*Edit Title* Louisiana what’s going on - 1 & 3 GET TESTED!

Info on the Lion's grip?

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"King of the jungle"
 
Ehhh.... there’s time for discussion and there’s time to shoot things down. “It’s the gay blacks making aids” is not a topic of discussion. You call that BS out and leave it be.
 
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: HIV/AIDS (The Basics)" and "Patient education: Tests to monitor HIV (The Basics)")

SUMMARY

●Human immunodeficiency virus (HIV) infection can be divided into the following stages: viral transmission, acute HIV infection with seroconversion, and chronic HIV infection with or without evidence of the acquired immunodeficiency syndrome (AIDS). (See 'Overview of stages of HIV infection' above.)

●HIV infection is usually acquired through sexual intercourse, exposure to contaminated blood, or perinatal transmission. Risk factors for transmission include high viral load, certain sexual behaviors, presence of ulcerative sexually transmitted infections (STIs), lack of circumcision, and certain host and genetic factors. (See 'Viral transmission' above.)

●Symptomatic acute HIV infection is characterized by fever, lymphadenopathy, sore throat, rash, myalgia/arthralgia, and headache; however, a substantial proportion of patients with early HIV infection are asymptomatic. Early HIV infection is a period of rapid viral replication with typically very high viral RNA levels. By approximately six months of infection, plasma viremia has reached a steady state level. (See 'Acute and early HIV infection' above and "Acute and early HIV infection: Clinical manifestations and diagnosis".)

●The period of chronic HIV infection following early infection and seroconversion but prior to the development of severe immunosuppression is characterized by relative stability of viral levels and a progressive decline in CD4 cell count. The rate of CD4 cell decline correlates with the level of viremia. During this stage, the majority of HIV-infected patients are asymptomatic, although some may have generalized lymphadenopathy. However, certain HIV-associated clinical findings, such as thrush, seborrheic dermatitis, and susceptibility to herpesvirus and human papillomavirus (HPV) infections, bacterial pneumonia, and tuberculosis, frequently occur despite a CD4 cell count >200 cells/microL. (See 'Chronic HIV infection, without AIDS' above.)

●AIDS is defined by a CD4 cell count <200 cells/microL or the presence of any AIDS-defining condition (table 5) regardless of the CD4 cell count. (See 'AIDS and advanced HIV infection' above.)

●AIDS-defining conditions are opportunistic illnesses that occur more frequently or more severely in immunocompromised hosts. These include mainly opportunistic infections, such as Pneumocystis jirovecii pneumonia, toxoplasmosis, and disseminated Mycobacterium avium infection. Certain malignancies (Kaposi sarcoma, lymphoma), as well as conditions without clear alternative etiology thought to be related to uncontrolled HIV infection itself, such as wasting or encephalopathy, are also AIDS-defining conditions. (See 'AIDS defining conditions' above.)

●A minority of HIV-infected patients, despite not being on antiretroviral therapy (ART), has very low levels of viremia. They are considered HIV controllers. A subset of these patients are referred to as non-viremic controllers because they have no detectable viremia, even on ultrasensitive diagnostic testing. (See 'HIV controllers' above.)

