Dissident AIDS Database

HIV drugsAZT/PIsIneffectivenessViral load
Constant Mean Viral Copy Number per Infected Cell in Tissues Regardless of High, Low, or Undetectable Plasma HIV RNA.
 Hockett RD et al.
  “The results obtained for patients with a broad range of plasma viral loads before and after antiretroviral therapy reveal a constant mean viral (v)RNA copy number (3.6 log10 copies) per infected cell, regardless of plasma virus load or treatment status.”
  Journal of Experimental Medicine. 1999 May 17;189(10):1545-54.1999
Residual human immunodeficiency virus (HIV) type 1 RNA and DNA in lymph nodes and HIV RNA in genital secretions and in cerebrospinal fluid after suppression of viremia for 2 years.
 Gunthard HF et al.
  “Shows ineffectiveness of HAART at eradicating HIV in the lymphoid compartment”
  JID. 2001 May 1;183(9):1318-27.2001
Effect of highly active antiretroviral therapy on outcomes in Veterans Affairs Medical Centers.
 Goetz MB et al.
  “ The virological failure of up to 60% of treatment-experienced patients and the increased recognition of the toxicities of antiretroviral therapy...”
  AIDS. 2001 Mar 9;15(4):530-2.2001
Quantification of integrated and total HIV-1 DNA after long-term highly active antiretroviral therapy in HIV-1-infected patients.
 Ibanez A et al.
  “Our findings suggest that 48 weeks of HAART does not significantly reduce the integrated HIV-1 proviral DNA load in the latently infected CD4 T cell reservoir”
  AIDS. 1999 Jun 18;13(9):1045-9.1999
Long-Term Highly Active Anti-Retroviral Therapy in an Anti-Retroviral Experienced Population.
 Ramirez CM, Gottlieb MS.
  “We examined 304 anti-retroviral-experienced patients who were placed on HAART for a period of 18 months. The baseline ... HIV RNA level was 3.2 log[10] copies/ml... The HAART regimens included 3-5 anti-retroviral agents at least one of which was a protease inhibitor...After 18 months,... the average ... HIV RNA level of 3.2 log[10] copies/ml. [i.e. HAART did not affect HIV RNA levels]”
  AIDS Weekly Plus. 1999 Jun 28.1999
Detection of infectious HIV in circulating monocytes from patients on prolonged highly active antiretroviral therapy.
 Lambotte O et al.
  “The existence of a reservoir of resting CD4+ T cells harboring latent replication-competent HIV has been demonstrated in patients on prolonged highly active antiretroviral therapy (HAART). Latently infected tissue macrophages may constitute a second HIV reservoir...These results demonstrate the long-term persistence of infectious virus in cells of the monocyte-macrophage lineage in patients receiving HAART.”
  JAIDS. 2000 Feb 1;23(2):114-9.2000
Study looks at HIV ‘Cocktail’.
 Loviglio J
  “According to the study, [published in 7/20/99 Annals of Internal Medicine] 37 percent of the Johns Hopkins patients getting the cocktail treatment had undetectable HIV levels one year after starting therapy. Only 23 percent suppressed the virus in all three time periods studied - 1-90 days, 3-7 months and 7-14 months. Clinical trials using similar drugs show suppression rates twice as high as those numbers.”
  Associated Press. 1999 July 19.1999
Persistence of HIV-1 Transcription in Peripheral-Blood Mononuclear Cells in Patients Receiving Potent Antiretroviral Therapy.
 Furtado M et al.
  “Potent antiretroviral therapy seems unable to eradicate latent HIV-1 reservoirs in CD4+ T cells.”
  NEJM. 1999 May 27;340(21):1614.1999
Sexual transmission of HIV.
 Royce RA et al.
  “Decreases in concentrations of and detection of seminal HIV in men taking zidovudine or newer antiretroviral drugs have been observed in some [2 referenced], but not all studies [4 referenced]. Antiretroviral therapy apparently does not affect the detection of HIV in cervicovaginal specimens”
  NEJM. 1997 Apr 10;336(15):1072-8.1997
HIV-1 and HAART: A time to cure, a time to kill.
 Saag MS, Kilby JM.
  “As the ADARC group suggested, immediate attention should focus on the reasons why three- and four-drug potent anti-retroviral therapy does not completely suppress virus replication. Based on their data, it is unlikely that anatomical sanctuaries are protecting cells from drugs; instead, the positive cells seem to be readily circulating through the body, as suggested by the presence of many of the HIV-expressing cells in lymphoid sinuses.”
  Nature Medicine. 1999 June;5(6):609-11.1999
Study Backs HIV Drug Combination
 No author
  'A combination of anti-HIV drugs that lacks the powerful protease inhibitors that have helped cut AIDS death rates might be just as effective at halting disease progression as those including protease inhibitors, researchers said Tuesday... Dr. Schlomo Staszewski, from Klinikum der Johann Wolfgang Goethe-Universitat in Frankfurt, Germany, and colleagues randomly assigned 562 HIV-positive people who had never been treated with AIDS drugs to receive treatment with one of two combinations. Some patients were given GlaxoSmithKline's abacavir (Ziagen) with 3TC and AZT, others got the Merck & Co. protease inhibitor indinavir (Crixivan) with 3TCand AZT. Like 3TC and AZT, abacavir is in the class of drugs known as nucleoside analogues. After 48 weeks of treatment, 51% of patients in both groups had the levels of HIV in their blood reduced to less than 400 copies permilliliter of blood. The investigators found no difference between the treatment combinations in their effects on blood levels of the CD4+ immune cells that are attacked by HIV..." (Journal of the American Medical Association, 7 March 2001;285:1155) : In other words, according to mainstream AIDS researchers, adding a PI to an AZT+ ddI combo doesn't seem to do much.
  Reuters Health NY, wednesday March 7, 20012001