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The Water Cooler
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CDC admits death toll is inflated! Of 161,392 deaths ONLY 6% / 9,683 ARE DIRECTLY CAUSED BY COVID.
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<blockquote data-quote="_CY_" data-source="post: 3507234" data-attributes="member: 7629"><p>They Fought HCQ So Hard Because it possibly Treats HIV at 1/80th - 1/100th of the Cost of Other Antiretrovirals and Likely Had Few to No Side Effects. Trump Ripped the Clothes Right Off the Pharma Emperor</p><p></p><p>please note this is a work in progress ..</p><p><strong></strong></p><p><strong>HCQ TREATS HIV</strong></p><p>sauce:</p><p></p><p><strong><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220506/" target="_blank">Mechanism of HIV Reverse Transcriptase Inhibition by Zinc: *Formation of a Highly Stable Enzyme-(Primer-Template) Compex with Profoundly Diminished Catalytic Activity</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220506/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220506/</a></li> </ul><p><em>Several physiologically relevant cations including Ca2+, Mn2+, and Zn2+ have been shown to inhibit HIV reverse transcriptase (RT), presumably by competitively displacing one or more Mg2+ ions bound to RT....... Essentially, the presence of Zn2+ promotes the formation of a highly stable slowly progressing RT-(primer-template) complex....In conclusion, Zn2+ inhibits HIV-RT synthesis not by directly stopping catalysis, but by forming a highly stable complex that has very slow incorporation kinetics. The RT-Zn2+-(primer-template) complex can be thought of as a “dead-end complex” since it ties up RT- potentially for hours, in a complex that is from a kinetic perspective, minimally productive.</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/9001825/" target="_blank">Inhibition of HIV-1 replication by hydroxychloroquine: mechanism of action and comparison with zidovudine</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://pubmed.ncbi.nlm.nih.gov/9001825/" target="_blank">https://pubmed.ncbi.nlm.nih.gov/9001825/</a></li> </ul><p><em>We have previously described the inhibition of human immunodeficiency virus serotype 1 (HIV-1) using the antimalarial hydroxychloroquine (HCQ), a weak base that inhibits the posttranslational modification of glycoprotein 120 (gp 120) in T cells and monocytes</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/8427717/" target="_blank">Inhibition of human immunodeficiency virus type 1 replication by hydroxychloroquine in T cells and monocytes</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://pubmed.ncbi.nlm.nih.gov/8427717/" target="_blank">https://pubmed.ncbi.nlm.nih.gov/8427717/</a></li> </ul><p><em>HCQ inhibited HIV-1 replication (> 75%), as measured by reverse transcriptase activity, in the primary T cells and monocytes as well as the T cell and monocytic cell lines. HCQ itself had no anti-reverse transcriptase activity and was not toxic to the cells at concentrations inhibitory to viral replication. Intracytoplasmic staining with an anti-p24 antibody, 24 h after infection, revealed the presence of intracytoplasmic virus, suggesting that the drug does not block viral entry. The production of steady-state HIV-1 mRNA was not affected by HCQ in that comparable levels of HIV-1 mRNA could be detected by Northern blot analysis and by in situ hybridization in both the HCQ-treated and untreated cells. However, HCQ does appear to affect production of infectious HIV-1 virions because viral isolates from HCQ-treated cells could not infect target CEM cells. These data suggest that HCQ may be useful adjunctive therapy in the treatment of HIV-1 infection.</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/8565026/" target="_blank">Hydroxychloroquine treatment of patients with human immunodeficiency virus type 1</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://pubmed.ncbi.nlm.nih.gov/8565026/" target="_blank">https://pubmed.ncbi.nlm.nih.gov/8565026/</a></li> </ul><p><em>Hydroxychloroquine (HCQ), an antimalarial agent used to treat patients with autoimmune diseases, has been shown to suppress human immunodeficiency virus type 1 (HIV-1) replication in vitro in T cells and monocytes by inhibiting posttranscriptional modification of the virus. These in vitro observations have been expanded into an in vivo study of HCQ as a potential anti-HIV-1 agent in HIV-1-infected patients. A randomized, double-blind, placebo-controlled clinical trial was conducted in 40 asymptomatic HIV-1-infected patients who had CD4+ counts between 200 and 500 cells/mm3. Patients were randomly assigned to receive either HCQ 800 mg/d or placebo for 8 weeks. Virologic and immunologic parameters, including HIV-1 ribonucleic acid (RNA) via use of polymerase chain reaction, viral culture, antigen and mitogen responses, and proinflammatory cytokine levels were measured at the beginning and end of the study......HCQ thus may be useful in the treatment of patients with HIV-1 infection.