral genome and stimulates viral genome replication, whereas group-specific antigen (gag) promotes the formation of fully infectious HIV-1 virions. Interestingly, RGE intake increases the frequency of gross deletions in Nef genes [51], [52], [53], [54] and the 5′ LTR/gag gene [53], [55], [56], leading to a delay in disease progression and increase of survival rate in HIV-1 patients.
Although most studies evaluating the effects of ginseng on HIV-1 have been carried out in HIV-1 patients, several in vitro studies have also been performed. For example, a homodimeric protein, quinqueginsin, isolated from the roots of American ginseng Panax quinquefolium, and xylanase, isolated from the roots of Panax notoginseng, have been shown to inhibit reverse transcriptase in a cell-free system [57], [58]. Additionally, ginsenoside Rh1, ginsenoside Rb1, and compound K have been reported to inhibit cytoprotective effects which may contribute to the long-term survival and persistent HIV-1 production in cells constitutively expressing transactivator (Tat) proteins [59], [60], [61].
In addition to antiviral effects, ginseng interacts with antiHIV drugs and changes their pharmacokinetic properties. Shi et al [62] have reported that ginsenoside Rh2 increased the accumulation and decreased the efflux of ritonavir through P-glycoprotein (P-gp) in Caco-2 cells and MDCK-MDR1 cells. An in vivo study using rats confirmed that intravenous administration of ginsenoside Rh2 inhibited ritonavir efflux and increased the plasma level of ritonavir. However, American ginseng, Panax quinquefolium, did not affect the pharmacokinetics of an antiHIV drug cotreated in humans, although it induced phase 2 enzyme quinone reductase [63]. Kaempferol isolated from ginseng has also been reported to inhibit P-gp-mediated efflux of ritonavir and cytochrome P-450 3A4 (CYP3A4) activities in vitro [64], but it has not been confirmed whether kaempferol would indeed induce the level of ritonavir in vivo.
6. Human herpesvirus
The herpesviruses are a group of large DNA viruses causing lytic, persistent, and latent/recurrent infections [65]. The human herpesviruses (HHV) are further divided into three subfamilies, alphaherpesvirinae [including herpes simplex virus-1 (HSV-1), herpes simplex virus-2 (HSV-2), and varicella-zoster virus (VZV)], betaherpesvirinae, and gammaherpesvirinae based on the differences in factors such as tissue tropism, pathogenesis, and site of latent infection [66]. HSV-1 is typically transmitted during childhood by contact with infected skin and is associated with orofacial infections and encephalitis [67], [68], although HSV-2 is transmitted by sexual activity and causes genital herpes mostly [68].
Notoginsenoside ST-4 is a dammarane-type saponin of Panax notoginseng and has been reported to show antiHSV activity by inhibiting the penetration of HSV-1 into Vero cells [69]. Another in vitro study has shown that ginsenoside Rb1 promotes cell proliferation and inhibits the apoptosis of human glioma cells upon HSV infection, suggesting the potential application of ginsenoside Rb1 to prevent neuronal cell death in viral encephalitis [70]. The antiHSV-1 activity of RGE has also been reported in vivo. When Balb/c mice were administered 200 mg/kg or 400 mg/kg of RGE orally for 10 days and infected with HSV-1, the RGE-treated mice became more resistant to vaginal and systemic infection as shown by a decrease in clinical severity and increase in survival rate and viral clearance. RGE also stimulated IFN-γ secretion in vaginal lavage fluid and increased the expression of IFN-γ, granzyme B, and Fas-Ligand mRNA in lymph nodes and vaginal tissue, suggesting that RGE protects the host from HSV-1 infection by stimulating natural killer (NK) cell activities [71]. Given the diverse antiviral activities of RGE through the inhibition of viral penetration and cell death and NK cell activation, prophylactic use of RGE would be beneficial for preventing or alleviating primary and recurrent HSV infection in combination with conventional antiviral drugs [72].
