1988, vieron "VIH" en pacientes SIN VIH. La referencia científica que DEBIÓ HABER TERMINADO con la h

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Ante todo la referencia indexada en Pubmed:

Hum Pathol. 1988 May;19(5):545-9.

The ultrastructural and immunohistochemical demonstration of viral particles in lymph nodes from human immunodeficiency virus-related and non-human immunodeficiency virus-related lymphadenopathy syndromes.

O'Hara CJ, Groopman JE, Federman M.

Source
Department of Pathology, England Deaconess Hospital, Harvard Medical School, Boston, MA 02215.

Abstract

Viral particles have been demonstrated by electron microscopy in lymph nodes from patients with acquired immune deficiency syndrome AIDS-related persistent generalized lymphadenopathy (PGL) syndrome. Immunohistochemical and in situ hybridization studies have identified these viruses as the human immunodeficiency virus (HIV). In this study, we examined 20 PGL lymph nodes and found viral particles in 18 cases. Immunohistochemical studies on these cases revealed positive staining for the HIV core protein P24 within germinal centers of secondary follicles. In addition we found viral particles, morphologically indistinguishable from those observed in PGL lymph nodes, in 13 of 15 non-HIV related reactive lymph nodes. Immunohistochemical staining of these lymph nodes for the P24 core protein was negative. None of the patients in this group had risk factors for developing AIDS and none exhibited clinical evidence of immune deficiency. We conclude that the viral particles observed in PGL lymph nodes are most likely HIV, but similar particles can be seen in reactive lymph nodes not associated with HIV infection. The discrete localization of these particles within germinal centers has been observed for other viruses and immune complexes and a possible mechanism of this antigen deposition is discussed.

The ultrastructural and immunohistochemical demon... [Hum Pathol. 1988] - PubMed - NCBI

Les traduzco lo subrayado: Encontraron "partículas indistinguibles" del "VIH"... en pacientes SIN "VIH" :8:.

Cuando me encontré con este abstract increíble, a la primera oportunidad oportunidad que tuve corrí a mi Alma Mater a leer el artículo completo. Sí: el artículo respalda exactamente lo que dice el Abstract. Aún me recuerdo tembloroso leyendo el polvoriento tomo de "Human Pathology" en el mismo archivo de mi Universidad. Ni siquiera me senté para leerlo. Allí estaba la Piedra Filosofal de todo disidente del SIDA: El artículo que demostraba que había "VIH"...en muestras "cocultivadas" de NO "INFECTADOS" con "VIH".

El Grupo de Perth ya había notado la existencia de este extraordinario artículo, y habían dedicado comentario al escaneado de las fotos de este artículo:

The Perth Group HIV-AIDS Debate Website

En el punto 4 el Grupo de Perth enlaza las micrografías de O'Hara 1988



Aquí "VIH" en paciente "infectado por el VIH".



Aquí, partícula "morfológicamente indistinguible del VIH" en persona... sin "VIH".

Comprobé en los archivos de mi alma mater que estas fotos alojadas por el Grupo de Perth corresponden exactamente (salvo letras explicativas) con las fotos de O´Hara 1988 .

Se lo digo de otra forma: Lo que les venden como "VIH"...



...está también presente en personas sin "VIH" :8:, lo cual echa por tierra (hay 1000 argumentos más, pero este es el K.O. final) toda la fantástica teoría de que un "retrovirus" llamado "VIH" cause una enfermedad llamada SIDA.

Y ahora, unos comentarios que deberían ser los clavos en la tapa del ataúd del cadáver de cualquier confianza que les puedan ustedes aún tener en nuestras "autoridades científicas":

* O´Hara 1988 es el único :8: estudio en 29 años de "VIH/SIDA" en el cual se busca "VIH" donde NO DEBERÍA estar, es decir, el único estudio con algo tan elemental en Ciencia como un control negativo. Los controles negativos están Olímpicamente ausentes en la "Ciencia VIH/SIDA".

* Nadie se ha molestado en averigüar qué diablos eran las partículas "morfológicamente indistinguibles de VIH" que tienen los pacientes sin "VIH" de Ó´Hara 1988. Nadie. Nadie a querido estudiar este "misterio". A nadie parece interesar la contestación a ciertas preguntas "incómodas". Este estudio es como si encontrase una Fosa Común de una Cheka del PSOE en el centro de Madrid. Se taparía de inmediato y se dejaría de hablar del tema. Nadie quiere "revolver" algo así. Salvo los "revoltosos" disidentes como yo.

* "We found viral particles, morphologically indistinguishable from those observed in PGL lymph nodes, in 13 of 15 non-HIV related reactive lymph nodes. Immunohistochemical staining of these lymph nodes for the P24 core protein was negative. Esta cita prueba que los "viriones VIH" pueden estar presentes SIN p24. Los Oficialistas -impertérritos- siguen utilizando la p24 como "prueba" de que hay "VIH" en alguien. La p24 está también en el gráfico de "VIH" que les he puesto más arriba. Su propio estudio les desmiente. Les da lo mismo.

* En 30 años que llevamos de "ver" el "VIH" (o LAV, o HTLV-III, que es lo mismo) nunca, jamás se le ha podido ver si no es "cocultivando" la muestra. "Al natural" el "VIH" jamás se ve :8:, y eso que oficialmente se producen decenas de millones al día en cada "infectado". Algunos Disidentes dicen que el "VIH" es un mero ARTEFACTO DE LABORATORIO, fruto de la misma técnica de "cocultivo". El que aparezca en "no infectados" respalda este punto de vista.​
 
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Para colmo, 15 meses antes, en marzo de 1987, Peter Duesberg publicó su celebérrimo artículo en Cancer Research...


...que fue la primera (...y no la última) publicación en revista peer review denunciando como científicamente insostenible la idea de que el "VIH" cause SIDA.

es un artículo libre, así que puden leerlo entero. Al "VIH" sólo dedica el último tercio del artículo. Pueden leerlo en más cómodo formato de texto en el sitio de Duesberg:

Duesberg on AIDS- Retroviruses as Carcinogens and Pathogens

Paea su comodidad les pego aquí lo relevante para el SIDA de ese artículo de 1987:

II. Retroviruses and AIDS

The isolation in 1983 of a retrovirus from a human patient with lymphadenopathy, a typical symptom of AIDS, led to the proposal that the virus, now termed lymphadenopathy-associated virus, is the cause of AIDS (26). Related viruses, termed HTLV-III, ARV, or HIV (209), have since been isolated from about one-half of the AIDS patients that have been sampled (210-214). In the United States about 26,000 AIDS cases and 15,000 AIDS fatalities have been reported between 1981, when the disease was first identified (215), and October 1986 (216). Women represent only 7% of the AIDS cases in the United States (216). The number of AIDS cases reported in the United States has increased from about 100 per 6-month period in 1981 to about 5,000 during the last three 6-month periods from January 1985 (216). At the same time the case-fatality rate has declined from a high of 88% in 1981 to 32% in 1986 (216). In absolute numbers the known deaths have declined from a high of 2,600 in the first 6 months of 1985 to 1,800 in the first 6 months of 1986. This suggests either that the virulence of the disease is dropping or that other diseases were diagnosed as AIDS. Recently the virus was also suggested to cause disease of the brain and of the nervous system (230, 255, 268, 274) and lymphoid interstitial pneumonia (275).
Antibody to the virus is found in about 90% of AIDS patients and correlates with chronic latent infection by the virus (217-221). Because of the nearly complete correlation between AIDS and immunity against the virus, the virus is generally assumed to be the cause of AIDS (13, 27). Accordingly, detection of antiviral antibody, rather than virus, is now most frequently used to diagnose AIDS and those at risk for AIDS (27, 217-224). This is paradoxical, since serum antibody from AIDS patients neutralizes AIDS virus (225-227) and since antiviral immunity or vaccination typically protects against viral disease. It is even more paradoxical that a low antibody titer is equated with a low risk for AIDS (228, 229).
Unlike all other retroviruses, AIDS viruses are thought to be direct pathogens that kill their host cells, namely T-lymphocytes (13, 27), and possibly cells of the brain (230, 255). This view is compatible with the phenotype of AIDS, the hallmark of which is a defect in T-cells (13, 27, 215), and with experimental evidence that many but not all viral isolates induce cytopathic fusion of T-lymphocytes under certain conditions in vitro (Section D). Further it is compatible with neurological disease (231, 232, 255). However, cell killing is incompatible with the obligatory requirement of mitosis for retrovirus replication (16, 25) and with the complete absence of cytocidal effects in all asymptomatic infections in vivo (Section D).

A. Infections with No Risk and Low Risk for AIDS Indicate That the Virus Is Not Sufficient to Cause AIDS

Since their original discoveries in AIDS patients, the virus and more frequently antibody to the virus have also been demonstrated in a large group of asymptomatic persons (212, 214). The virus has been estimated to occur in about 1 to 2 x 106 or about 0.5 to 1% of all Americans (223, 224). In the United States persons at high risk for infection include promiscuous homosexual and bisexual men, of whom 17 to 67% are antibody positive; intravenous drug users, of whom 50 to 87% are positive; and hemophiliacs, of whom 72 to 85% are positive according to some studies (13, 218, 223). On the basis of this particular epidemiology, it was concluded that the virus is not transmitted as a cell-free agent like pathogenic viruses but only by contacts that involve exchange of cells (13, 27).

In these virus-infected groups the annual incidence of AIDS was found to average 0.3% (224) and to reach peak values of 2 to 5% (218, 223, 233). However even in these groups there are many more asymptomatic than symptomatic virus carriers. Other infected groups appear to be at no risk for AIDS. In Haiti and in certain countries in Africa antibody-positive individuals range from 4 to 20% of the population, whereas the incidence of AIDS is estimated at less than 0.01% (223, 229, 234). Several reports describe large samples of children from Africa who were 20 (228) to 60% (221) antibody positive and of female prostitutes who were 66 to 80% antibody positive (221,235), yet none of these had AIDS. Among male homosexuals and hemophiliacs of Hungary about 5% are AIDS virus positive, yet no symptoms of AIDS were recorded (161). Among native male and female Indians of Venezuela 3.3 to 13.3% have antiviral immunity, but none have symptoms of AIDS (236). Since these Indians are totally isolated from the rest of the country, in which only one hemophiliac was reported to be virus positive (236), the asymptomatic nature of their infections is not likely to be a consequence of a recent introduction of the virus into their population. Thus it is not probable that these infections will produce AIDS after the average latent period of 5 years (Section B).
Since the percentage of virus carriers with symptoms of AIDS is low and in particular since it varies between 0 and 5% depending on the AIDS risk group of the carrier, it is concluded that the virus is not sufficient to cause AIDS and that it does not encode an AIDS-specific function. The virus is also not sufficient to cause neurological disease, since it has been detected in the brains of persons without neurological disease and of healthy persons who had survived transient meningitis (230-232).
Thus the virus appears only rarely compatible with Koch's third postulate as an etiological agent of AIDS. It may be argued that the asymptomatic infections reflect latent infections or infections of only a small percentage of susceptible cells, compared to presumably acute infections with symptoms of AIDS. However, it is shown in Section C that infections of neither symptomatic nor asymptomatic carriers are acute; instead both are equally latent and limited to a small percentage of susceptible cells.
Further, the observations that some virus carriers are at high and others at essentially no risk for AIDS directly argue for a cofactor (218, 237) or else for a different cause for AIDS. The strong bias against women, because only 2.5% (479 of 17,000 cases) of the sexually transmitted AIDS cases in the United States are women (216), is a case in point. The virus-positive but AIDS-negative children and prostitutes of Africa (221) or Indians from Venezuela (236) are other examples.

B. Long Latent Period of AIDS Incompatible with Short Latent Period of Virus Replication

The eclipse period of AIDS virus replication in cell culture is on the order of several days, very much like that of other retroviruses (238). In humans virus infection of a sufficient number of cells to elicit an antibody response appears to take less than 4 to 7 weeks. This estimate is based on an accidental needle-stick infection of a nurse, who developed antibody 7 weeks later (239), and on reports describing 12 (240) and 1 (232) cases of male homosexuals who developed antibody 1 to 8 weeks after infection. During this period a mononucleosis-like illness associated with transient lymphadenopathy was observed. In contrast to AIDS (see below), this illness appeared 1 to 8 weeks after infection and lasted only 1 to 2 weeks until antiviral immunity was established. The same early mononucleosis-like disease, associated with lymphocyte hyperplasia, was observed by others in primary AIDS virus infections (234). This is reminiscent of the direct, early pathogenic effects observed in animals infected with retroviruses prior to the onset of antiviral immunity (Part I, Section B).
By contrast the lag between infection and the appearance of AIDS is estimated from transfusion-associated AIDS to be 2 to 7 years in adults (220, 223, 241, 242) and 1 to 2 years in children from infected mothers (220, 223). The most likely mean latent period was estimated to be 5 years in adults (220, 223). Unexpectedly, most of the AIDS virus-positive blood donors identified in transfusion-associated AIDS transmission did not have AIDS when they donated blood and were reported to be in good health 6 years after the donation (220). Likewise there is evidence that individuals shown to be antibody positive since 1972 have not developed AIDS (228). Further, 16 mothers of babies with AIDS did not have AIDS at the time of delivery but three of them developed AIDS years later (276). This indicates that the latent period may be longer than 5 years or that AIDS is not an obligatory consequence of infection.
In view of the claim that the virus directly kills T-cells and requires 5 years to cause disease, we are faced with two bizarre options: Either 5 year old T-cells die 5 years after infection or the offspring of originally infected T-cells die in their 50th generation, assuming a generation time of one month for an average T-cell (176). It may be argued that the virus is biochemically inactive during the first five years of infection and then activated by an unknown cause. However, AIDS virus is biochemically inactive even during the acute phase of the disease (Section C). Moreover it would be difficult for the retrovirus to become acute five years after it had induced chronic antiviral immunity.
Because of the 5 year latency between infection and AIDS, the virus has been likened to the lentiviruses (277), a group of animal retroviruses that is thought to cause debilitating diseases only after long latent periods (13) (Part I, Section B). However, recently an ovine lentivirus, the visna or maedi virus of sheep, was shown to cause lymphoid interstitial pneumonia in 2 to 4 weeks if expressed at high titer (269). [The same disease is believed to be caused by AIDS virus in humans (see below)]. Therefore lentiviruses are not models for retroviruses that are only pathogenic after long latency (Part I, Section B).
Based on the 5-year latent period of the disease and on the assumption that virus infection is sufficient to cause AIDS, one would expect the number of AIDS cases to increase to 1 to 2 x 106 in the United States in the next 5 years. The virus has reportedly reached its present endemic level of 1 to 2 x 106 in the United States (223, 224) since it was introduced there, presumably, less than 10 years ago (27). Yet the spread of AIDS from 1981 to 1986 has not followed the spread of virus with a latent period of 5 years. Instead, recent statistics (see above) indicate no further increases in the number of AIDS cases and a significant decline in the number of AIDS fatalities in the United States (216, 244).
Clearly, the long lag between infection and AIDS and the large number of virus-positive cases in which as yet no AIDS is observed, even after long latent periods, lead to the conclusion that the virus is not sufficient to induce AIDS and does not encode an AIDS-specific function. Indeed, this conclusion is directly supported by genetic evidence against a viral AIDS gene. Deletion analysis has proved that all viral genes are essential for replication (28, 245), which requires not more than 1 or 2 days, yet AIDS follows infection only with an average lag of 5 years and even then only very rarely.