</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/21576701/" target="_blank">Hydroxychloroquine drastically reduces immune activation in HIV-infected, antiretroviral therapy-treated immunologic nonresponders</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://pubmed.ncbi.nlm.nih.gov/21576701/" target="_blank">https://pubmed.ncbi.nlm.nih.gov/21576701/</a></li> </ul><p><em>HCQ reduces lipopolysaccharide/TLR-mediated immune activation; this compound could be a useful immunomodulant in HIV-infected patients</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/15320751/" target="_blank">Chloroquine and hydroxychloroquine as inhibitors of human immunodeficiency virus (HIV-1) activity</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://pubmed.ncbi.nlm.nih.gov/15320751/" target="_blank">https://pubmed.ncbi.nlm.nih.gov/15320751/</a></li> </ul><p><em>Chloroquine and its analog hydroxychloroquine are two inexpensive agents that are widely used for the treatment of malaria and have been shown to achieve some level of anti-HIV activity. The exact mechanism of chloroquine and hydroxychloroquine's anti-HIV activity has not yet been discerned but may be related to effects on HIV's surface envelope glycoprotein 120. If found efficacious, both drugs would offer significant advantages to current therapy including a unique mechanism of action, lack of cross-resistance with other antiretrovirals, and low cost.</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/11166661/" target="_blank">The anti-HIV-1 activity of chloroquin</a></strong></p><p><em>Chloroquine (CQ) and its derivative hydroxychloroquine (HCQ) are endowed with a broad anti-HIV-1 activity inhibiting X4, R5, and X4/R5 stains in lymphocytic and monocytic cells. Interestingly, CQ is capable of inhibiting HIV-1 replication at concentrations within the range reported in plasma of individuals chronically treated with doses of the drug which have well-known and limited toxicity. These effects have been confirmed in vivo in two clinical trials. The principal mechanism of HIV-1 inhibition by CQ seems to be an effect on gp120 on a post-transcriptional level. Because CQ and HCQ appear to have a novel site of action (i.e. post-transcriptional inhibition of gp120), these drugs may be particularly useful in combination with other anti-retroviral agents (e.g. ZDV, ddI and HU)</em></p><p></p><p><strong><a href="https://pubmed.ncbi.nlm.nih.gov/9385480/" target="_blank">Comparison of hydroxychloroquine with zidovudine in asymptomatic patients infected with human immunodeficiency virus type 1</a></strong></p><ul> <li data-xf-list-type="ul"><a href="https://pubmed.ncbi.nlm.nih.gov/9385480/" target="_blank">https://pubmed.ncbi.nlm.nih.gov/9385480/</a></li> </ul><p><em>Hydroxychloroquine (HCQ), an antimalarial agent used to treat patients with autoimmune diseases, has been shown to suppress human immunodeficiency virus type 1 (HIV-1) replication in T cells and monocytes in vitro by inhibiting posttranscriptional modification of the virus. An initial randomized, placebo-controlled clinical trial conducted in 38 asymptomatic HIV-1-infected patients who had CD4+ counts between 200 and 500 cells/mm3 demonstrated that the amount of recoverable virus declined significantly in the HCQ group compared with the placebo group over the 8-week study period...Thus HCQ may be potentially useful in the treatment of patients with HIV-1 infection.</em></p></blockquote><p></p>
[QUOTE="_CY_, post: 3507234, member: 7629"] They Fought HCQ So Hard Because it possibly Treats HIV at 1/80th - 1/100th of the Cost of Other Antiretrovirals and Likely Had Few to No Side Effects. Trump Ripped the Clothes Right Off the Pharma Emperor please note this is a work in progress .. [B] HCQ TREATS HIV[/B] sauce: [B][URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220506/']Mechanism of HIV Reverse Transcriptase Inhibition by Zinc: *Formation of a Highly Stable Enzyme-(Primer-Template) Compex with Profoundly Diminished Catalytic Activity[/URL][/B] [LIST] [*][URL]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220506/[/URL] [/LIST] [I]Several physiologically relevant cations including Ca2+, Mn2+, and Zn2+ have been shown to inhibit HIV reverse transcriptase (RT), presumably by competitively displacing one or more Mg2+ ions bound to RT....... Essentially, the presence of Zn2+ promotes the formation of a highly stable slowly progressing RT-(primer-template) complex....In conclusion, Zn2+ inhibits HIV-RT synthesis not by directly stopping catalysis, but by forming a highly stable complex that has very slow incorporation kinetics. The RT-Zn2+-(primer-template) complex can be thought of as a “dead-end complex” since it ties up RT- potentially for hours, in a complex that is from a kinetic perspective, minimally productive.