●HIV-1 causes the vast majority of HIV infections worldwide, although HIV-2 is an important cause of infection in certain regions of the world, such as West Africa. Compared with HIV-1, HIV-2 infection is characterized by lower levels of plasma virus, slower declines in the CD4 cell count, and a longer asymptomatic period of chronic infection. (See "Epidemiology, transmission, natural history, and pathogenesis of HIV-2 infection" and "Clinical manifestations and diagnosis of HIV-2 infection" and "Treatment of HIV-2 infection".)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge John G Bartlett, MD, who contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
  1. Mocroft A, Ledergerber B, Katlama C, et al. Decline in the AIDS and death rates in the EuroSIDA study: an observational study. Lancet 2003; 362:22.
  2. Samji H, Cescon A, Hogg RS, et al. Closing the gap: increases in life expectancy among treated HIV-positive individuals in the United States and Canada. PLoS One 2013; 8:e81355.
  3. Centers for Disease Control and Prevention (CDC). Revised surveillance case definition for HIV infection--United States, 2014. MMWR Recomm Rep 2014; 63:1.
  4. World Health Organization. WHO case definitions of HIV for surveillance and revised clinical staging and immunologic classification of HIV-related disease in adults and children. World Health Organization, Geneva, Switzerland, 2007, 1-48.
  5. Adler MW. ABC of Aids: Development of the epidemic. BMJ 2001; 322:1226.
  6. Quinn TC, Wawer MJ, Sewankambo N, et al. Viral load and heterosexual transmission of human immunodeficiency virus type 1. Rakai Project Study Group. N Engl J Med 2000; 342:921.
  7. Gray RH, Wawer MJ, Brookmeyer R, et al. Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda. Lancet 2001; 357:1149.
  8. Dorak MT, Tang J, Penman-Aguilar A, et al. Transmission of HIV-1 and HLA-B allele-sharing within serodiscordant heterosexual Zambian couples. Lancet 2004; 363:2137.
  9. Wawer MJ, Gray RH, Sewankambo NK, et al. Rates of HIV-1 transmission per coital act, by stage of HIV-1 infection, in Rakai, Uganda. J Infect Dis 2005; 191:1403.
  10. Buchbinder SP, Vittinghoff E, Heagerty PJ, et al. Sexual risk, nitrite inhalant use, and lack of circumcision associated with HIV seroconversion in men who have sex with men in the United States. J Acquir Immune Defic Syndr 2005; 39:82.
  11. Pilcher CD, Fiscus SA, Nguyen TQ, et al. Detection of acute infections during HIV testing in North Carolina. N Engl J Med 2005; 352:1873.
  12. Bailey RC, Moses S, Parker CB, et al. Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial. Lancet 2007; 369:643.
  13. Gray RH, Kigozi G, Serwadda D, et al. Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial. Lancet 2007; 369:657.
  14. Gray R, Kigozi G, Kong X, et al. The effectiveness of male circumcision for HIV prevention and effects on risk behaviors in a posttrial follow-up study. AIDS 2012; 26:609.
  15. Auvert B, Taljaard D, Lagarde E, et al. Randomized, controlled intervention trial of male circumcision for reduction of HIV infection risk: the ANRS 1265 Trial. PLoS Med 2005; 2:e298.
  16. Baeten JM, Donnell D, Kapiga SH, et al. Male circumcision and risk of male-to-female HIV-1 transmission: a multinational prospective study in African HIV-1-serodiscordant couples. AIDS 2010; 24:737.
  17. Fiebig EW, Wright DJ, Rawal BD, et al. Dynamics of HIV viremia and antibody seroconversion in plasma donors: implications for diagnosis and staging of primary HIV infection. AIDS 2003; 17:1871.
  18. Branson BM, Stekler JD. Detection of acute HIV infection: we can't close the window. J Infect Dis 2012; 205:521.
  19. Branson BM, Ginocchio CC. Introduction to 2013 Journal of Clinical Virology supplement on HIV testing algorithms. J Clin Virol 2013; 58 Suppl 1:e1.
  20. Pedersen C, Lindhardt BO, Jensen BL, et al. Clinical course of primary HIV infection: consequences for subsequent course of infection. BMJ 1989; 299:154.
  21. Niu MT, Stein DS, Schnittman SM. Primary human immunodeficiency virus type 1 infection: review of pathogenesis and early treatment intervention in humans and animal retrovirus infections. J Infect Dis 1993; 168:1490.
  22. Pantaleo G, Demarest JF, Schacker T, et al. The qualitative nature of the primary immune response to HIV infection is a prognosticator of disease progression independent of the initial level of plasma viremia. Proc Natl Acad Sci U S A 1997; 94:254.
  23. Musey L, Hughes J, Schacker T, et al. Cytotoxic-T-cell responses, viral load, and disease progression in early human immunodeficiency virus type 1 infection. N Engl J Med 1997; 337:1267.
  24. Mellors JW, Kingsley LA, Rinaldo CR Jr, et al. Quantitation of HIV-1 RNA in plasma predicts outcome after seroconversion. Ann Intern Med 1995; 122:573.
  25. Lavreys L, Baeten JM, Chohan V, et al. Higher set point plasma viral load and more-severe acute HIV type 1 (HIV-1) illness predict mortality among high-risk HIV-1-infected African women. Clin Infect Dis 2006; 42:1333.
  26. Schacker TW, Hughes JP, Shea T, et al. Biological and virologic characteristics of primary HIV infection. Ann Intern Med 1998; 128:613.
  27. Madec Y, Boufassa F, Porter K, et al. Spontaneous control of viral load and CD4 cell count progression among HIV-1 seroconverters. AIDS 2005; 19:2001.
  28. Osmond D, Chaisson R, Moss A, et al. Lymphadenopathy in asymptomatic patients seropositive for HIV. N Engl J Med 1987; 317:246.
  29. Sterling, T and Chaisson, R. General clinical manifestations of Human Immunodeficiency Virus infection (including the acute antiretroviral syndrome and oral, cutaneous, renal, ocular, metabolic, and cardiac diseases). In: Principles and Practice of Infectious Diseases, 7, Mandell GL, Bennet JE, and Dolin R (Eds), 2010. p.1705.
  30. Farizo KM, Buehler JW, Chamberland ME, et al. Spectrum of disease in persons with human immunodeficiency virus infection in the United States. JAMA 1992; 267:1798.
  31. Popovich KJ, Hota B, Aroutcheva A, et al. Community-associated methicillin-resistant Staphylococcus aureus colonization burden in HIV-infected patients. Clin Infect Dis 2013; 56:1067.
  32. Zervou FN, Zacharioudakis IM, Ziakas PD, et al. Prevalence of and risk factors for methicillin-resistant Staphylococcus aureus colonization in HIV infection: a meta-analysis. Clin Infect Dis 2014; 59:1302.
  33. Wei X, Ghosh SK, Taylor ME, et al. Viral dynamics in human immunodeficiency virus type 1 infection. Nature 1995; 373:117.
  34. Ho DD, Neumann AU, Perelson AS, et al. Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. Nature 1995; 373:123.
  35. Henrard DR, Phillips JF, Muenz LR, et al. Natural history of HIV-1 cell-free viremia. JAMA 1995; 274:554.