C. Levels of AIDS Virus Expression and Infiltration Appear Too Low to Account for AIDS or Other Diseases

If AIDS viruses were pathogenic by killing susceptible lymphocytes, one would expect AIDS to correlate with high levels of virus infiltration and expression, because uninfected cells would not be killed by viruses nor would unexpressed or latent viruses kill cells. As yet no report on virus titers of AIDS patients has appeared, despite the record interest in the epidemiology and nucleic acid structure of this virus (13, 27, 223). In view of the consistent antiviral immunity of AIDS patients and the difficulties in isolating virus from them (213), the virus titers are probably low. Titers have been said to range between only 0 and 102 per ml blood (213).8
Proviral DNA has been detected in only 15% (9 of 65) AIDS patients; in the remaining 85% the concentration of provirus, if present, was apparently too low for biochemical detection (246). Moreover, among positive samples less than 1 in 102 to 103 lymphocytes contained the provirus (246). Viral RNA was detected in 50 to 80% of AIDS blood samples. However, among the positive samples, RNA was found in only less than 1 of 104 to 105 presumably susceptible lymphocytes (247). The relatively high ratios of provirus-positive (10-2 to 10-3) to viral RNA positive cells (10-4 to 10-5) of AIDS patients indicate latent infections. Further there is no evidence that the virus titer or the level of virus infiltration increases during the acute phase of the disease. It is probably for this reason that cells from AIDS patients must be propagated several weeks in culture, apart from the host's immune system, before either spontaneous (210-214) or chemically induced (248) virus expression may occur. Further, the AIDS virus is completely absent from the Kaposi sarcoma (27, 246), which is associated with 15% (216) to 30% (249) of AIDS cases and is one of the most characteristic symptoms of the disease.
Similar extremely low levels of virus infiltration and expression were also recorded in AIDS virus-associated brain disease (274). Likewise, in interstitial lymphoid pneumonia less that 0.1% of lung cells expressed viral RNA (275).
Indeed there is evidence that even latent virus may not be necessary for AIDS, since 85% of AIDS patients lack proviral DNA (246) and since over 10% of AIDS patients have been observed to lack antiviral immunity (214, 221, 222, 234). Further, in a study from Germany 3 of 91 AIDS patients were found to be virus free, based on repeated negative efforts to detect antibody or to rescue virus.9
It is concluded then that the AIDS virus infects less than 1%, and is expressed in less than 0.01%, of susceptible cells both in carriers with or without AIDS. This raises the question of how the virus could possibly be pathogenic and responsible for immunodeficiency or other diseases. For instance even if the virus were to claim its 10-4 or 10-5 share of T-cells that express viral RNA every 24 to 48 h, the known eclipse period of retroviruses, it would hardly ever match or beat the natural rate of T-cell regeneration (176).
All other viruses function as direct pathogens only if they are biochemically active and expressed at high levels. For instance, the titers that correlate with direct pathogenicity for avian retroviruses are 105-12 (31, 35, 250)4 and they are 104-7 for murine retroviruses (12, 38, 40, 42, 251) (Section B). Hepatitis viruses reach titers of 1012-13 when they cause hepatitis (15), and latent infections are not pathogenic (83). Further, the very low levels of AIDS virus expression in vivo are difficult to reconcile with reports based on in vitro studies with synthetic indicator genes that the AIDS virus encodes a potent transcription-stimulating protein (28, 153, 245). Clearly such activators are not at work in vivo.
The extremely low virus titers of symptomatic and asymptomatic carriers also explain why infection by the virus in the United States is essentially limited to contacts that involve transmission of cells (244) rather than being transmitted as a cell-free, infectious agent like pathogenic viruses. For instance, among 1750 health care workers with exposure to AIDS, only 1 or 2 were found to be antibody positive (252). Another study failed to find a single antibody-positive person among 101 family contacts of 39 AIDS patients, all of whom had lived in the same household with an AIDS patient for at least 3 months (253).

D. AIDS Viruses Not Directly Cytocidal

The AIDS viruses are reported to display in culture a fast cytocidal effect on primary T-cells within 1 to 2 months after infection (13, 27, 254). The cytocidal effect was shown to involve cell fusion (27, 238, 254). The effect is thought to reflect the mechanism of how the virus generates AIDS after a latent period of 5 years (27, 254).
This is debatable on several grounds: (a) above all, the in vitro assay cannot account for the large discrepancy between the short latent period of cell death in vitro and the 5-year latent period of the disease; (b) Tcell fusion is not observed in vivo in chronic, asymptomatic virus carriers and not in prospective AIDS patients during the long latent period of the disease (255), although virus expression is not lower than during the acute phase of AIDS; (c) T-cell killing is also not observed in T-cell lines in vitro (27) and not in primary lymphocytes under appropriate conditions (238). Further primary lymphocytes infected by AIDS virus were shown to double every 5 days in cell culture for three weeks; at the same time the previously latent AIDS virus was activated to high levels of expression (278); (d) virus strains that do not cause cytopathic fusion in vitro have been isolated from 7 of 150 AIDS patients.9 This demonstrates that the fusion-inducing function of the virus can be dissociated from a putative AIDS function.
Thus T-cell killing by fusion is apparently a cell culture artifact that depends on the virus strain and the cell used, as has been shown for many other retroviruses including HTLV-I (Part I, Section B), and not an obligatory feature of virus infection. As with other retroviruses, fusion involves binding of viral envelope antigens on the surface of infected cells with receptors of uninfected cells. Accordingly, fusion is inhibited by AIDS virus-neutralizing antibody (256). It apparently depends on high local virus titers that in particular in the case of AIDS are not observed in vivo. This view of the cell-killing effect also resolves the apparent contradiction between the postulated cytocidal effects of AIDS viruses and the obligatory requirement of all retroviruses for mitosis in order to replicate (16, 25). Indeed AIDS viruses have been reported to replicate without cytocidal effects not only in T-cells but also in human monocytes and macrophages (257, 278), which share the same virus-specific receptors (258), and in B-cell lines (259), in fibroblasts (261) in human brain and the lung (213, 230, 232, 257, 261).