7. Hepatitis A virus
Hepatitis A virus (HAV) is a positive-sense, single-stranded RNA virus, belonging to the family Picornaviridae. Unlike hepatitis B virus (HBV), which is transmitted through exposure to blood and various body fluids of infected people, HAV is largely transmitted by the fecal–oral route and causes acute hepatitis. Although hepatitis A infection does not lead to chronic liver disease and has very low mortality, it may cause enervating symptoms and fulminant hepatitis (acute liver failure) [4]. Currently, no specific antiviral agent is available for HAV, and thus, prevention via vaccination and improvement of hygiene and sanitation is the most effective approach against the HAV infection.
Lee et al [73] examined the antiviral effects of RGE and purified ginsenosides Rb1 and Rg1 against HAV infection. They demonstrated that pretreatment or cotreatment with RGE and ginsenosides Rb1 and Rg1 on FRhK-4 cells derived from the monkey kidney decreased the HAV titer upon HAV infection in vitro. Although the antiviral effect of RGE and ginsenosides remained limited to the in vitro model, the report suggested that regular intake of KRG as a dietary supplement may help prevent HAV infection.
8. Hepatitis B virus
Hepatitis B virus (HBV) is a double-stranded DNA virus classified as being in the family Hepadnaviridae [74]. HBV can cause acute hepatitis, but it can also develop into a long-term, chronic infection. As chronic hepatitis B can lead to life-threatening cirrhosis or hepatocarcinoma, HBV infection is one of the most serious health problems worldwide [75]. During viral replication, large amounts of HBV surface antigen (HBsAg), HBV envelope antigen (HBeAg), and virions are released in the blood, and accordingly, diagnostic tests for HBV infection involve the detection of those viral antigens, virions, and antibodies to the viral antigens.
The antiHBV effect of ginsenoside Rg3 has been well-described [76]. Ginsenoside Rg3 remarkably inhibited the secretion of HBsAg, HBeAg, and viral particles in HBV-infected HepG2.2.15 cells. Another mechanistic study revealed that ginsenoside Rg3 downregulated TNF receptor-associated factor 6 (TRAF6)/transforming growth factor β activated kinase-1 (TAK1) and inhibited the mitogen-activated protein kinase (MAPK) signaling pathway by impeding c-Jun phosphorylation and reducing AP-1 expression. Consequently, the expression of proinflammatory cytokines such as IL-8 and TNF-α was reduced. Although the anti-inflammatory activity of ginsenoside Rg3 is explicitly described, it is unclear how the anti-inflammatory effect of ginsenoside Rg3 affects HBV replication. Future studies should strive to better understand the link between antiHBV and anti-inflammatory activities of ginsenoside Rg3.
9. Norovirus
Norovirus is a positive-sense, single-stranded RNA virus causing nausea, vomiting, abdominal pain, and diarrhea in humans [77]. The virus is spread through the fecal–oral route by ingestion of contaminated water or food, especially fish and shellfish [78]. As human norovirus is not culturable, norovirus surrogates such as feline calicivirus (FCV), murine norovirus (MNV), and Tulane virus (TV) are used to test the antiviral activity of natural or chemical compounds against norovirus [79]. FCV and MNV have a similar genome organization, physical properties, and replication cycle to those of human norovirus and can be cultivated in Crandell–Reese feline kidney (CRFK) cells and murine Raw264.7 cells, respectively [80].
Lee et al [81] have shown that pretreatment of CRFK or RAW264.7 cells with RGE and ginsenosides Rb1 or Rg1 significantly reduced FCV and MNV titers in vitro, whereas cotreatment or posttreatment had no antiviral effects. In a subsequent study, the same research group demonstrated that RGE and ginsenosides pretreatment induced antiviral proteins in FCV-infected CRFK cells. The expressions of IFN-α, IFN-β, IFN-ω, zinc finger antiviral protein shorter isoform (ZAPS), and Mx protein, an IFN-inducible protein with antiviral activity, were all increased which contributed to the decrease of viral titers in CRFK cells. Future studies are needed to establish a culture system for human norovirus and subsequently evaluate the antiviral effects of RGE and ginsenosides against human norovirus.