  36. Pantaleo G, Graziosi C, Demarest JF, et al. HIV infection is active and progressive in lymphoid tissue during the clinically latent stage of disease. Nature 1993; 362:355.
  37. Henrich TJ, Hanhauser E, Marty FM, et al. Antiretroviral-free HIV-1 remission and viral rebound after allogeneic stem cell transplantation: report of 2 cases. Ann Intern Med 2014; 161:319.
  38. Gottlieb GS, Sow PS, Hawes SE, et al. Equal plasma viral loads predict a similar rate of CD4+ T cell decline in human immunodeficiency virus (HIV) type 1- and HIV-2-infected individuals from Senegal, West Africa. J Infect Dis 2002; 185:905.
  39. Touloumi G, Pantazis N, Pillay D, et al. Impact of HIV-1 subtype on CD4 count at HIV seroconversion, rate of decline, and viral load set point in European seroconverter cohorts. Clin Infect Dis 2013; 56:888.
  40. Mlisana K, Werner L, Garrett NJ, et al. Rapid disease progression in HIV-1 subtype C-infected South African women. Clin Infect Dis 2014; 59:1322.
  41. Stein DS, Korvick JA, Vermund SH. CD4+ lymphocyte cell enumeration for prediction of clinical course of human immunodeficiency virus disease: a review. J Infect Dis 1992; 165:352.
  42. Lodi S, Phillips A, Touloumi G, et al. Time from human immunodeficiency virus seroconversion to reaching CD4+ cell count thresholds <200, <350, and <500 Cells/mm³: assessment of need following changes in treatment guidelines. Clin Infect Dis 2011; 53:817.
  43. Schacker T, Collier AC, Hughes J, et al. Clinical and epidemiologic features of primary HIV infection. Ann Intern Med 1996; 125:257.
  44. Simon V, Ho DD, Abdool Karim Q. HIV/AIDS epidemiology, pathogenesis, prevention, and treatment. Lancet 2006; 368:489.
  45. Galai N, Vlahov D, Margolick JB, et al. Changes in markers of disease progression in HIV-1 seroconverters: a comparison between cohorts of injecting drug users and homosexual men. J Acquir Immune Defic Syndr Hum Retrovirol 1995; 8:66.
  46. Lang W, Perkins H, Anderson RE, et al. Patterns of T lymphocyte changes with human immunodeficiency virus infection: from seroconversion to the development of AIDS. J Acquir Immune Defic Syndr 1989; 2:63.
  47. Margolick JB, Muñoz A, Vlahov D, et al. Changes in T-lymphocyte subsets in intravenous drug users with HIV-1 infection. JAMA 1992; 267:1631.
  48. Hughes MD, Stein DS, Gundacker HM, et al. Within-subject variation in CD4 lymphocyte count in asymptomatic human immunodeficiency virus infection: implications for patient monitoring. J Infect Dis 1994; 169:28.
  49. Moir S, Malaspina A, Pickeral OK, et al. Decreased survival of B cells of HIV-viremic patients mediated by altered expression of receptors of the TNF superfamily. J Exp Med 2004; 200:587.
  50. Moir S, Malaspina A, Ogwaro KM, et al. HIV-1 induces phenotypic and functional perturbations of B cells in chronically infected individuals. Proc Natl Acad Sci U S A 2001; 98:10362.
  51. Greene M, Covinsky KE, Valcour V, et al. Geriatric Syndromes in Older HIV-Infected Adults. J Acquir Immune Defic Syndr 2015; 69:161.
  52. Aberg JA. Aging, inflammation, and HIV infection. Top Antivir Med 2012; 20:101.
  53. Jones JL, Hanson DL, Dworkin MS, et al. Surveillance for AIDS-defining opportunistic illnesses, 1992-1997. MMWR CDC Surveill Summ 1999; 48:1.
  54. Hanson DL, Chu SY, Farizo KM, Ward JW. Distribution of CD4+ T lymphocytes at diagnosis of acquired immunodeficiency syndrome-defining and other human immunodeficiency virus-related illnesses. The Adult and Adolescent Spectrum of HIV Disease Project Group. Arch Intern Med 1995; 155:1537.
  55. Taylor JM, Sy JP, Visscher B, Giorgi JV. CD4+ T-cell number at the time of acquired immunodeficiency syndrome. Am J Epidemiol 1995; 141:645.
  56. Karon JM, Buehler JW, Byers RH, et al. Projections of the number of persons diagnosed with AIDS and the number of immunosuppressed HIV-infected persons--United States, 1992-1994. MMWR Recomm Rep 1992; 41:1.
  57. Freedberg KA, Malabanan A, Samet JH, Libman H. Initial assessment of patients infected with human immunodeficiency virus: the yield and cost of laboratory testing. J Acquir Immune Defic Syndr 1994; 7:1134.
  58. Yarchoan R, Venzon DJ, Pluda JM, et al. CD4 count and the risk for death in patients infected with HIV receiving antiretroviral therapy. Ann Intern Med 1991; 115:184.
  59. Phillips AN, Elford J, Sabin C, et al. Immunodeficiency and the risk of death in HIV infection. JAMA 1992; 268:2662.
  60. Easterbrook PJ, Emami J, Moyle G, Gazzard BG. Progressive CD4 cell depletion and death in zidovudine-treated patients. J Acquir Immune Defic Syndr 1993; 6:927.
  61. Hsue PY, Hunt PW, Schnell A, et al. Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV-associated atherosclerosis. AIDS 2009; 23:1059.
  62. Pereyra F, Lo J, Triant VA, et al. Increased coronary atherosclerosis and immune activation in HIV-1 elite controllers. AIDS 2012; 26:2409.
  63. Pereyra F, Palmer S, Miura T, et al. Persistent low-level viremia in HIV-1 elite controllers and relationship to immunologic parameters. J Infect Dis 2009; 200:984.
  64. Dinoso JB, Kim SY, Siliciano RF, Blankson JN. A comparison of viral loads between HIV-1-infected elite suppressors and individuals who receive suppressive highly active antiretroviral therapy. Clin Infect Dis 2008; 47:102.
  65. Migueles SA, Connors M. Long-term nonprogressive disease among untreated HIV-infected individuals: clinical implications of understanding immune control of HIV. JAMA 2010; 304:194.
  66. Klein MR, Miedema F. Long-term survivors of HIV-1 infection. Trends Microbiol 1995; 3:386.
  67. Migueles SA, Osborne CM, Royce C, et al. Lytic granule loading of CD8+ T cells is required for HIV-infected cell elimination associated with immune control. Immunity 2008; 29:1009.
  68. Sedaghat AR, Rastegar DA, O'Connell KA, et al. T cell dynamics and the response to HAART in a cohort of HIV-1-infected elite suppressors. Clin Infect Dis 2009; 49:1763.
  69. Leon A, Perez I, Ruiz-Mateos E, et al. Rate and predictors of progression in elite and viremic HIV-1 controllers. AIDS 2016; 30:1209.
  70. Walker BD. Elite control of HIV Infection: implications for vaccines and treatment. Top HIV Med 2007; 15:134.
  71. Pereyra F, Addo MM, Kaufmann DE, et al. Genetic and immunologic heterogeneity among persons who control HIV infection in the absence of therapy. J Infect Dis 2008; 197:563.
cracks me up when "physicians" think they got all the answers
all doctors are
are folks who memorized a damn textbook
anyone can memorize a textbook and become a doctor
doctors think they so smart
i work in the medical field
and have met plenty of idiot doctors
who are dumb as a bag of rocks
mind u
does take a lot of work to be a doctor
but again
they just all memorizing a damn book
 