E. No Simian Models for AIDS

Since retroviruses have been isolated from monkeys in captivity with immunodeficiencies and since experimental viremia can depress immune functions in monkeys, such systems are considered to be animal models of human AIDS. For example, 42 of 68 newborn monkeys died with a broad spectrum of diseases that included runting and lymphadenopathy 4 to 6 weeks after inoculation with Mason-Pfizer monkey virus (91). However, this virus has since been found in healthy macaques (262). More recently a retrovirus termed simian AIDS or SAIDS virus was isolated from monkeys with immunodeficiency (92, 262). Inoculation of three juvenile rhesus monkeys by one isolate was reported to cause splenomegaly and lymphadenopathy within 2 to 5 weeks. One animal became moribund and two others were alive with simian AIDS at the time of publication (92). However, in another study only transient lymphadenopathy but no lasting AIDS-like disease was observed in macaques inoculated with this virus (263). Another simian virus that is serologically related to AIDS virus, termed STLV-III, was isolated from immunodeficient macaques and from one macaque with a lymphoma. Macaques inoculated with blood or tissue samples of the viral lymphoma died 50 to 60 days later with various diseases (93). However, asymptomatic infections by the same virus have since been identified in no less than 50% of wild green monkeys that did not show any symptoms of a disease (264).
Eight chimpanzees infected with human AIDS virus had not developed symptoms of AIDS 1.5 years past inoculation (265). However, each animal developed antiviral immunity about 1 month after infection, followed by persistent latent infection, as in the human cases (265). A follow-up of champanzees inoculated with sera from AIDS patients in 1983 reports no evidence for AIDS in 1986 although the animals had developed antibodies to the virus (243).
Several reasons suggest that these experimental infections of monkeys are not suitable models for human AIDS. Above all, the human virus is not pathogenic in animals. The diseases induced in monkeys by experimental infections with simian viruses all occur fast compared to the 5-year latency for AIDS. Moreover the simian viruses are never associated with a disease in wild animals. Therefore these diseases appear to be exactly analogous to the direct, early pathogenic effects caused by other retroviruses in animals prior to antiviral immunity (see Part I, Section B), and thus are probably models for the early mononucleosis-like diseases which occur in humans infected with AIDS virus prior to antiviral immunity (232, 234, 240) (Section B). Indeed the persistent asymptomatic infections of wild monkeys with simian retroviruses appear to be models for the many asymptomatic infections of humans with AIDS virus or HTLV-I.

F. AIDS Virus As an Indicator of a Low Risk for AIDS

The only support for the hypothesis that the AIDS virus causes AIDS is that 90% of the AIDS patients have antibody to the virus. Thus it would appear that the virus, at least as an immunogen, meets the first of Koch's postulates for an etiological agent. This conclusion assumes that all AIDS patients from whom virus cannot be isolated (about 50%) (278) or in whom provirus cannot be demonstrated (85%) and the antibody-negative cases (about 10%) and the virus-free cases reported in one study (3%) (Section C) are false negatives. Indeed, the diagnosis of AIDS virus by antibody has recently been questioned on the basis of false positives (234).
At this time the hypothesis that the virus causes AIDS faces several direct challenges. (a) First it fails to explain why active antiviral immunity, which includes neutralizing antibody (225-227) and which effectively prevents virus spread and expression, would not prevent the virus from causing a fatal disease. This is particularly paradoxical since antiviral immunity or "vaccination" typically protects against viral pathogenicity. It is also unexpected that AIDS patients are capable of mounting an apparently highly effective, antiviral immunity, although immunodeficiency is the hallmark of the disease. (b) The hypothesis is also challenged by direct evidence that the virus is not sufficient to cause AIDS. This includes (i) the low percentage of symptomatic infections, (ii) the fact that some infected groups are at a relatively high and others at no risk for AIDS, (iii) the long latent period of the disease (Section B), and (iv) the genetic evidence that the virus lacks a late AIDS function. Since all viral genes are essential for virus replication (28, 245), the virus should kill T-cells and hence cause AIDS at the time of infection rather than 5 years later. (c) The hypothesis also fails to resolve the contradiction that the AIDS virus, like all retroviruses, depends on mitosis for replication yet is postulated to be directly cytocidal (Section D). (d) The hypothesis offers no convincing explanation for the paradox that a fatal disease would be caused by a virus that is latent and biochemically inactive and that infects less than 1% and is expressed in less than 0.01% of susceptible lymphocytes (Section D). In addition the hypothesis cannot explain why the virus is not pathogenic in asymptomatic infections, since there is no evidence that the virus is more active or further spread in carriers with than in carriers without AIDS.
In view of this it seems likely that AIDS virus is just the most common among the occupational viral infections of AIDS patients and those at risk for AIDS, rather than the cause of AIDS. The disease would then be caused by an as yet unidentified agent which may not even be a virus, since cell-free contacts are not sufficient to transmit the disease.
Other viral infections of AIDS patients and those at risk for AIDS include Epstein-Barr and cytomegalovirus in 80 to 90% (222, 268), and herpes virus in 75 to 100%.10
In addition hepatitis B virus is found in 90% of drug addicts positive for antibody to AIDS virus (267). Among these different viruses, retroviruses are the most likely to be detectable long after infection and hence are the most probable passenger viruses of those exposed to multiple infectious agents. This is because retroviruses are not cytocidal and are unsurpassed in establishing persistent, nonpathogenic infections even in the face of antiviral immunity. Therefore AIDS virus is a useful indicator of contaminated sera that may cause AIDS (13, 27) and that may contain other cell-free and cell-associated infectious agents. It is also for these reasons that latent retroviruses are the most common nonpathogenic passenger viruses of healthy animals and humans. For the same reasons, they are also frequently passenger viruses of slow diseases other than AIDS like the feline, bovine and human leukemias (see Part I) or multiple sclerosis (268) in which latent or defective "leukemia viruses" are occasionally found.
It is concluded that AIDS virus is not sufficient to cause AIDS and that there is no evidence, besides its presence in a latent form, that it is necessary for AIDS. However, the virus may be directly responsible for the early, mononucleosis-like disease observed in several infections prior to antiviral immunity (Section B). In a person who belongs to the high risk group for AIDS, antibody against the AIDS virus serves as an indicator of an annual risk for AIDS that averages 0.3% and may reach 5%, but in a person that does not belong to this group antibody to the virus signals no apparent risk for AIDS. Since nearly all virus carriers have antiviral immunity including neutralizing antibody (225-227), vaccination is not likely to benefit virus carriers with or without AIDS.