10. Rotavirus
Rotavirus is the leading cause of acute gastroenteritis in young children age ≤ 5 years [82]. Two live oral rotavirus vaccines (Rotarix by GlaxoSmithKline, Unitied Kingdom, and RotaTeq by Merck, United States) are available, and the implementation of rotavirus vaccines in childhood immunization programs has significantly reduced the morbidity and mortality associated with Rotavirus infection [6]. Nevertheless, there is no antiviral drug to treat rotavirus infection, and mostly, therapeutics involve the prevention of dehydration [83], [84].
In traditional medicine, ginseng has been known to improve gastrointestinal function and prevent gastrointestinal problems such as diarrhea [3]. A recent study researched the active constituent in ginseng and reported that two pectic polysaccharides isolated from hot water extract of ginseng prevented cell death from viral infection [3]. The polysaccharides, named GP50-dHR and GP50-her, did not have virucidal effects but inhibited viral attachment to the host cells thereby protecting them from virus-induced cell death. Given these results and an additional report that other pectin-type polysaccharides in ginseng inhibited the adherence of Helicobacter pylori to gastric epithelial cells and the ability of Porphyromonas gingivalis to agglutinate erythrocytes [85], further evaluation of the antimicrobial effects of acidic polysaccharides with the structure of pectin is merited.
11. Enterovirus
Human enterovirus 71 (EV71) and coxsackievirus A16 (CVA16) are the two major causes of hand-foot-and-mouth disease (HFMD) in young children [86]. Although HFMD is a mild and self-limited disease characterized by fever, rash, bumps, blisters, or ulcers in the mouth, feet, hands, and buttocks, some affected children may develop neurological, cardiovascular, and respiratory complications in rare cases [87], [88]. Presently, there are no specific treatments or vaccines for HFMD.
In order to identify ginsenosides with antiviral activity against EV71, Song et al [26] tested panaxadiol-type ginsenosides (Rb1, Rb2, Rc, and Rd) and panaxatriol-type ginsenosides (Re, Rf, and Rg2). They found that only ginsenoside Rg2 had antiviral activity against EV71 infection in Vero cells, but it has not been determined whether the anticytopathic effect of Rg2 is due to the virucidal activity or the inhibition of viral attachment.
12. Coxsackievirus
Coxsackievirus is a positive-sense, single-stranded RNA virus, belonging to Picornaviridae. Coxsackieviruses are divided into the group A virus with 23 serotypes and the group B virus with six serotypes [89], [90]. Among those, the most common pathogens are coxsackievirus A16 (CVA16) causing HFMD as described above and coxsackievirus B3 (CVB3) causing myocarditis, aseptic meningitis, and pancreatitis [91], [92]. At present, there is no effective therapeutic agent against CVB3, and only ribavirin is available for CVB3 infection despite its weak antiviral activity [93].
20(S)-Protopanaxtriol is one of the major triterpenes isolated from Panax notoginseng [94]. It has been shown that 20(S)-protopanaxtriol has potent antiCVB3 activities in vitro and in vivo. The IC50 of 20(S)-protopanaxtriol for inhibition of CVB3 replication in HeLa cells was even lower than that of ribavirin, indicating a stronger antiviral effect than ribavirin. In vivo experiments showed that treatment of CVB3-infected mice with 20(S)-protopanaxtriol significantly improved CVB3-induced myocarditis represented by a decrease in the activities of lactase dehydrogenase and creatine kinase, markers for myocardial injury.
In addition, panaxatriol-type ginsenosides such as ginsenosides Re, Rf, and Rg2 also showed significant antiCVB3 activity represented by a decrease in the CVB3-induced cytopathic effect and an increase in the cell viability of infected Vero cells [26]. The antiCVB3 activity of ginsenosides Re and Rf was comparable to that of ribavirin. However, panaxadiol-type ginsenosides such as Rb1, Rb2, Rc, and Rd did not exhibit antiCVB3 activity.