cracks me up when "physicians" think they got all the answers
all doctors are
are folks who memorized a damn textbook
anyone can memorize a textbook and become a doctor
doctors think they so smart
i work in the medical field
and have met plenty of idiot doctors
who are dumb as a bag of rocks
I’m not “anti doctor” but I’ve seen plenty of cases where they’ve destroyed kids with medications. Sad and irreversible
 
cracks me up when "physicians" think they got all the answers
all doctors are
are folks who memorized a damn textbook
anyone can memorize a textbook and become a doctor
doctors think they so smart
i work in the medical field
and have met plenty of idiot doctors
who are dumb as a bag of rocks
mind u
does take a lot of work to be a doctor
but again
they just all memorizing a damn book
When one of your kids are sick, who do you seek help from?

Your local Youtube conspiracy theorist?
 
cracks me up when "physicians" think they got all the answers
all doctors are
are folks who memorized a damn textbook
anyone can memorize a textbook and become a doctor
doctors think they so smart
i work in the medical field
and have met plenty of idiot doctors
who are dumb as a bag of rocks
mind u
does take a lot of work to be a doctor
but again
they just all memorizing a damn book
I spoke their language and cited the credentials that they usually would to validate their point of view.I should've just posted this from the jump and left it at that.

From
Dr Eleni Papadopulos-Eleopulos

Reappraising AIDS Dec. 1999

Eleni Papadopulos-Eleopulos (1) Valendar F.Turner (2) John M Papadimitriou (3) Helman Alphonso (4) David Causer (1)

There is a tide in the affairs of men, which, taken at the flood, leads on to fortune; Omitted, all the voyage of their life is bound in shallows and in miseries. On such a full sea are we now afloat; And we must take the current when it serves, or lose our ventures.

-- Julius Caesar Act V Scene III



Over recent months debate has been taking place amongst the HIV/AIDS dissident groups regarding the wisdom of taking up the issue of HIV isolation as an argument in our fight against mainstream AIDS science. According to some dissidents this question should not be raised because:

  1. it will provide HIV/AIDS protagonists with additional ammunition with which to discredit us;
  2. it makes little difference if people are being killed in the name of a non-existent or a merely harmless virus;
  3. it is an "existentialist" discussion.
On the other hand, other dissidents are of the opinion that we have no strong arguments. To quote Vladimir Koliadin, "There are many observations…which seem to provide strong support for the official theory and to refute dissident views. Dissidents must "not turn the blind eye to inconvenient facts".