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Gallo, R.C., Salahuddin, S.Z., Popovic, M., Shearer, G.M., Kaplan, M., Haynes, B.F., Palher, F.J. Redfield, R., Oleske, J, Safai, B., White, F., Foster, P., and Markham, P.D. Frequent detection and isolation of cytopathic retroviruses (HTLV III) from patients with AIDS and at risk for AIDS. Science, 224: 500-503, 1984.
Salahuddin, S.A., Markham, P.D., Popovic, M., Sarngadharan, M.G., Orudorff, S., Fladagar, A., Patel, A., Gold, J., and Gallo, R.C. Isolation of infectious T-cell leukemia/lymphoma virus type III (HTLV-III) from patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) and from healthy carriers: a study of risk groups and tissue sources. Proc. Natl. Acad. Sci. USA, 82: 5530-5534, 1985.
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Blattner, W.A., Biggar, R.J., Weiss, S.H., Melbye, M., and Goedert, J.J. Epidemiology of human T-lymphotropic virus type III and the risk of the acquired immunodeficiency syndrome. Ann. Intern. Med., 103: 665-670, 1985.
Kaminsky, L.S., McHugh, T., Stites, D., Volberding, P., Henle, G, Henle, W., and Levy, J.A. High prevalence of antibodies to acquired immune deficiency syndrome (AIDS)-associated retrovirus (ARV) in AIDS and related conditions but not in other disease states. Proc. Natl. Acad. Sci. USA, 82: 5535-5539, 1985.
Peterman, T.A., Jaffe, H.W., Feorino, pm, Haverkos, H.W., Stoweburner, R.L., and Curran, J.W. Transfusion-associated acquired immunodeficiency syndrome in the United States. JAMA, 254: 2913-2917, 1985.
Clumeck, N., Robert-Guroff, M., Van De Perre, P., Jennings, A., Sibomana, J., Demol, P., Cran, S., and Gallo, R.C. Seroepidemiological studies of HTLV-III antibody prevalence among selected groups of heterosexual Africans. JAMA, 254: 2599-2602, 1985.
Gottlieb, M.S., Wolfe, P.R., Fahey, J.L., Knight, S., Hardy, D., Eppolito, L., Ashida, E., Patel, A., Beall, G.N., and Sun, N. The syndrome of persistent generalized lymphadenopathy: experience with 101 patients. Adv. Exp. Med. Biol., 187: 85-91, 1985.
Curran, J.W., Morgan, M.W., Hardy, A.M., Jaffe, H.W., Darrow, W.W., and Dowdle, W.R. The epidemiology of AIDS: current status and future prospects. Science, 229: 1352-1357, 1985.
Sivak, S.L., and Wormset, G.P. How common is HTLV-III infection in the United States? N. Engl. J. Med., 313: 1352, 1985.
McDougal, J.S., Cort, S.P., Kennedy, M.S., Cabridilla, C.D., Feorino, pm, Francis, D.P., Hicks, D, Kalyanaraman, V.S., and Martin, L.S. Immunoassay for the detection and quantitation of infectious human retrovirus, lymphadenopathy-associated virus (LAV). J. Immunol. Methods, 76: 171-183, 1985.
Robert-Guroff, M., Brown, M., and Gallo, R.C. HTLV-III neutralizing antibodies in patients with AIDS and ARC. Nature, 316: 72-74, 1985.
Weiss, R.A., Clapham, P.R., Cheingsong-Popov, R., Dalgleish, A.G., Carne, C. A, Weller, I.V.D., and Tedder, R.S. Neutralization of human T-lymphotropic virus type III by sera of AIDS and AIDS-risk patients. Nature, 316: 69-72, 1985.
Saxinger, C., Levine, P.H., Lange-Wantzin, G., and Gallo, R. Unique pattern of HTLV-III (AIDS-related) antigen recognition by sera from African children in Uganda (1972). Cancer Res. (Suppl.), 45: 4624-4626, 1985.
Bayley, A.C., Cheingsong-Popov, R., Dalgleish, A.G., Downing, R.G., Tedder, R.S., and Weiss, R.A. HTLV-III serofogy distinguishes atypical and endemic Kaposi's sarcoma in Africa. Lancet, 1: 359-361, 1985.
Black, P.H. HTLV-III, AIDS, and the brain. N. Engl. J. Med., 313: 1538-1540, 1985.
Resnick, L., DiMarzo-Veronese, F., Schupbach, J., Tortellotte, W.W., Ho, D. D, Muller, F., Shapshak, P., Vogt, M., Groopman, J.E., Markham, P. D, and Gallo, R.C. Intra-blood-brain-barrier synthesis of HTLV-III-specific IgG in patients with neurologic symptoms associated with AIDS or AIDS-related complex. N. Engl. J. Med., 313:1498-1510, 1985.
Ho, D.D., Rota, T.R., Schooley, R.T., Kaplan, J.C., Allan, J.D., Groopman, J.E., Resnick, L., Felsenstein, D., Andres, G.A., and Hirsch, M.S. Isolation of HTLV-III from cerebrospinal fluid and neural tissue of patients with neurologic syndromes related to the acquired immunodeficiency syndrome. N. Engl. J. Med., 313: 1493-1497, 1985.
Goedert, J.J., Biggar, R.J., Weiss, S.H., Eyster, M.E., Melbye, M., Wilson, S., Ginzburg, H.M., Grossman, R.J., DiGiola, R.A., Sanchez, W.C., Giron, J.A., Ebbesen, P., Gallo, R.C., and Blattner, W.A. Three-year incidence of AIDS in five cohorts of HTLV-III-infected risk group members. Science, 231: 992-995, 1986.
Biggar, R.J. The AIDS problem in Africa. Lancet, 1: 79-83, 1986.
Kreiss, J.K., Koech, D., Plummer, F.A., Holmes, K.K., Lightfoote, M., Piot, P., Ronald, A.R., Ndinya-Achola, J.O., D'Costa, L.J., Roberts, P., Ngugi, E.N., and Quinn, T.C. AIDS virus infection in Nairobi prostitutes‹spread of the epidemic to East Africa. N. Engl. J. Med., 314: 414-417, 1986.
Rodriquez, L., Sinangil, F., Godoy, G., Dewhurst, S., Merino, F., and Volsky, D.J. Antibodies to HTLV-III/LAV among aboriginal Amazonian Indians in Venezuela. Lancet, 2:1098-1100, 1985.
Levy, J.A., and Ziegler, J.L. Acquired immune deficiency syndrome is an opportunistic infection and Kaposi's sarcoma results from secondary stimulation. Lancet, 2:78-81, 1983.
Hoxie, J.A., Haggarty, B.S., Rachowski, J.L., Pilsbury, N., and Levy, J.A. Persistent noncytopathic infection of human lymphocytes with AIDS-associated retrovirus. Science, 229: 1400-1402, 1985.
Anonymous Report. Needle-stick transmission of HTLV-III from a patient infected in Africa. Lancet, 2:1376-1377, 1984.
Cooper, D.A., Maclean, P., Finlayson, R., Michelmore, H.M., Gold, J., Donovan, B., Barnes, T.G., Brooke, P., and Penny, R. Acute AIDS retrovirus infection. Definition of a clinical illness associated with seroconversion. Lancet, 1: 537-540, 1985.
Eyster, M.E., Goedert, J.J., Sarngadharan, M.G., Weiss, S.H., Gallo, R. C., and Blattner, W.A. Development and early natural history of HTLV-III antibodies in persons with hemophilia. JAMA, 253: 2219-2223, 1985.
Feorino, pm, Jaffe, H.W., Palmer, E., Peterman, T.A., Francis, D.E., Kalzunaran, V.S., Weinstein, R.A., Stoneburner, R.L., Alexander, W.J., Ruersky, C., Getcheil, J.P., Weinfield, D., Haverkos, H.W., Kilbourne, B.W. Nicholson, J.K.A., and Curran, J.W. Transfusion-associated acquired immune deficiency syndrome. N. Engl. J. Med., 312: 1293-1296, 1985.
Sarin, P.S., and Gallo, R.C. The involvement of human T-lymphotropic viruses in T-cell leukemia and immune deficiency. Cancer Rev., 1: p. 1-17, Copenhagen: Einar Munksgaard, 1986.
Sande, M.A. Transmission of AIDS. The case against casual contagion. N. Engl. J. Med., 314: 380-382, 1986.
Dayton, A.I., Sodroski, J.G., Rosen, G.A., Goh, W.C., and Haseltine, W.A. The trans-activator gene of the human T cell lymphotropic virus type III is required for replication. Cell, 44: 941-947, 1986.