13. Conclusion
The swift emergence of new infectious viruses and drug-resistant variants has limited the availability of effective antiviral agents and vaccines. Thus, the development of broad-spectrum antivirals and immunomodulating agents that stimulate host immunity and improve host resilience is essential. Although ginseng itself can exert direct antiviral effects by inhibiting viral attachment, membrane penetration, and replication, the foremost antiviral activities of ginseng are attributed to the enhancement of host immunity. Future studies should include the identification of essential components responsible for the enhanced immunity against any viral attack.
Conflicts of interest
None declared.
Acknowledgments
This work was supported by the National Research Foundation (NRF) funded by the Ministry of Science, ICT, and Future Planning (NRF-2013R1A1A3005097).
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90. Muir P., Kammerer U., Korn K., Mulders M.N., Poyry T., Weissbrich B., Kandolf R., Cleator G.M., van Loon A.M. Molecular typing of enteroviruses: current status and future requirements. The European Union concerted action on virus meningitis and encephalitis. Clin Microbiol Rev. 1998;11:202–227. [ PubMed] 91. Gupta S., Markham D.W., Drazner M.H., Mammen P.P. Fulminant myocarditis. Nat Clin Pract Cardiovasc Med. 2008;5:693–706. [ PubMed] 92. Tracy S., Gauntt C. Group B coxsackievirus virulence. Curr Top Microbiol Immunol. 2008;323:49–63. [ PubMed] 93. Heim A., Grumbach I., Pring-Åkerblom P., Stille-Siegener M., Müller G., Kandolf R., Figulla H.-R. Inhibition of coxsackievirus B3 carrier state infection of cultured human myocardial fibroblasts by ribavirin and human natural interferon-α Antiviral Res. 1997;34:101–111. [ PubMed] 94. Wang X., Wang Y., Ren Z., Qian C., Li Y., Wang Q., Zhang Y., Zheng L., Jiang J., Yang C. Protective effects of 20(s)-protopanaxtriol on viral myocarditis infected by coxsackievirus B3. Pathobiology. 2012;79:285–289. [ PubMed]
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Last Updated on Sunday, 24 December 2017 10:36 |
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Written by Guy Mong Ky TRAN
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Thursday, 09 November 2017 16:17 |
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There are no translations available.
C.115-Justifications par la biologie moléculaires de la dangérosité du vaccin contre l’hépatite B
Alors que les effets secondaires très graves de la vaccination contre l’hépatite B, rendu obligatoire par nos pouvoirs publics, sont niés tant par les laboratoires, des médecins incompétents ou corrompus, et les pouvoirs publics qui lui sont infeodés , nous allons apporter des éléments de preuves incontestables basés sur la biologie moléculaire. Au niveau des faits constatés nous reprenons ceux décrits dans le Livre de Lucienne Foucras « Le nouveau dossier noir de la vaccination contre l’hépatite B » (Resurgence). Le mari de Lucienne Foucras a subi un vrai calvaire: SLA, SGS et démyélinisation. On n'ose imaginer l'hécatombe d'enfants qui vont être sacrifiés à l'autel du veau d'or des financiers de Big Pharma.
