Dating sites hiv positive people usa

29-Feb-2020 12:37 by 6 Comments

Dating sites hiv positive people usa

Finally the author should be congratulated for “daring where Angels feared to tread.” -PROFESSOR P S IGBIGBI “I have never learned so much in such a short time – your book, “AIDS : What the Discoverers of HIV Never Admitted”, is absolutely the most revealing and clearly documented work I’ve ever read!

Rather such a dramatic drop in tubercular mycobacterial avium suggested to him a direct affect on the part of “antiretrovirals” against AIDS-borne fowl tuberculosis. Barré had been trained in mouse retroviral techniques requiring the measurement of reverse transcriptase in Robert Bassin’s National Cancer Institute (NCI) lab. avium victims having the same nausea or diarrhea so frequently attributed to ‘HIV’. In a follow-up study, Hirsch found that destruction through apoptosis of immune cells was increased at the site of active MTB infection in patients with pleural TB, regardless of whether the patient had “HIV” or did not have “HIV”. And it was the annihilation of just such infection swallowing macrophages, critical to reticuloendothelial ultrastructure, that M. avium (4), or more almost certainly both working in concert, furnished the key to AIDS comprehensive devastation to the human immune system. Apoptosis of Mycobacterium avium-infected macrophages is mediated by both tumour necrosis factor TNF and Fas, and involves the activation of caspases. In conjunction with colleagues in San Francisco and at the University of Nebraska, he first pursued, as lead author and originator, a novel technique to kill AIDS mycobacteria and tuberculosis, producing outstanding results [see Journal of Infectious Diseases 186, no. Recently he contributed a chapter regarding these findings to Sleator and Hill’s textbook Patho-biotechnology, published by Landes Bioscience. [16] Whether this situation will change with novel strategies now in the pipeline [3] remains to be seen. In addition, Broxmeyer has written many peer-reviewed articles, available on Pub Med of the US Library of Medicine, National Institutes of Health, at: It is only fitting that a bizarre tale — the history and promoting of “HIV” and its drug cocktails — end in a bizarre way: that drugs called antiretrovirals only real benefit is to toxically try to contain tubercular infections, which they were not designed to do in the first place. Central nervous system tuberculosis with the acquired immunodeficiency syndrome and its related complex. One argument often used by HIV pharmaceutical-sponsored devotees is to show how their antiretrovirals increase life spans of AIDS victims. This patient did not yet have full-blown AIDS, but his history and symptoms were strongly suggestive. Montagnier put the tissue into cell cultures of T-lymphocytes. Looking only for a retrovirus, the team cultured whole tissue lymph node lysates. It would be the beginning of a long, long line of research work based on indirect evidence. Morphological, biological, and immunological studies on isolates from tumors and leukemic blood. And at least one person is infected with it per second — someone dying from TB every ten seconds. [32] In 1978, the first European measurement of a low CD4 in AIDS was on a patient with disseminated atypical tuberculosis [Mycobacteria fortuitum], [5] closely related to Mycobacterium tuberculosis. Patterns of CD4 cell changes after HIV-1 infection indicate the existence of a codeterminant of AIDS. But does antiretroviral therapy [HAART] really prolong lives? To some orthodox believers, yes, by an average of 13-15 years. Later, looking at Montagnier’s tissue cultures microscopically there were many granules, some of which were felt to look like retroviruses. Tuberculosis, indeed kills two to three million people each year, more than any other infectious disease in the world today. Mycobacterial disease in patients with human immunodeficiency virus infection. As early as 1987, Canadian researchers realized that mycobacteria such as tuberculosis alone could be responsible for direct CD4 killing and much of the immunosuppression found in AIDS. On the other hand the growing number of scientists that doubt that the HIV retrovirus or any other retrovirus could not be behind the AIDS epidemic, stand on firm ground. TRAGIC COST OF PREMATURE CONSENSUS Pasteur Institute, Paris, January, 1983 The Pasteur Institute squeezed head of cancer virology, Luc Montagnier, into the pressure cooker of finding an AIDS retrovirus when its production of Hepatitis B vaccine, accounting for a significant part of its income, and in part processed from pooled American homosexual blood, came under fire. Montagnier, who for his part was exclusively looking for a retrovirus related to Gallo’s failed HTLV-1, instead came upon the retrovirus “LAV” which, in wastebasket category fashion, stood for “Lymphadenopathy Associated Virus”. Because his assistant Françoise Barré-Sinoussi said that she found it………at least she found something that looked like it. By 1983, the certain knowledge that AIDS had begun its wholesale slaughter of Africans, mainly through heterosexual sex, sent shudders down the back of a world in which, not since the last great sexual pandemic of syphilis five centuries before, had there been the specter of anything comparable. [28] And although attempt after attempt has been made to say that low CD4 is synonymous with HIV, the fact is that known AIDS-risk groups may have low CD4, even in the face of persistently negative HIV antibody tests.

