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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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          Abstract

          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 references 11

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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.
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            • Article: not found

            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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              Neuronal cell killing by the envelope protein of HIV and its prevention by vasoactive intestinal peptide.

              The clinical manifestations of AIDS (acquired immune deficiency syndrome) often include neuropsychiatric and neurological deficits, including early memory loss and progressive dementia. HIV (human immunodeficiency virus), the aetiological agent of AIDS, is probably carried by infected macrophages in the central nervous system. The virus enters cells by binding its envelope glycoprotein gp120 to the CD4 antigen present on brain and immune cells. From the data reported in this paper, we now suggest that the neuronal deficits associated with HIV may not be entirely a result of infectivity, but that gp120 shed from HIV could directly produce the neuropathology as a result of its interference with endogenous neurotrophic substances. It is known that an analogue of a sequence contained in vasoactive intestinal peptide (VIP) occurs in all known sequenced gp120 isolates and that VIP is important for neuronal survival in cell culture. Here we show that purified gp120 from two diverse HIV isolates and a recombinant gp120 from a third isolate were all potent in specifically producing significant neuronal cell death in dissociated hippocampal cultures derived from fetal mice, and that this could be reduced by monoclonal antibodies against the murine CD4 antigen and completely antagonized by VIP.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                978-3-8055-7683-3
                978-3-318-01049-7
                0253-5068
                1421-9735
                2004
                July 2004
                20 January 2004
                : 22
                : 1
                : 84-91
                Affiliations
                Aethlon Medical, Inc., San Diego, Calif., USA
                Article
                74928 Blood Purif 2004;22:84–91
                10.1159/000074928
                14732816
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 1, References: 27, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/74928
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