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Preliminary Findings in Cure of Two HAART Experienced HIV Patients by Stopping Reverse Dissemination from Bone Marrow CD4 Progenitors

Received: 15 May 2013     Published: 20 June 2013
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Abstract

Elucidation of reverse dissemination as the true mechanism by which HIV maintains chronic infection while discounting of the generally accepted model of latent reserve can open a new frontier in research that could result in radical cure. HIV may cause and maintain chronic infection by reverse disseminating from differentiating CD4 T-lymphocyte progenitor cells (LPCs) within the bone marrow niche, and that breaking the cross-infection between older and new cells can lead to elimination of the reserve infection result in radical cure. By using a mechanism that prevents the rapid expansion of HSCs that give rise to LPCs, I collected data and information from two patients that show achievement of radical cure of HIV by absence of viral resurgence for eight months after stoppage of highly active antiretroviral therapy.

Published in International Journal of Immunology (Volume 1, Issue 2)
DOI 10.11648/j.iji.20130102.11
Page(s) 14-23
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2013. Published by Science Publishing Group

Keywords

HIV, Reserve Infection, Reverses Dissemination, Radical Cure

References
[1] Muller-Sieburg CE, Cho RH, Thoman M, Adkins B, Sieburg HB, Deterministic regulation of haematopoietic stem cell self-renewal and differentiation. Blood. 2002; 100; 1302-9
[2] Allen TD, Dexter TM.,The essential cells of the hemopoietic microenvironment. Exp Hematol. 1984 Aug 12(7)517-21 http://www.ncbi.nlm.nih.gov/pubmed/6745328
[3] Zauli G, Furlini G, Vitale M, Re MC, Gibellini D, et al. A subset of human CD34+ hematopoietic progenitors express low levels of CD4, the high-affinity receptor for human immunodeficiency virus-type 1. Blood. 1994;84:1896–1905. [PubMed].
[4] Louache F, Debili N, Marandin A, Coulombel L, Vainchenker W. Expression of CD4 by human hematopoietic progenitors. Blood. 1994;84:3344–3355. [PubMed].
[5] Lichtman MA, Beutler E, Kipps TJ, Seligsohn U, Kaushansky K, et al. Williams Hematology. McGraw-Hill Companies, Inc; 2006.
[6] Chen JJ, Huang JC, Shirtliff M, Briscoe E, Ali S, et al. CD4 lymphocytes in the blood of HIV (+) individuals migrate rapidly to lymph nodes and bone marrow: support for homing theory of CD4 cell depletion. J Leukoc Biol. 2002; 72: 271–278. [PubMed].
[7] Barasa S, True story about HIV: Theory of viral sequestration and reserve infection HIV AIDS (Auckl). 2011; 3: 125–133. Published online 2011 December 8. doi: 10.2147/HIV.S26578.
[8] Hariharan D, Li Y, Campbell DE, Douglas SD, Starr SE, et al. Human immunodeficiency virus infection of human placental cord blood CD34+AC133+ stem cells and their progeny. AIDS Res Hum Retroviruses. 1999; 15:1545–1552. [PubMed].
[9] Shen H, Cheng T, Preffer FI, Dombkowski D, Tomasson MH, et al. Intrinsic human immunodeficiency virus type 1 resistance of hematopoietic stem cells despite coreceptor expression. J Virol. 1999; 73:728–737. [PMC free article] [PubMed].
[10] Liu Y, Tang XP, McArthur JC, Scott J, Gartner S. Analysis of human immunodeficiency virus type 1 gp160 sequences from a patient with HIV dementia: evidence for monocyte trafficking into brain. J Neurovirol. 2000;6(Suppl 1):S70–81. [PubMed].
[11] Steinberg HN, Crumpacker CS, Chatis PA. In vitro suppression of normal human bone marrow progenitor cells by human immunodeficiency virus. J Virol. 1991; 65:1765–1769. [PMC free article] [PubMed].
[12] Kitano K, Abboud CN, Ryan DH, Quan SG, Baldwin GC, et al. Macrophage-active colony-stimulating factors enhance human immunodeficiency virus type 1 infection in bone marrow stem cells. Blood. 1991; 77:1699–1705. [PubMed].
[13] Ruiz ME, Cicala C, Arthos J, Kinter A, Catanzaro AT, et al. Peripheral blood-derived CD34+ progenitor cells: CXC chemokine receptor 4 and CC chemokine receptor 5 expression and infection by HIV. J Immunol. 1998; 161:4169–4176. [PubMed].
[14] Isgro A, Aiuti A, Mezzaroma I, Addesso M, Riva E, et al. Improvement of interleukin 2 production, clonogenic capability and restoration of stromal cell function in human immunodeficiency virus-type-1 patients after highly active antiretroviral therapy. Br J Haematol. 2002; 118: 864–874. [PubMed].
[15] Canque B, Marandin A, Rosenzwajg M, Louache F, Vainchenker W, et al. Susceptibility of human bone marrow stromal cells to human immunodeficiency virus (HIV). Virology. 1995; 208:779–783. [PubMed].
[16] Gill V, Shattock RJ, Freeman AR, Robinson G, Griffin GE, et al. Macrophages are the major target cell for HIV infection in long-term marrow culture and demonstrate dual susceptibility to lymphocytotropic and monocytotropic strains of HIV-1. Br J Haematol. 1996; 93:30–37. [PubMed].
[17] Freedman AR, Gibson FM, Fleming SC, Spry CJ, Griffin GE. Human immunodeficiency virus infection of eosinophils in human bone marrow cultures. J Exp Med. 1991; 174: 1661–1664. [PMC free article] [PubMed].
[18] Scadden DT, Zeira M, Woon A, Wang Z, Schieve L, et al. Human immunodeficiency virus infection of human bone marrow stromal fibroblasts. Blood. 1990; 76:317–322. [PubMed].