From the very beginning the Perth group questioned the evidence which may well prove the most significant "inconvenient" fact to fly in the face of all HIV/AIDS protagonists. If the data do not prove beyond reasonable doubt the existence of HIV then, in terms of a putative exogenous retrovirus, there can be no "observations…to provide strong support for the official theory". This is a point from which the staunchest of each side cannot escape. However, although our group has long published many scientific and epidemiological reasons for questioning the existence of HIV, we largely chose to leave the facts speak for themselves rather than making pronouncements such as "HIV does not exist". There were two reasons for this:

  1. To facilitate publication;
  2. To avoid a split in the group which Charles Thomas founded. Also, we could not exclude the possibility that the HIV theory of AIDS could be deconstructed without questioning the existence of HIV.
In 1996, when Peter Duesberg wrote a paper claiming the Continuum prize, he directly challenged the Perth group. We then had no choice but to openly defend our position, and we repeated the reasons in our lecture given at the 1998 Geneva International AIDS Conference. At present there are four reasons why it is necessary to question the isolation and thus the existence of HIV:

  1. Since 1996 it has become clear that, as far as the existence of HIV is concerned, the Group for Reappraising AIDS is divided. Some of the best known HIV experts are aware of this fact and it is now too late to pretend otherwise.
  2. There is no proof that such an entity exists. To claim the opposite is to deny the scientific evidence. Certainly conduct an anti-HIV debate avoiding this issue as exemplified by many in our midst. However, in arguing against the HIV hypothesis of AIDS in this manner one has to be content with half truths.
  3. "HIV" is the main obstacle, indeed, the only obstacle, in deconstructing the HIV theory of AIDS.
  4. Demonstrating that HIV has not been isolated is not an "existentialist" debate. In fact we consider this to be the strongest argument we can muster.
If we accept there is no proof for the existence of HIV then undoubtedly "the construction AIDS, also called HIV disease, collapses immediately and all so called "HIV tests" are automatically unmasked as being useless". If, on the other hand, we accept the existence of HIV, the debate could be endless, no matter how courageously one fights and what sacrifices one makes. In this regard Peter Duesberg’s unprecedented contribution is a wise and timely reminder to all of us.

Why HIV isolation is necessary

The word "isolation" appears frequently in scientific papers and in debate concerning HIV and indeed in virology in general. For example, Montagnier’s 1983 and two of Gallo’s 1984 Science papers contain the word in their titles as well as the text. Use of this word signals the reader that the experimenter is claiming that the data presented proves that a virus exists. If this is the first such report the authors may claim to the discovery of a particular virus. What all scientists must consider is whether the data presented as "isolation" do indeed justify the claims.

A virus is an obligatory intracellular, replicating particle of particular physical and chemical properties. Thus the first absolutely necessary, but not sufficient step in proving the existence of a retrovirus is to isolate retrovirus-like particles. That is, obtain the particles separate from everything else. In other words, purify them. There are many reasons for this including the following:

1. To prove that the retrovirus-like particles are infectious, that is, the particles are a virus.

Finding a retrovirus either in vitro or in vivo is not proof that it originated from outside, that is, the virus is infectious, exogenous. Furthermore, Gallo was well aware of this problem as far back as 1976 when he wrote: "Release of virus-like particles morphologically and biochemically resembling type-C virus but apparently lacking the ability to replicate have been frequently observed from leukaemic tissue". In other words, it is not sufficient to claim a particle is a retrovirus merely on appearances. To prove that retrovirus-like particles observed in a culture are virus particles one must isolate (purify) the particles, characterise their proteins and RNA and introduce them in a secondary culture, preferably containing cells of a different type than the primary culture. If any particles are released in the secondary culture, isolate them and prove that their proteins and RNA are exactly the same as those of the particles isolated from the primary culture. In these types of experiments one must not ignore the pivotal importance of proper controls.

2. To determine their biological effects.

For this one must use pure particles otherwise it is impossible to determine whether the effects are due to the virus particle or to contaminants. As Peter Duesberg has pointed out in "Koch's second postulate: The microbe must be isolated from the host and grown in pure culture", "was designed to prove that a given disease was caused by a particular germ, rather than by some undetermined mixture of non-infectious substances". Ironically Peyton Rous, the discoverer of retroviruses, issued the same caveat for "filterable agents", "retroviruses" in 1911.

3. To characterise the viral proteins.

The only way to prove that a protein is a viral protein is to obtain it from that object, or when the object is very small, as is the case of viruses, from material which contains nothing else but virus particles. In the material contains impurities which also have proteins it is not possible to determine what is viral and what is not. Only after the viral proteins are characterised they can be used as antigens in the antibody tests.

4. To characterise the viral genome.

As for viral proteins the only way to prove that a stretch of RNA is viral, it is to obtain it from material which contains nothing else but virus particles. If the material contains impurities, the impurities must not contain RNA. Then, and only then, can the RNA and its cDNA be used as probes and primers for genomic hybridisation and PCR studies.

