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      Mathematical Model of the Effect of Affinity Hemodialysis on the T-Cell Depletion Leading to AIDS

      Blood Purification
      S. Karger AG
      Affinity dialysis, AIDS, Bystander effect, Envelope proteins, gp120, HIV, Mathematical models

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          HIV-derived envelope proteins appear to be intimately involved in the destruction of uninfected T cells that leads to AIDS in a process known as the ‘bystander effect’. Affinity hemodialysis has been proposed as an effective means of reducing these viral toxins. Using deterministic mathematical models based on the well-known Perelson formulations, the effectiveness of affinity hemodialysis in reducing the levels of viral gp120 was analyzed. Incorporating experimental data on the function of the affinity dialysis system and data from published analyses of HIV viral dynamics, two different models of HIV and AIDS were analyzed. Both models predict a rapid and sustained reduction in gp120 levels. In the model incorporating stem cell dynamics, affinity hemodialysis treatment under several different scenarios was associated with a significant increase in T-cell levels independent of any release from lymphatic tissues. The calculations support the contention that affinity hemodialysis is a potentially useful adjunctive therapy, which can be employed to treat HIV-infected patients in conjunction with drug therapy. For those patients resistant to anti-retroviral drugs or those unable to take the drugs due to the side effects of those medications, affinity hemodialysis treatment may become a viable option.

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          Most cited references11

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          The dynamics of CD4+ T-cell depletion in HIV disease.

          J. McCune (2001)
          The size and composition of the CD4+ T-cell population is regulated by balanced proliferation of progenitor cells and death of mature progeny. After infection with the human immunodeficiency virus, this homeostasis is often disturbed and CD4+ T cells are instead depleted. Such depletion cannot result simply from accelerated destruction of mature CD4+ T cells - sources of T-cell production must also fail. Ironically, this failure may be precipitated by physiological mechanisms designed to maintain homeostasis in the face of accelerated T-cell loss.
            • Record: found
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            T cell depletion in HIV-1 infection: how CD4+ T cells go out of stock.

            HIV-1 infection is characterized by a gradual loss of CD4+ T cells and progressive immune deficiency that leads to opportunistic infections, otherwise rare malignancies and ultimately death. Extensive research over the past two decades has increased our insight into the pathogenic mechanisms underlying these features of HIV-1 infection. Here, we will give a brief overview of the most recent findings and present a model that fits most of the relevant aspects of HIV-1 infection as known. We hypothesize that HIV-1 infection depletes T cell supplies (which are not replaced because of low and static thymic function) by direct infection and killing of cells and through hyperactivation of the immune system.
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              Identification of a common sphingolipid-binding domain in Alzheimer, prion, and HIV-1 proteins.

              The V3 loop of the human immunodeficiency virus (HIV)-1 surface envelope glycoprotein gp120 is a sphingolipid-binding domain mediating the attachment of HIV-1 to plasma membrane microdomains (rafts). Sphingolipid-induced conformational changes in gp120 are required for HIV-1 fusion. Galactosylceramide and sphingomyelin have been detected in highly purified preparations of prion rods, suggesting that the prion protein (PrP) may interact with selected sphingolipids. Moreover, a major conformational transition of the Alzheimer beta-amyloid peptide has been observed upon interaction with sphingolipid-containing membranes. Structure similarity searches with the combinatorial extension method revealed the presence of a V3-like domain in the human prion protein PrP and in the Alzheimer beta-amyloid peptide. In each case, synthetic peptides derived from the predicted V3-like domain were found to interact with monomolecular films of galactosylceramide and sphingomyelin at the air-water interface. The V3-like domain of PrP is a disulfide-linked loop (Cys(179)-Cys(214)) that includes the E200K mutation site associated with familial Creutzfeldt-Jakob disease. This mutation abrogated sphingomyelin recognition. The identification of a common sphingolipid-binding motif in gp120, PrP, and beta-amyloid peptide underscores the role of lipid rafts in the pathogenesis of HIV-1, Alzheimer, and prion diseases and may provide new therapeutic strategies.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                July 2004
                20 January 2004
                : 22
                : 1
                : 84-91
                Aethlon Medical, Inc., San Diego, Calif., USA
                74928 Blood Purif 2004;22:84–91
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 27, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/74928
                Self URI (text/html): https://www.karger.com/Article/FullText/74928
                Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology

                Cardiovascular Medicine,Nephrology
                Affinity dialysis,AIDS,Bystander effect,Envelope proteins,gp120,HIV,Mathematical models


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