[19] Gibellini D, Vitone F, Buzzi M, Schiavone P, De Crignis E, et al. HIV-1 negatively affects the survival/maturation of cord blood CD34 (+) hematopoietic progenitor cells differentiated towards megakaryocytic lineage by HIV-1 gp120/CD4 membrane interaction. J Cell Physiol. 2007; 210:315–324. [PubMed]
[20] Chan D, Kim P (1998). "HIV entry and its inhibition". Cell 93 (5): 681–4. doi:10.1016/S0092-8674(00)81430-0. PMID 9630213.
[21] Wyatt R, Sodroski J (1998). "The HIV-1 envelope glycoproteins: fusogens, antigens, and immunogens". Science 280 (5371): 1884–8. Bibcode 1998Sci...280.1884W. doi:10.1126/science.280.5371.1884. PMID 9632381.
[22] Pollard, V. W. and Malim, M. H. (1998). "The HIV-1 Rev protein". Annu. Rev. Microbiol. 52: 491–532. doi:10.1146/annurev.micro.52.1.491. PMID 9891806.
[23] Donahue JP, Vetter ML, Mukhtar NA, D'Aquila RT (July 2008). "The HIV-1 Vif PPLP motif is necessary for human APOBEC3G binding and degradation". Virology 377 (1): 49–53. doi: 10.1016/j.virol.2008.04.017. PMC 2474554. PMID 18499212.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2474554.
[24] Allers, K.; Hutter, G.; Hofmann, J.; Loddenkemper, C.; Rieger, K.; Thiel, E.; Schneider, T. (2010). "Evidence for the cure of HIV infection by CCR5 32/ 32 stem cell transplantation". Blood 117 (10): 2791–2799. doi:10.1182/blood-2010-09-309591. PMID 21148083.edit.
[25] Hütter G, Nowak D, Mossner M, Ganepola S, Ganepola A, Allers K, Schneider T, Hofmann J, Kücherer C, Blau O, Blau IW, Hofmann WK, Thiel E (2009). "Long-Term Control of HIV by CCR5 Delta32/Delta32 Stem-Cell Transplantation". N Engl J Med 360 (7): 692–698.doi:10.1056/NEJMoa0802905. PMID 19213682. http://content.nejm.org/cgi/content/abstract/360/7/692.
[26] Watson J (2006). "Scientists, activists sue South Africa's AIDS 'denialists'". Nat. Med. 12 (1): 6. doi: 10.1038/nm0106-6a. PMID 16397537.
[27] Baleta A (2003). "S Africa's AIDS activists accuse government of murder". Lancet 361 (9363): 1105. doi: 10.1016/S0140-6736(03)12909-1. PMID 12672319.
[28] Cohen J (2000). "South Africa's new enemy". Science 288 (5474): 2168–70. doi: 10.1126/science.288.5474.2168. PMID 10896606.
[29] Fiore AE, Bridges CB, Cox NJ (2009). "Seasonal influenza vaccines". Curr. Top. Microbiol. Immunol.. Current Topics in Microbiology and Immunology 333: 43–82. doi:10.1007/978-3-540-92165-3_3.ISBN 978-3-540-92164-6. PMID 19768400.
[30] Chang Y, Brewer NT, Rinas AC, Schmitt K, Smith JS (July 2009). "Evaluating the impact of human papillomavirus vaccines". Vaccine 27 (32): 4355–62. doi: 10.1016/j.vaccine.2009.03.008. PMID 19515467.
[31] Liesegang TJ (August 2009). "Varicella zoster virus vaccines: effective, but concerns linger". Can. J. Ophthalmol. 44 (4): 379–84. doi: 10.3129/i09-126. PMID 19606157
[32] Piatak, M., Jr, Saag, M. S., Yang, L. C., Clark, S. J., Kappes, J. C., Luk, K. C., Hahn, B. H., Shaw, G. M. and Lifson, J.D. (1993). "High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR". Science 259 (5102): 1749–1754. Bibcode 1993Sci...259.1749P. doi:10.1126/science.8096089. PMID 8096089.
[33] Pantaleo G, Demarest JF, Schacker T, Vaccarezza M, Cohen OJ, Daucher M, Graziosi C, Schnittman SS, Quinn TC, Shaw GM, Perrin L, Tambussi G, Lazzarin A, Sekaly RP, Soudeyns H, Corey L, Fauci AS. (1997). "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. 94 (1): 254–258. Bibcode 1997PNAS...94..254P. doi:10.1073/pnas.94.1.254. PMC 19306. PMID 8990195. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=19306.
[34] Kahn, J. O. and Walker, B. D. (1998). "Acute Human Immunodeficiency Virus type 1 infection". N. Engl. J. Med. 331 (1): 33–39. doi:10.1056/NEJM199807023390107. PMID 9647878.
[35] Smith D, Richman D, Little S (2005). "HIV Superinfection". Journal of Infectious Diseases 192 (3): 438–44. doi:10.1086/431682. PMID 15995957.
[36] Levy Y, Lacabaratz C, Weiss L, et al. (April 2009). "Enhanced T cell recovery in HIV-1–infected adults through IL-7 treatment". J. Clin. Invest. 119 (4): 997–1007. doi:10.1172/JCI38052. PMC 2662568. PMID 19287090. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2662568.
[37] Tincati, C.; d'Arminio Monforte, A.; Marchetti, G. (2009). "Immunological mechanisms of interleukin-2 (IL-2) treatment in HIV/AIDS disease". Current molecular pharmacology 2 (1): 40–45. PMID 20021444.
[38] HIV vaccine 'reduces infection'. BBC News. September 24, 2009. http://news.bbc.co.uk/2/hi/health/8272113.stm. Retrieved March 30, 2010.The Lancet (2009). "A (prime) boost for HIV vaccine research?". Lancet 374 (9696): 1119. doi: 10.1016/S0140-6736(09)61720-7.
[39] Ball TB, Ji H, Kimani J, McLaren P, Marlin C, Hill AV, Plummer FA. Polymorphisms in IRF-1 associated with resistance to HIV-1 infection in highly exposed uninfected Kenyan sex workers. AIDS. 2007 May 31; 21(9): 1091-1101. PMID: 17502719.
[40] Joint United Nations Programme on HIV/AIDS (2006). "Overview of the global AIDS epidemic" (PDF). 2006 Report on the global AIDS epidemic. ISBN 9291734799. http://data.unaids.org/pub/GlobalReport/2006/2006_GR_CH02_en.pdf. Retrieved 2006-06-08.
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    Barasa Simon Situma. (2013). Preliminary Findings in Cure of Two HAART Experienced HIV Patients by Stopping Reverse Dissemination from Bone Marrow CD4 Progenitors. International Journal of Immunology, 1(2), 14-23. https://doi.org/10.11648/j.iji.20130102.11