5. To use it as a gold standard.

Just because a virus or viral protein reacts with an antibody present in a patient's sera, this does not prove that the antibody is directed against the virus or its proteins. That is, the reaction is specific. To determine the specificity of an antibody reaction one must use the virus as a gold standard. Protagonist HIV experts such as Dr. Donald Francis agree. Speculating on a viral cause for AIDS in 1983, Francis wrote, "One must rely on more elaborate detection methods through which, by some specific tool, one can "see" a virus. Some specific substances, such as antibody or nucleic acids, will identify viruses even if the cells remain alive. The problem here is that such methods can be developed only if we know what we are looking for. That is, if we are looking for a known virus we can vaccinate a guinea pig, for example, with pure virus...Obviously, though, if we don't know what virus we are searching for and we are thus unable to raise antibodies in guinea pigs, it is difficult to use these methods...we would be looking for something that might or might not be there using techniques that might or might not work" (italics ours). The only way to perform hybridisation and PCR studies is to use the viral RNA or its cDNA or small fragments of it, as probes and primers. However, as with antibodies which react with viral proteins, a positive result, especially a positive PCR result, does not guarantee that what is detected is viral RNA. To determine the specificity of the PCR the virus must be used as a gold standard.

HIV "Isolation"

All retrovirologists agree that one of the principal defining physical characteristics of retroviruses is their density. In sucrose density gradients they band at the density of 1.16g/ml. Using the method of sucrose density banding in 1983 Francoise Barre-Sinoussi, Luc Montagnier and their colleagues claimed to have isolated a retrovirus, that is, to have obtained material which contained nothing else but "purified labelled virus" which now is known as HIV. Similar claims were reported by Robert Gallo’s group in 1984. It goes without saying that if the material was pure HIV, then all the proteins present in such material must be HIV proteins. Instead, only the proteins which were found to more often react with sera from AIDS patients and those at risk were said to be HIV proteins, and the antibodies which reacted with them the specific HIV antibodies. Since then the reaction of these proteins with antibodies is considered proof for HIV infection. Again, if their material was pure HIV then all the nucleic acids present in their material must be the HIV genome. Instead, only some fragments of RNA rich in adenine were arbitrary chosen and were said to constitute the HIV genome. Since then, these fragments have been used as probes and primers for hybridisation and PCR studies, including the determination of "viral load".

The biggest problem in accepting Montagnier's and Gallo's groups claims is the fact that neither published even one electron microscope picture of the "pure" HIV to prove that the material contained nothing else but isolated, retrovirus-like particles, "purified labelled virus". In 1997 Montagnier was asked by the French Journalist Djamel Tahi why such pictures were not published. Incredibly Montagnier replied because in what his group called "purified" HIV there were no particles with the "morphology typical of retroviruses". When he was asked if the Gallo group purified HIV, Montagnier replied: "I don't know if he really purified. I don't believe so". If this is the case then the 1983 Montagnier findings and the 1984 Gallo's finding, prove beyond all reasonable doubt that they did not have any retrovirus much less a unique retrovirus, and that the proteins and the RNAs which were present in their "purified" material could not have been of retroviral origin.

In the same year, 1997, some of the best known HIV experts accepted that no evidence existed which proved HIV isolation and thus a "virus to be used for biochemical and serological analyses or as an immunogen". In that year, two papers were published in Virology with the first electron micrographs of "purified HIV" obtained by banding the supernatant of "infected" cultures in sucrose density gradients. The authors of both studies claimed that their "purified" material contained some particles which looked like retroviruses and were said to be the HIV particles. But they admitted that their material predominantly contained particles which were not viruses but "mock virus", that is, "budding membrane particles frequently called microvesicles". Furthermore, "The cellular vesicles appear to be a heterogeneous population of both electron-lucent and electron-dense membrane delineated vesicles ranging in size from about 50 to 500nm". Many, but not all of these mock viruses "appear "empty" by electron microscopy". According to the authors of these studies, one of the reasons that some of the "mock virus" particles appear to have no core "might be that the vesicles contain large amounts of protein and nucleic acid which are unstructured". They showed that the microvesicles "are a major contaminant" of the "purified" HIV. Indeed, the caption to one of the electron micrographs reads, "Purified vesicles from infected H9 cells (a) and activated PBMC (b) supernatants", not purified HIV.


In a further experiment the supernatant from non-infected cultures was also banded in sucrose gradients. They claimed that the banded material from these cultures contained only microvesicles, "mock virus" particles but no particles with the morphology of HIV. The mock virus particles contains both DNA and RNA, including mRNA which is known to be poly-A rich.

No reason(s) is given, other than morphological, for why some of the particles in the fractions from the "infected" cells are virus particles and the others "mock virus". As far as morphology is concerned, none of the particles have all the morphological characteristics attributed to HIV, or even retroviruses.

The minimum absolutely necessary but not sufficient condition to claim that what are called "HIV-1 particles" are a retrovirus and not cellular microvesicles is to show that the sucrose density fractions obtained from the "infected" cells contain proteins which are not present in the same fractions obtained from non-infected cells. However, Bess et al have shown this is not the case. The only difference one can see in their SDS-polyacrylamide gel electrophoresis strips of "purified virus" and "mock virus" is quantitative, not qualitative. This quantitative difference may be due to many reasons including the fact that there were significant differences in the history and the mode of preparation of the non-infected and "infected" H9 cell cultures.