A l'aulne des données du livre, je développe mes constatations scientifiques:
GenHevac B Sanofi-Pasteur-MSD : Pour la fabrication (ADN recombinant), ils utilisent larga manu:
1°) un promoteur de MMTV (le MMTV, Mouse Mammary Tumor Virus, comme son nom ne l'indique pas, donne des LYMPHOMES; c'est archi-connu, c'est publié) et
2°) un promoteur de SV40 (même famille que les polyomavirus responsables de la LEMP DÉMYÉLINISANTE du Sida),
3°) ainsi que des cellules de hamster (animal faisant du diabète avec une facilité déconcertante: UN HAMSTER EST TOUJOURS spontanément peu ou prou DIABÉTIQUE)
L'utilisation de promoteurs rappelle les bébés-bulles de l'hôpital Necker (Pr Fischer A, consultant pro-vaccin du Ministère de la Santé, qui d'ailleurs n'a consulté aucun membre du Revhab, pour conclure à l'obligation vaccinale, par ordonnances: Il avait administré larga manu le LTR (un sigle bien mystérieux Long Terminal Repeat) du Moloney Mu LV (Murine Leukemia Virus), lequel LTR s'est empressé de provoquer des leucémies en pagaie chez les bébés-bulles. Le LTR était considéré, bien qu'extrait d'un virus LEUCEMOGENE, COMME TOTALEMENT INOFFENSIF; si ce n'est pas une expérimentation humaine, qu'est-ce que c'est? On n'a PAS prévu que le LTR soit si dangereux; en fait, on aurait dû, car dans la littérature, c'était déjà publié que cela donnait des leucémies chez le rongeur, mais comme personne ne lit de façon exhaustive la littérature mondiale, même ceux qui sont les plus spécialisés dans un seul domaine pointu, ce fait a été malheureusement méconnu).
Je me rappelle toujours quand j'en ai parlé (TRÈS RAPIDEMENT, LORS D'UN CROISEMENT FURTIF DANS LE COULOIR) à Klatzmann à Eurocancer, il n'y a pas prêté d'attention, car à l'époque personne ne pensait que le danger proviendrait de là: du LTR; un sigle bien mystérieux Long Terminal Repeat.
NOUS JOUONS AUX APPRENTIS SORCIERS AVEC LE GÉNOME.
et qu'est-ce que l'on trouve comme complications? (Revhab)
1°) Leucémies de l'enfance
2°) et affections démyélinisantes diverses (encephalopathies, encéphalites)
3°) ainsi que du diabète
N'importe quel médecin dirait que cela n'a rien à voir avec l'hépatite B (sauf le 2°),
mais n'importe quel quidam se poserait des questions légitimes sur les lymphomes du MMTV, les démyélinisations des polyomavirus et le diabète spontané du hamster.
Autre problème: les cellules d'ovaire de hamster chinois (CHO) sont contaminées par des RETROVIRUS,
autant dire que l'on injecte ces rétrovirus aux enfants.
qu'est ce qui donne un LUPUS? un rétrovirus (chez le chien)
qu'est-ce qui donne un syndrome de Gougerot-Sjogren? Un Rétrovirus (Tax d'HTLV-1, Mariette X)
qu'est-ce qui donne une paraparésie spastique (tropicale)? un rétrovirus le HTLV-1 (Gessain)
qu'est-ce qui donne une sclérose latérale amyotrophique mortelle à 100% en 2-3 ans (LA SLA EST UNE PARAPLÉGIE SPASTIQUE)?
Le vaccin de Sanofi (utilisant des rétrovirus de CHO)
en gros , en tenant compte des non-notifications (les déclarations de SLA SONT INTROUVABLES, ELLES ONT DISPARUES, en particulier la déclaration du cas de SLA du mari de Lucienne Foucras- disparue, comme si cela n'avait JAMAIS existé), il y a 400 cas de SLA MORTELLES recensés par le Revhab. Ce qui est terrifiant avec la SLA, c'est que jusqu'au dernier souffle, le malade reste pleinement conscient qu'il va mourir, même trachéotomisé en chaise roulante puis dans son lit.
Qu'est-ce qu'on trouve dans la liste des complications?
Lupus, SGS, SLA
Chez GSK ENGERIX, ils utilisent la LEVURE
CE N'EST PAS MIEUX, car personne ne sait si un composant de la levure n'est pas dangereux
J'en veux pour preuve que lorsqu'on fabrique l'asparaginase (avec E.Coli), elle donne des pancréatites aigues; pourquoi ?