Shaw, G.M., Hahn, B.H., Arya, S.K., Groopman, J.E., Gallo, R.C., and Wong-Staal, F. Molecular characterization of human T-cell leukemia (lymphotropic) virus type III in the acquired immune deficiency syndrome. Science, 226:1165-1167, 1984.
Harper, M.E., Marselle, L.M., Gallo, R.C., and Wong-Staal, F. Detection of lymphocytes expressing T-lymphotropic virus type III in lymph nodes and peripheral blood from infected individuals by in situ hybridization. Proc. Natl. Acad. Sci. USA, 83: 772-776, 1986.
Folks, T., Powell, D.M., Lightfoote, M.M., Benn, S., Martin, M., and Fauci, A. Induction of HTLV-III/LAV from a nonvirus-producing T-cell line: implications for latency. Science, 231: 600-602, 1986.
Centers for Disease Control. Update: acquired immunodeficiency syndrome-United States. Morbidity Mortality Weekly Rep., 34: 245-248, 1985.
Beard, J.W. Avian virus growth and their etiological agents. Adv. Cancer Res., 7: 1-127, 1963.
Fischinger, P.J., Ihle, J.N., Levy, J.-P., Bolognesi, D.P., Elder, J., and Schiller, W. Recombinant murine leukemia viruses and protective factors in leukemogenesis. Cold Spring Harbor Conf. Cell Proliferation, 7: 989-1103, 1980.
Centers for Disease Control. Update: evaluation of human T-lymphotropic virus type III/lymphadenopathy-associated virus infection in health care personnel‹United States. Morbidity Mortality Weekly Rep., 34: 575-578, 1985.
Friedland, G.H., Satzman, B.R., Rogers, M.F., Kahl, P.A., Lesser, M.L., Mayers, M.M., and Klein, R.S. Lack of transmission of HTLV-III/LAV infection to household contacts of patients with AIDS or AIDS-related complex with oral candidiasis. N. Engl. J. Med., 314: 344-349, 1986.
Klatzmann, D., Barre-Sinoussi, F., Nugeyre, M.T., Dauguet, C., Vilmer, E., Griscelli, C., Brun-Vezinet, F., Rouzioux, C., Gluckman, J.C., Chermann, J.C., and Montagnier, L. Selective tropism of lymphadenopathy associated virus (LAV) for helper-inducer T lymphocytes. Science, 225: 59-63, 1984.
Barnes, D.M. AIDS-related brain damage unexplained. Science, 232: 1091-1093, 1986.
Lifson, G.D., Feinberg, M.B., Reyes, G.R., Rabin, L., Banapour, B., Chakrabarti, S., Moss, B., Wong-Staal, F., Steiner, K.S., and Engleman, E.G., Induction of CD4-dependent cell fusion by HTLV-III/LAV envelope glycoprotein. Nature, 323: 725-728, 1986.
Gartner, S., Markovits, P., Markovitz, D., Kaplan, M., Gallo, R., Popovic, M. The role of mononuclear phagocytes in HTLV-III/LAV infection. Science, 233: 215-219, 1986.
Stewart, S.J., Fujimoto, J., and Levy, R. Human T lymphocytes and monocytes bear the same leu-3 (T4) antigen. J. Immunol., 136: 3773-3778, 1986.
Montagnier, L., Gruest, J., Chamaret, S., Dauguet, C., Axler, C., Guetard, D., Nugeyre, M.T., Barre-Sinoussi, F., Chermann, J.-C., Burnet, J. B, Klatzmann, D., and Gluckman, J.C. Adaptation of lymphoadenopathy associated virus (LAV) to replication in EBV-transformed B lymphoblastoid cells lines. Science, 225: 63-66, 1984.
Levy, J.A., Cheng-Mayer, C., Dina, D., and Luciw, P. AIDS retrovirus (ARV) replicates in human and animal fibroblasts transfected with a molecular clone. Science, 232: 998-1011, 1986.
Shaw, G.M., Harper, M.E. Hahn, B.H., Epstein, L.G., Gajdusek, D.C., Price, R.W., Naria, B.A., Petito, C.K., O'Hara, C.J., Groopman, J.E., Cho, E.-S., Oleske, J.M., Wong-Staal, F., and Gallo, R.C. HTLV III infection in brains of children and adults with AIDS encephalopathy. Science, 277: 177-181, 1985.
Daniel, M.D., King, N.W., Letvin, N.L., Hunt, R.D., Seghal, P.K., and Desrosiers, R.C. A new type D retrovirus isolated from macaques with immune-deficiency syndrome. Science, 223: 602-605, 1984.
Letvin, N.L., Daniel, M.A., Seghal, P.K., Chaliloux, L.V., King, N.W., Hunt, R.D., Aldrich, W.R., Holley, K., Schmidt, D.K., and Desrosiers, R.C. Experimental infection of rhesus monkeys with type D retrovirus. J. Virol., 52: 683-686, 1984.
Kanki, P.J., Alroy, J., and Essex, M. Isolation of T-lymphotropic retrovirus related to HTLV-III/LAV from wild-caught African green monkeys. Science, 230:951-954, 1985.
Fultz, P.N., McClure, H.M., Swenson, R.B., McGrath, C.R., Brodie, A., Getcheil, J.P., Jensen, F.C., Anderson, D.C., Broderson, J.R., and Francis, D.P. Persistent infection of chimpanzees with human T-lymphotropic virus type III/lymphadenopathy-associated virus: a potential model for acquired immunodeficiency syndrome. J. Virol., 58:116-124, 1986.
Purtilo, D.T., Kipscomb, H., Krueger, G., Sonnabend, J., Casareale, D., and Volsky, D.J. Role of Epstein-Barr virus in acquired immune deficiency syndrome. Adv. Exp. Med. Biol., 187: 53-65, 1985.
Peutherer, J.F., Edmond, E., Simmonds, P., Dickson, J.D., and Bath, G.E. HTLV-III antibody in Edinburgh drug addicts. Lancet, 2:1129-1130, 1985.
Koprowski, H., DeFreitas, E., Harper, M.E., Sandberg-Wollheim, M., Sheremata, W., Robert-Guroff, M., Saxinger, C.W., Feinberg, M.B., Wong-Staal, F., and Gallo, R.C. Multiple sclerosis and human T-cell lymphotropic retroviruses. Nature, 318: 154-160, 1985.
Lairmore, M.D., Rosadio, R.H., and De Martini, J.C. Ovine lentivirus lymphoid interstitial pneumonia. Rapid induction in neonatal lambs. Am. J. Path., 125: 173-181, 1986.
Chen, I.Y., Wachsman, W., Rosenblatt, J.D., and Cann, A.J. The role of the X gene in HTLV associated malignancy. Cancer Surveys, 5 (2): 331-342, 1986.
Gallo, R.C. The first human retrovirus. Scientific American, 255 (6): 88-98, 1986.
Zijlstra, M., and Melief, C.J.M. Virology, genetics and immunology of murine lymphomagenesis. Biochem. et Biophys. Acta, 865: 197-231, 1986.
Duesberg, P.H. Cancer genes: rare recombinants instead of activated oncogenes. Proc. Natl. Acad. Sci. USA, 84: 2117-2124, 1987.
Stoler, M.H., Eskin, T.A., Been, S., Angerer, R.C., and Angerer, L.M. Human T-cell lymphotropic virus type III infection of the central nervous system. J. Am. Med. Assoc., 256: 2360-2364, 1986.
Chayt, K.J., Harper, M.E., Marselle, L.M., Lewin, E.B., Rose, R.M., Oleske, J.M., Epstein, L.G., Wong-Staal, F., and Gallo, R.C. Detection of HTLV-III RNA in lungs of patients with AIDS and pulmonary involvement. J. Am. Med. Assoc., 256: 2356-2371, 1986.
Scott, G.B., Fischl, M.A., Klimas, N., Fletcher, M.A., Dickinson, G.M., Levine, R.S., and Parks, W.P. Mothers of infants with the acquired immuno-deficiency syndrome. J. Am. Med. Assoc., 253: 363-366, 1985.
Gonda, M., Wong-Staal, F., Gallo, R., Clements, J., Narayan, O., and Gilden, R. Sequence homology and morphologic similarity of HTLV-III and visna virus: a pathogenic lentivirus. Science, 227: 173-177, 1985.
Walker, C.M., Moody, D.J., Stites, D.P., and Levy, J.A. CD8+ lymphocytes can control HIV infection in vitro by suppressing virus replication. Science, 234: 1563-1566, 1986.