That the "viral" proteins are nothing more than cellular proteins was further demonstrated by Arthur, Bess and their associates. In their efforts to make an HIV vaccine they immunised macaques with, amongst other antigens, "mock virus", that is sucrose density banded material from the supernatants of non-infected H9 cell cultures. After the initial immunisation the monkeys were given boosters at 4, 8 and 12 weeks. The animals were then challenged with "SIV" propagated either in H9 cells or macaque cells. When the WBs obtained after immunisation but before "SIV" challenge were compared with the WBs post-challenge, it was found that challenge with "SIV" propagated in macaque cells had some additional bands. However, the WBs obtained after the challenge with SIV propagated in H9 cells were identical with the WBs obtained after immunisation, but before challenge. In other words, the protein immunogens in the "virus" were identical with the immunogens in the "mock virus".

Since both the "mock virus" and "purified" virus contain the same proteins, then all the particles seen in the banded materials including what the authors of the 1997 virology papers call "HIV" particles must be cellular vesicles. Since there is no proof that the banded, "purified virus", material contains retrovirus particles then there can be no proof that any of the banded RNA is retroviral RNA. When such RNA (or its cDNA) is used as probes and primers for hybridisation and PCR studies, no matter what results are obtained, they cannot be considered proof for infection with a retrovirus, any retrovirus.

To quote dissident Paul Philpott "I think a very convincing case can be made against the HIV model. It's just that the points that really do refute the HIV model have not been taken up as the principal weapons of our most visible advocates." Any scientist of any persuasion acquainted with these data must question the evidence for the existence of HIV.

(1) Department of Medical Physics, Royal Perth Hospital, Wellington Street, Perth 6001; (2) Department of Emergency Medicine, Royal Perth Hospital; (3) University of Western Australia; (4) Department of Research, Unversidad Metropolitana Barranquilla, Colombia

References

1. Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med Hypotheses 1988;25:151-162.

2. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Is a positive Western blot proof of HIV infection? Bio/Technology 1993;11:696-707.

3. Duesberg PH. Peter Duesberg responds. Continuum 1996;4:8-9.

4. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, et al. The Isolation of HIV: Has it really been achieved? Continuum 1996;4:1s-24s.

5. Gallo RC, Wong-Staal F, Reitz M, et al. Some evidence for infectious type-C virus in humans. In: Balimore D, Huang AS, Fox CF, eds. Animal Virology. New York: Academic Press Inc., 1976:385-405.

6. Rous P. A Sarcoma of the Fowl transmissible by an agent separable from the Tumor Cells. J Exp Med 1911;13:397-411.

7. Francis DP. The search for the cause. In: Cahill KM, ed. The AIDS epidemic. 1st ed. Melbourne: Hutchinson Publishing Group, 1983:137-150.

8. Tahi D. Did Luc Montagnier discover HIV? Text of video interview with Professor Luc Montagnier at the Pasteur Institute July 18th 1997. Continuum 1998;5:30-34.

9. Bess JW, Gorelick RJ, Bosche WJ, et al. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virol 1997;230:134-144.

10. Gluschankof P, Mondor I, Gelderblom HR, et al. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virol 1997;230:125-133.

11. Arthur LO, Bess JW, Jr., Urban RG, et al. Macaques immunized with HLA-DR are protected from challenge with simian immunodeficiency virus.
 
I’m not “anti doctor” but I’ve seen plenty of cases where they’ve destroyed kids with medications. Sad and irreversible

I was talking about this the other day. Despite genetic parental history increasing ADHD risk, some parents just cant properly raise or discipline children. I have parents who demand their child's Adderall, Concerta, Ritalin, etc. ADHD medications are so damn overprescribed in white male children under 12 years old its unbelievable. If you read in between the lines, the DSM-5 criteria are basically a combination of children who....

-lose focus in school
-dont wait their turn to get called on
-talk excessively
-have sloppy handwriting
-need to be constantly reminded of things

You can argue that that's pretty much a majority of children. Hell that was all of us at one point. Then guidelines recommend maximizing the dose till you see benefit without running into side effects. One of the parts of health care that I disagree with on many levels.
 
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Should've been posted this, but the headline of that article was click bait in it self and the racist undertones are present. 99% of the people in this thread haven't to Zimbabwe yet automatically make the mental connection that it's some aids riddled country because what's reported to us.

"AIDS in Africa: distinguishing fact and fiction The data widely purporting to show the existence and heterosexual transmission in Africa of a new syndrome caused by a retrovirus which induces immune deficiency are critically evaluated. It is concluded that both acquired immune deficiency (AID) and the symptoms and diseases which constitute the clinical syndrome (S) are of long standing in Africa, affect both sexes equally and are caused directly and indirectly by factors other than human immunodeficiency virus (HIV). Seropositivity to HIV in Africans represents no more than cross-reactivity caused by an abundance of antibodies induced by the numerous infectious and parasitic diseases which are endemic in Africa. The apparently high prevalence of 'AIDS' and 'HIV seropositives is therefore not surprising and is not proof of heterosexual transmission of either HIV or AIDS."

http://www.theperthgroup.com/SCIPAPERS/EPEWorldJMicro&BiotechOCR1995.pdf
 
The Perth Group is a group of HIV/AIDS denialists based in Perth, Western Australia who claim, in opposition to the scientific consensus, that the existence of HIV (Human Immunodeficiency Virus) is not proven, and that AIDS and all the "HIV" phenomena are caused by changes in cellular redox due to the oxidative nature of substances and exposures common to all the AIDS risk groups, and are caused by the cell conditions used in the "culture" and "isolation" of "HIV".[1]