[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/9001825/']Inhibition of HIV-1 replication by hydroxychloroquine: mechanism of action and comparison with zidovudine[/URL][/B] [LIST] [*][URL]https://pubmed.ncbi.nlm.nih.gov/9001825/[/URL] [/LIST] [I]We have previously described the inhibition of human immunodeficiency virus serotype 1 (HIV-1) using the antimalarial hydroxychloroquine (HCQ), a weak base that inhibits the posttranslational modification of glycoprotein 120 (gp 120) in T cells and monocytes[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/8427717/']Inhibition of human immunodeficiency virus type 1 replication by hydroxychloroquine in T cells and monocytes[/URL][/B] [LIST] [*][URL]https://pubmed.ncbi.nlm.nih.gov/8427717/[/URL] [/LIST] [I]HCQ inhibited HIV-1 replication (> 75%), as measured by reverse transcriptase activity, in the primary T cells and monocytes as well as the T cell and monocytic cell lines. HCQ itself had no anti-reverse transcriptase activity and was not toxic to the cells at concentrations inhibitory to viral replication. Intracytoplasmic staining with an anti-p24 antibody, 24 h after infection, revealed the presence of intracytoplasmic virus, suggesting that the drug does not block viral entry. The production of steady-state HIV-1 mRNA was not affected by HCQ in that comparable levels of HIV-1 mRNA could be detected by Northern blot analysis and by in situ hybridization in both the HCQ-treated and untreated cells. However, HCQ does appear to affect production of infectious HIV-1 virions because viral isolates from HCQ-treated cells could not infect target CEM cells. These data suggest that HCQ may be useful adjunctive therapy in the treatment of HIV-1 infection.[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/8565026/']Hydroxychloroquine treatment of patients with human immunodeficiency virus type 1[/URL][/B] [LIST] [*][URL]https://pubmed.ncbi.nlm.nih.gov/8565026/[/URL] [/LIST] [I]Hydroxychloroquine (HCQ), an antimalarial agent used to treat patients with autoimmune diseases, has been shown to suppress human immunodeficiency virus type 1 (HIV-1) replication in vitro in T cells and monocytes by inhibiting posttranscriptional modification of the virus. These in vitro observations have been expanded into an in vivo study of HCQ as a potential anti-HIV-1 agent in HIV-1-infected patients. A randomized, double-blind, placebo-controlled clinical trial was conducted in 40 asymptomatic HIV-1-infected patients who had CD4+ counts between 200 and 500 cells/mm3. Patients were randomly assigned to receive either HCQ 800 mg/d or placebo for 8 weeks. Virologic and immunologic parameters, including HIV-1 ribonucleic acid (RNA) via use of polymerase chain reaction, viral culture, antigen and mitogen responses, and proinflammatory cytokine levels were measured at the beginning and end of the study......HCQ thus may be useful in the treatment of patients with HIV-1 infection.[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/21576701/']Hydroxychloroquine drastically reduces immune activation in HIV-infected, antiretroviral therapy-treated immunologic nonresponders[/URL][/B] [LIST] [*][URL]https://pubmed.ncbi.nlm.nih.gov/21576701/[/URL] [/LIST] [I]HCQ reduces lipopolysaccharide/TLR-mediated immune activation; this compound could be a useful immunomodulant in HIV-infected patients[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/15320751/']Chloroquine and hydroxychloroquine as inhibitors of human immunodeficiency virus (HIV-1) activity[/URL][/B] [LIST] [*][URL]https://pubmed.ncbi.nlm.nih.gov/15320751/[/URL] [/LIST] [I]Chloroquine and its analog hydroxychloroquine are two inexpensive agents that are widely used for the treatment of malaria and have been shown to achieve some level of anti-HIV activity. The exact mechanism of chloroquine and hydroxychloroquine's anti-HIV activity has not yet been discerned but may be related to effects on HIV's surface envelope glycoprotein 120. If found efficacious, both drugs would offer significant advantages to current therapy including a unique mechanism of action, lack of cross-resistance with other antiretrovirals, and low cost.[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/11166661/']The anti-HIV-1 activity of chloroquin[/URL][/B] [I]Chloroquine (CQ) and its derivative hydroxychloroquine (HCQ) are endowed with a broad anti-HIV-1 activity inhibiting X4, R5, and X4/R5 stains in lymphocytic and monocytic cells. Interestingly, CQ is capable of inhibiting HIV-1 replication at concentrations within the range reported in plasma of individuals chronically treated with doses of the drug which have well-known and limited toxicity. These effects have been confirmed in vivo in two clinical trials. The principal mechanism of HIV-1 inhibition by CQ seems to be an effect on gp120 on a post-transcriptional level. Because CQ and HCQ appear to have a novel site of action (i.e. post-transcriptional inhibition of gp120), these drugs may be particularly useful in combination with other anti-retroviral agents (e.g. ZDV, ddI and HU)[/I] [B][URL='https://pubmed.ncbi.nlm.nih.gov/9385480/']Comparison of hydroxychloroquine with zidovudine in asymptomatic patients infected with human immunodeficiency virus type 1[/URL][/B] [LIST] [*][URL]https://pubmed.ncbi.nlm.nih.gov/9385480/[/URL] [/LIST] [I]Hydroxychloroquine (HCQ), an antimalarial agent used to treat patients with autoimmune diseases, has been shown to suppress human immunodeficiency virus type 1 (HIV-1) replication in T cells and monocytes in vitro by inhibiting posttranscriptional modification of the virus. An initial randomized, placebo-controlled clinical trial conducted in 38 asymptomatic HIV-1-infected patients who had CD4+ counts between 200 and 500 cells/mm3 demonstrated that the amount of recoverable virus declined significantly in the HCQ group compared with the placebo group over the 8-week study period...Thus HCQ may be potentially useful in the treatment of patients with HIV-1 infection.[/I] [/QUOTE]
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