A mi juicio en un mundo racional el paper de Duesberg de 1987 debió dejar seriamente tocada a la hipótesis "VIH/SIDA", y O¨Hara 1988 debió haber sido el K.O. total de una hipótesis insostenible, que para 1989 a más tardar debió haberse reunido en el basurero de hipótesis médicas fatalmente (literal) erróneas, junto con las Lobotomías y las teorías sobre el origen infeccioso del escorbuto y la pelagra.

* Lobotomía. Dieron un Premio Nobel :8: a su inventor. Hoy quien hiciese una terminaría en la cárcel. la última se hizo en 1967.

* Escorbuto infeccioso. una chorrada acientífica que se mantuvo 100 años después de que se supiese que el zumo de Lima prevenía la enfermedad.

* Pelagra infecciosa, un error médico que costó la vida a millones, pese a que ya había evidencias clarísimas de que con dieta se curaba esta enfermedad carencial.

* SIDA infeccioso. Un error médico aún no reconocido.​

He dicho mil veces que el "VIH/SIDA" dejó de ser Ciencia a finales de los años 80. Desde entonces es Dogma pseudo-científico soportado por el aparato punitivo del Estado, exactamente igual que el Lysenkoismo.

¿Creían que sólo la URSS era capaz de respaldar una teoría pseudocientífica?. ¡Pues nosotros también lo estamos haciendo como Civilización con el "VIH/SIDA"!.

La diferencia es que en la URSS ejecutaban a los disidentes de Lysenko, y aquí (por ahora) nos dejan expresarnos a los Disidentes del SIDA.

Por ahora...

"Los negacionistas del VIH son unos criminales" - Público.es

...la disensión científica e intelectual calificada como "crimen". Quien sostiene esto no es un científico, es un Inquisidor.

Esta señora que dice estas barbaridades es la co-descubridora oficial del "VIH". Una TRofim Lysenko de nuestros días que llama "criminales" a quienes no están de acuerdo con ella en temas científicos.​

Mis hilos sobre el "VIH/SIDA":

 
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workforfood

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Es la teoría de Luis Carlos Campos, entonces porque los antiretrovirales funcionan en los pacientes con SIDA y positivos a VIH.
 

Karonte

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Tienes toda la razón porque desde 1988 hasta hoy no se ha avanzado nada en el tema de analisis.....
 

AYN RANDiano2

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Tienes toda la razón porque desde 1988 hasta hoy no se ha avanzado nada en el tema de analisis.....
¿No sabes leer?.

A ver, resuma por favor con sus propias palabras el primer post del hilo, porque o no las ha leído o carece de comprensión lectora.

Los experimentos de Pasteur echando por tierra la generación espontánea siguen siendo válidos 140 años después de su realización:



El golpe mortal a la generación espontánea : Biología

Igualmente: O´Hara 1988 echa por tierra hoy Y PARA SIEMPRE la hipótesis VIH.

O´Hara 1988 es un CISNE NEGRO...



...que destruye para siempre la pretensión de los VIHistas de que todos los cisnes son blancos, esto es, de que el "VIH" es privativo de los "infectados por el VIH".

Eliminamos la Filosofía del bachillerato y este es el resultado: la gente NO SABE PENSAR.
 
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MiNombreEsLegión

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Una pregunta, sin mala intención:

¿A qué se debe que el VIH/SIDA sea la única dolencia en la que no se permite la disidencia?

Pongamos, por ejemplo, con la Malaria, enfermedad infinitamente más peligrosa que el SIDA. Imaginemos que alguien demuestra que ha encontrado Plasmodium en gente sana, es mas, esa gente está repleta de ellos, pero en cambio no tiene síntoma alguno (damos por hecho que no han desarrollado inmunidad por convivir durante generaciones con ella); asimismo, demuestra que hay gente padeciendo Malaria y en la que no se encuentran esos microorganismos.

¿Les parecería lógico que gran parte de los médicos y toda la industria farmacéutica se dedicase a crucificar a esa persona, y a terminar con su carrera?
 

AYN RANDiano2

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Una pregunta, sin mala intención:

¿A qué se debe que el VIH/SIDA sea la única dolencia en la que no se permite la disidencia?
Es un tema político y militar.

Mira al capitoste del organismo que controla el "VIH/SIDA", el CDC:



Ali S. Khan - Wikipedia, the free encyclopedia

Este señor es militar, y por lo tanto sigue órdenes. El organismo que dirige NADA TIENE QUE VER CON LA CIENCIA.

Lee esto:

PLOS Medicine: The National Security Implications of HIV/AIDS

El "VIH" es un asunto de "seguridad nacional". Ya sabes que en ese tipo de ausuntos NO HAY DISCUSIONES.

Por qué los USA han escogido "militarizar" esta magufada lo ignoro. Hay especulaciones mil:

* Herramienta de control de población mundial: Eugenesia, control demográfico...hay todo tipo de especulaciones.