So reasonable is the latter assumption, in fact, that eventually Dr. LAV was so named because the French homosexual fashion designer it was first isolated from had enlarged, inflamed neck nodes [lymphadenopathy], a common early AIDS feature. Tuberculosis or persistent generalized lymphadenopathy in HIV disease. Men and woman were transmitting AIDS back and forth sexually in heretofore unheralded numbers. [7,9,26] That HIV is not the cause of apoptosis [a sort of remote-control immune cell destruction] of CD4 cells is more than amply shown in chronically infected retroviral cell lines, where although what is claimed to be “HIV” is produced, apoptosis is not detected.

Yet we are still led to believe that we are fortunate, even ‘lucky’ that retroviruses, only discovered in the 1970s, were uncovered just in time to label them the culprit in a killer AIDS epidemic.

And ‘lucky’ that two ‘HIVs’ were discovered in rapid succession and the technology and theory to link AIDS to the ‘HIV’ retrovirus were fully in place, for the first time in history, only a few years prior to the recognition of the AIDS epidemic. Even as of the 20th anniversary of the first reported AIDS cases passed, AIDS had infected nearly 60 million people of which almost 22 million, including nearly half a million Americans died, and 8,500 AIDS deaths occurred daily.

However logic insists that such immediate benefit cannot be the result of any antiretroviral action, whose supposed benefits [decrease in ‘viral load’, rise in CD4] come slowly. Jackson marveled at the many forms of tuberculosis, including the tiny granules which the German Hans Much saw in 1908, that soon became known as Much’s granules. Mellon, Fisher New studies on the filterability of pure cultures of the tubercle group of microorganisms. This deeply disturbed her, as retroviruses typically didn’t kill cells. By January 25th, 1983, Barré-Sinoussi’s reverse transcriptase radioactivity counter was clicking-away with increased activity, which to her, as a retrovirologist, meant that her lymph node ‘retrovirus’ LAV must be multiplying. The ultrastructural and immunohistochemical demonstration of viral particles in lymph nodes from human immunodeficiencyvirus-related and non-human immunodeficiency virus-related lymphadenopathy syndromes. But in the developing countries of Asia and Africa, where the AIDS epidemic was still new in 1983, epidemic waves of tuberculosis had not yet reached their zenith. [25] Moreover, TB often presented before the development of immune dysfunction, either with or without HIV. tuberculosis in their blood had significantly lower CD4 counts. It has long been known that a low CD4 count in and of itself did not automatically lead to the severe immunodepression found in AIDS.

Rather such testimony likely reflects an antibiotic or anti-inflammatory effect. [4] In 1910 Fontes proved that Much’s granules, as a sub-classification of Kleinberger’s L-forms, were filterable and therefore also often mistaken for viruses. Bemerkungen uber die Tuberkulose Infektion und ihr virus. But reverse transcriptase was nonspecific and was also found elevated in events leading to the death of CD4 lymphocytes by tuberculosis [16], as well as in M. [10] As this TB epidemic continued to seethe, it was these very continents that would show the highest TB mortality and morbidity, even before AIDS came into the picture [7] — and would prove to be the future epicenters for AIDS. [30] In fact of all the infections involved in AIDS, none were associated with as low CD4 cell counts as were tubercular infections. [18] Case Western Reserve University, Ohio, July, 1998 Although previously demonstrated [19,8], the actual ferociousness of CD4 tubercular attack was amply shown in papers such as Hirsh’s 1999 Ohio study, which showed that not only were 30% of CD4 but also non-CD4 slaughtered within 98 hours of co-culture with TB, a 20-fold increase. Disseminatred mycobacterial histiocytosis due to M. fortuitum associated with helper T-lymphocyte immune deficiency.

To others, this is absurd —citing that the rate of death among “HIV/AIDS” was just being increasingly redefined by the HIV powers that be to include illnesses less life-threatening than that behind the original AIDS epidemic. But they were inside cells and tissues – not whole viral particles — and had different shapes and sizes. They seemed to show all forms of ‘viral maturation’, but were they viral? Die Variation des tuberkelbacillus in form and wirkung. THE RACE Pasteur Institute, Paris, 1983 Gallo’s leukemic retrovirus (HTLV), which Barré and Montagnier thought they had isolated, should have led to the wild proliferation of lymphocytes. It did not need to be defined by any harmless retrovirus………did its own defining. Furthermore, such a tubercular immune system throttle could persist for life, even when the disease wasn’t progressive.