The group's activism has negatively affected the epidemic of HIV/AIDS in South Africa due to their influence on the AIDS policies of South African President Thabo Mbeki. The resulting governmental refusal to provide effective anti-HIV treatment in South Africa has been blamed for hundreds of thousands of premature AIDS-related deaths in South Africa.[2]

https://en.wikipedia.org/wiki/The_Perth_Group
 
I was talking about this the other day. Despite genetic parental history increasing ADHD risk, some parents just cant properly raise or discipline children. I have parents who demand their child's Adderall, Concerta, Ritalin, etc. ADHD medications are so damn overprescribed in white male children under 12 years old its unbelievable. If you read in between the lines, the DSM-5 criteria are basically a combination of children who....

-lose focus in school
-dont wait their turn to get called on
-talk excessively
-have sloppy handwriting
-need to be constantly reminded of things

You can argue that that's pretty much a majority of children. Hell that was all of us at one point. Then guidelines recommend maximizing the dose till you see benefit without running into side effects. One of the parts of health care that I disagree with on many levels.
I tell parents it takes years to build skills but it lasts a life time. TRY first. You can put kids on meds in an instant and after that reaching “normal” just never happens. It’s a horrible cycle. I’m not against meds but WAIT.
 
Let me get this straight, we're using Wikipedia, an open platform that anyone can edit as evidence, yet a licensed doctor and biophysicist who gives a thorough dissertation on her stance is not addressed? Mind you this physician has gave her stance on a multitude of levels where no has been able to refute what she says. I considered this before I even posted the link but I honestly didn't think you would really use wikipedia as a reference.

That easy to switch the narrative.

Screenshot (7).png


How is a wikipedia page any different then your average youtube conspiracy theorist that yall are so quick to point out?
 
I don't think you fully grasp how Wikipedia works.

In an academic setting, Wikipedia would not be an appropriate source. But the articles cited in the wiki article would. Just editing a wiki page and take a snip of it doesn't just "change the narrative"
 
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We do not expect you to trust us
It is in the nature of an open collaboration and work-in-progress like Wikipedia that quality may vary over time, and from article to article. While some articles are of the highest quality of scholarship, others are admittedly complete rubbish. Also, since Wikipedia can be edited by anyone at any time, articles may be prone to errors, including vandalism so Wikipedia is not a reliable source. So please do not use Wikipedia to make critical decisions. This encyclopedia is especially useful for improving familiarity with a subject and its jargon, and for learning search terms with which to further explore a subject beyond Wikipedia. Helpful external links are also provided to assist you in learning more.

Further information: Wikipedia:General disclaimer
 
A recap:

First: A source from “Atlanta’s Hottest Hip Hop.” The OP uses a link with no context, no analysis of the source that asserts an “epidemic.” Why are people drawn to this kind of knowledge/information? What counts as a legitimate source?

Second: Homophobic, anti-gay politics fueled by the usual NT suspects.

Third: What some call trolling, and others engage as worthy of discussion. Shout out to the physicians who clarified the differences between HIV and AIDS, and how the viruses actually works.

Fourth: an odd display of “receipts” from someone who then questions a collaborative, democratic process of knowledge production.

Fifth: An overlook of Rusty’s prescient, and elementary question: to whom do you send your kids when they’re sick?

Sixth: The elevation of masonic, hand-shaking, illuminati explanations.

At the end of the day, if we’re looking for an entry into how and why AIDS continues to devastate various communities in the United States in general, and black men and women in particular, we can start here:

https://www.nytimes.com/2017/06/06/magazine/americas-hidden-hiv-epidemic.html

Here's an accessible, if disheartening account of state negligence, individual choices, narrow networks, and public health, among other factors, that explain the disparate health outcomes.
 
I don't think you fully grasp how Wikipedia works.

In an academic setting, Wikipedia would not be an appropriate source. But the articles cited in the wiki article would. Just editing a wiki page and take a snip of it doesn't just "change the narrative"

Nice edit btw. All of my post on the topic have been academic and based on science from professions in the field. If you read through the sources, half of them don't work, some are rebuttals to one another, and others are reporting news with no scientific explanations for their stance. As it pertains to the South Africa there's varying theories on the death toll and what contributed to them, yet conveniently a white politician shows up with the answer to save the savage uncivilized people, sounds familiar. Through out all my post in this thread I have been consistent on my stance that from a scientific standpoint the HIV virus has never been proven to exist per the guidelines set forth by the scientific community. Neither physician that posted were able to refute what was presented. Simple as that. Furthermore, whites make up the majority of the homosexual demographic, which makes up the majority of "HIV +" demographic (homosexuals), yet blacks and predominantly black cities are facing an epidemic.. if you dont see the psy-op idk what else to say.
 
When one of your kids are sick, who do you seek help from?

Your local Youtube conspiracy theorist?
Did I say it was bad to go to a doctor or no :nerd:
They know more about stuff than I would
But just cause they have the knowledge
Doesn’t mean
They are necessarily always right
 
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