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    Barasa Simon Situma. Preliminary Findings in Cure of Two HAART Experienced HIV Patients by Stopping Reverse Dissemination from Bone Marrow CD4 Progenitors. Int. J. Immunol. 2013, 1(2), 14-23. doi: 10.11648/j.iji.20130102.11

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    AMA Style

    Barasa Simon Situma. Preliminary Findings in Cure of Two HAART Experienced HIV Patients by Stopping Reverse Dissemination from Bone Marrow CD4 Progenitors. Int J Immunol. 2013;1(2):14-23. doi: 10.11648/j.iji.20130102.11

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  • @article{10.11648/j.iji.20130102.11,
      author = {Barasa Simon Situma},
      title = {Preliminary Findings in Cure of Two HAART Experienced HIV Patients by Stopping Reverse Dissemination from Bone Marrow CD4 Progenitors},
      journal = {International Journal of Immunology},
      volume = {1},
      number = {2},
      pages = {14-23},
      doi = {10.11648/j.iji.20130102.11},
      url = {https://doi.org/10.11648/j.iji.20130102.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.iji.20130102.11},
      abstract = {Elucidation of reverse dissemination as the true mechanism by which HIV maintains chronic infection while discounting of the generally accepted model of latent reserve can open a new frontier in research that could result in radical cure. HIV may cause and maintain chronic infection by reverse disseminating from differentiating CD4 T-lymphocyte progenitor cells (LPCs) within the bone marrow niche, and that breaking the cross-infection between older and new cells can lead to elimination of the reserve infection result in radical cure. By using a mechanism that prevents the rapid expansion of HSCs that give rise to LPCs, I collected data and information from two patients that show achievement of radical cure of HIV by absence of viral resurgence for eight months after stoppage of highly active antiretroviral therapy.},
     year = {2013}
    }
    

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    AB  - Elucidation of reverse dissemination as the true mechanism by which HIV maintains chronic infection while discounting of the generally accepted model of latent reserve can open a new frontier in research that could result in radical cure. HIV may cause and maintain chronic infection by reverse disseminating from differentiating CD4 T-lymphocyte progenitor cells (LPCs) within the bone marrow niche, and that breaking the cross-infection between older and new cells can lead to elimination of the reserve infection result in radical cure. By using a mechanism that prevents the rapid expansion of HSCs that give rise to LPCs, I collected data and information from two patients that show achievement of radical cure of HIV by absence of viral resurgence for eight months after stoppage of highly active antiretroviral therapy.
    VL  - 1
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Author Information
  • Department of Istititution Technical, University of Kenya Pharmaceutical Technology, Nairobi, Kenya

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