* Poder envenenar a placer al grupo que deseen con designarlo "grupo de riesgo".

* Royalties de patentes relacionadas con el "VIH" (compartidas por USA y Francia).

* Prestigio y poder de ser considerados los conocedores de los "remedios" de una supuesta "plaga mortal".

* La lluvia de reclamaciones y el desprestigio atroz que sufrirían si dijesen "nos equivocamos en 1984".​



En 1984 la secretaria de salud USA presentó ante el mundo "la causa probable del SIDA se ha encontrado", y lo presentó como "un triunfo de la Ciencia Americana". Anunció también una vacuna para 1986... vacuna que aún estamos esperando.

El gobierno Reagan puso todo su peso detrás de esta magufada: La conferencia de prensa de abril de 1984 se celebró antes de la publicación de los mierdo-artículos (los he leído y son atroces) de Gallo en prensa científica.

Hay quienes dicen que "No hay vuelta atrás" porque el bochorno del desprestigio estatal y las reclamaciones millonarias serían la puntillas a unos USA en un estado financiero conocido por todos.

Además: ¿Qué mejor excusa para poder "tratar" con quimioterapia tóxica a quien te de la gana en cualquier parte del mundo?.

Más aún: La verdadera causa del primer SIDA de los años 1980 eran principalmente...drogas, gran parte de las cuales eran... drogas farmaceúticas:





"Poison" a los lados. Con buen motivo...

Observa el fabricante...es el mismo que años más tarde fabricaba AZT:



Otros laboratorios también fabricaron Poppers:



Esta imagen la aloja la Welcome: ¿Crees que les gustaría reconocer que su producto tuvo algo que ver con el SIDA de los años 1980?.



¿O crees que prefieren echarle la culpa a un "retrovirus"?.

El "VIH" permite que en vez de tener que pagar indemnizaciones tengas nuevos beneficios.

Ya sabes que las farmaceúticas dan dinero a TODOS los candidatos en las elecciones USA.

Ah, con respecto a los Poppers es como si Jimmy Carter siguiese en la casa Blanca: Nada ha cambiado.



Poppers – the Sweet Smell of Hypocrisy « Gay Mafia Watch

...hasta siguen con el de receta médica:

 
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Ancient Power 2

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Desde luego como eso sea así, y no tengo razones para pensar lo contrario, esta época podría llamarse la era de la desinformación. Basta ir a un kiosko y ver cómo, incluso en la revista científica más seria que pueda encontrarse, hay abundantes artículos sobre el VIH y su morfología, comportamiento o color.

Aynrandiano no se pone a ver más allá del hecho puntual en sí del engaño del SIDA, pero, lo mismo que con tantos otros engaños, las implicaciones políticas y sociológicas son inmensas y terribles.

¿En qué sistema vivimos? ¿Cómo podríamos mejorarlo? ¿Está tan seguro el autor del hilo que el liberalismo es una buena forma de combatir esta conspiración, cuando es en el libre mercado que venden sus revistas y propagan sus ideas ciertos grupos en la sombra?
 

AYN RANDiano2

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¿Está tan seguro el autor del hilo que el liberalismo es una buena forma de combatir esta conspiración, cuando es en el libre mercado que venden sus revistas y propagan sus ideas ciertos grupos en la sombra?
El respaldo último del "VIH/SIDA" es ESTATAL.

Son INDIVIDUOS como Peter Duesberg, Kary Mullis o el último Disidente de a pie (yo mismo, sin ir más lejos) los que combatimos a este Behemot pseudocientífico.

No hay "libre mercado" desde el momento en el cual EL ESTADO te "regala" los "tests de VIH" y los "tratamientos".

Sin intervención estatal este asunto hubiese terminado para 1989 a más tardar.

Pídeles a los "infectados" 50€ por "testarse" o 30.000€ al año por "tratarse" y ya verás como empiezan a preguntarse si realmente hacen falta esos gastos.
 

MiNombreEsLegión

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Por qué los USA han escogido "militarizar" esta magufada lo ignoro. Hay especulaciones mil:
* Herramienta de control de población mundial: Eugenesia, control demográfico...hay todo tipo de especulaciones.

* Poder envenenar a placer al grupo que deseen con designarlo "grupo de riesgo".

* Royalties de patentes relacionadas con el "VIH" (compartidas por USA y Francia).

* Prestigio y poder de ser considerados los conocedores de los "remedios" de una supuesta "plaga mortal".

* La lluvia de reclamaciones y el desprestigio atroz que sufrirían si dijesen "nos equivocamos en 1984".
Puede ser un poco de todo, al fin y al cabo, el SIDA es, después de la investigación acerca de la disfunción eréctil y el aumento de pene, lo que mas dinero recibe en el campo de la medicina (también habría que preguntarse si no es un poco de coña, porque su "gracia" tiene).

Lo de los militares no lo sabía, aunque era de esperar.
 

Manoliko

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El respaldo último del "VIH/SIDA" es ESTATAL.

Pídeles a los "infectados" 50€ por "testarse" o 30.000€ al año por "tratarse" y ya verás como empiezan a preguntarse si realmente hacen falta esos gastos.
Hombre... si la gente piensa que esos 30.000 van a salvarle la vida; seguro que el que los pueda pagar los pagaría.
 

AYN RANDiano2

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Hombre... si la gente piensa que esos 30.000 van a salvarle la vida; seguro que el que los pueda pagar los pagaría.
Seguro que investigarían un poquito (un bastante) más de si realmente está justificado gastarse 30.000€.

Para empezar los fabricantes tendrían que convencer SIN AYUDA DEL ESTADO a la gente que ser "VIH+" supone que uno va a morir.

Mucha gente se volvería escéptica de golpe si el estado se saliese del negocio propagandístico de convencer a la gente de semejante magufada:







Saque usted el "prestigio" del estado de estas magufadas y mucha gente empezaría a olerse la tostada al ver anuncios pagados por la Farmafia para que te hagas una prueba de la Farmafia que si das positivo te obliga a pagar 30.000€/año a la Farmafia "para no morir".
 
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AYN RANDiano2

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Puede ser un poco de todo, al fin y al cabo, el SIDA es, después de la investigación acerca de la disfunción eréctil y el aumento de pene, lo que mas dinero recibe en el campo de la medicina (también habría que preguntarse si no es un poco de coña, porque su "gracia" tiene)
Tiene más gracia aún: Los Poppers funcionaban (y funcionan) con los mismos efectos que el Sildenafil.

¡Un homólogo (en efectos) al Sildenafil disponible desde finales de los años 1960!. La "pega" es que los Poppers son (en palabras de Peter Duesberg) "tóxicos infernales". Se dice que después de consumir Poppers el tejido muscular de una persona no sería apto para el consumo (su fuese un animal) debido al exceso de Nitritos (se usan también como conservantes de carnes y embutidos).

Si todo esto lo hubiesen montado los "dioses" de Salvador Freixedo no les hubiese salido mejor: Hacen enfermar primero a los homosexuales por sus ansias sexuales (Poppers) y después los hacen enfermar por el miedo y la culpa que crea el sexo ("antiretrovirales").
 
  Es duro pedir pero más duro es robar
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