Parce que le RIBOSOME D'E.COLI contient dans sa sequence en acides aminés du CCKPZ (Cholecystokininepancreazymine) (mimétisme moléculaire : séquence commune WMDF Trp-Met-Asp-Phe) et que le CCKPZ provoque une pancréatite aiguë.
Mais seules certaines souches d'E.Coli en contiennent, d'autres pas.
L'asparaginase donne une pancréatite quand l'E.Coli contient le CCKPZ, mais quand une autre souche employée d'E.Coli n'en contient pas, il n'y a PAS de PANCRÉATITE.
Il y a donc 2 asparaginases: l'une dangereuse, l'autre pas. Tout dépend du process de fabrication; d'un "petit détail".
JE REVIENS À LA LEVURE DE GSK: L'Engerix est fabriqué avec de la levure, on pourrait croire que la levure, bof…
MAIS SI ON SE RAPPELLE E.Coli, ET LA PANCREATITE AIGUE de l'asparaginase, c'est bof aussi, le colibacille tout le monde en a; tout dépend de quel colibacille il s'agit.
La levure, elle, contamine le vaccin Engerix :
c'est là le danger; si la levure est une souche dangereuse, le vaccin sera dangereux; IL PEUT ARRIVER QUE, PARMI LES NOMBREUSES SOUCHES, LA LEVURE EMPLOYEE DANS LE VACCIN, SOIT DANGEREUSE (comme pour E.Coli).
(non publié, je ne peux pas m'avancer plus, en l'état actuel des recherches, car cela demande beaucoup de travail supplémentaire)
Pour les autres complications, c'est du mimétisme moléculaire avec HBs lui-même, l'antigène employé:
Périartérite noueuse (PAN) (non publié)
SEP (que j'ai publié il y a tellement longtemps (Journées de l'Internat, Auto-Immunité, 1998), mimétisme moléculaire de HBs avec la MBP de la MYÉLINE au niveau du tryptophane (il n'y a qu'un SEUL tryptophane dans la MBP, si on l’enlève, la myéline cesse d’être encéphalitogène), mais ils font tout pour étouffer l'info; heureusement, un Ecossais a vu mon poster, et il a empêché que l'Angleterre ne soit vaccinée par le vaccin anti-HBs). A l'époque le Dr Saliou (Institut Pasteur) m'avait répondu qu'on ne referait pas le vaccin, car ça coûterait trop cher. (Je lui avais suggéré de muter le tryptophane en sérine, comme dans l'hépatite du canard).
TRAN Guy Mong Ky
Retraité depuis 2014 de Santé Publique
Agence Régionale de Santé Auvergne Rhônes Alpes
Hôpital Hôtel Dieu Clermont-Ferrand
31 Avenue du Bois 92290 Châtenay Malabry
Tel : 09 81 89 38 70
Portable : 06 63 39 13 25 |
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Last Updated on Sunday, 12 November 2017 23:35 |
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Written by Guy Mong Ky TRAN
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Saturday, 04 November 2017 18:05 |
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There are no translations available.
C.114- Highly pathogenic Influenza virus A H5N1 (Vietnam, Hong Kong) polymerase PB2 contains a snake disintegrin homologous to platelet integrin ITGA2b (gpIIb), which blocks the formation of platelet clot.
Présentation Poster au 8TH EUROPEAN MEETING ON VIRAL ZOONOSES( Saint Raphaël, France, Octobre 2017)
Guy Mong Ky Tran(1) & Adrien Caprani(2)
(1) Retired since 2014 from University of Auvergne Rhone-Alpes, Health Regional Agency, Public Health Department, Hospital Hotel-Dieu, Clermont-Ferrand ; 31 Av du Bois - Chatenay Malabry, France. email:
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(2) Association "Positifs", 147 chemin de la futaie, 83550 Vidauban, email:
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Last Updated on Saturday, 04 November 2017 18:12 |
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