AIDS immunoadsorption therapy apparatus

Abstract

The invention discloses an AIDS immunoadsorption therapy apparatus, which is applicable to the medicine field. The AIDS immunoadsorption therapy apparatus is characterized in that blood and plasma separators, by which plasma, individual blood cells and multinuclear giant cells which are formed due to HIV boarding, are prepared; by virtue of a hybridoma technique and an exogenous gene transfection technique, a hybridoma macrophage cell line and a CD4+T cell line, which can bond HIV, are prepared, the cell lines, as adsorbing agents, are prepared in cell cryopreservation liquid, and the cell lines are filled with high polymer materials, so that adsorbers are prepared; the adsorbers, together with the separators, function as key parts of an extracorporeal circulation device; when blood passes through the blood separator, the multinuclear giant cells which contain the HIV are filtered out, subsequently, when the plasma, which is separated by virtue of the plasma separator, passes through the purifier, HIV in the plasma is adsorbed and scavenged by virtue of a purifying agent, the purified plasma joins with the individual blood cells which are separated by virtue of the plasma separator, and then the plasma is returned back, so that the purpose of scavenging the HIVs inside and outside the blood cells is achieved.

Description

technical field [0001] The invention relates to the preparation and application of an AIDS immunoadsorption therapeutic apparatus in the field of biomedicine, which is mainly used for removing HIV inside and outside blood cells of AIDS patients, so as to achieve the purpose of preventing, controlling and treating AIDS. Background technique [0002] Human immunodeficiency virus is a lentivirus that infects human immune cells. It is a type of retrovirus, with a diameter of about 120 nanometers and a roughly spherical shape. The outer membrane of the virus is a lipid envelope (derived from the host cell) and embedded with the viral proteins gp120 and gp41. gp41 is a transmembrane protein, and gp120 is located on the surface and binds to gp41 through non-covalent interaction. Inside is a spherical matrix (Matrix) formed by protein p17, and a semi-conical capsid (Capsid) formed by protein p24. The capsid has a high electron density under the electron microscope and contains the ...

AI Technical Summary

Problems solved by technology

However, the antibody cannot contact the virus remaining in the mononuclear macrophage, and the HIV envelope protein is prone to antigenic variation, and the original antibody loses its effect, so that the neutralizing antibody cannot play its due role

During the latent infection stage, the HIV provirus is integrated into the host cell genome, so HIV will not be recognized by the immune system, so it cannot be eliminated by autoimmunity alone

Another very important reason should be that, based on the mechanism of antibody killing and clearing antigens, it is speculated that after the immune antibody binds to the antigen, if it wants to produce an immune effect, it must either activate the complement and mediate the ADCC effect to dissolve the cellular antigen, but HIV It is not a cellular antigen; either it attracts phagocytes to phagocytize and clear the antigen through chemotaxis, but HIV is protected and proliferates in the phagocytes instead; or the antibody binds to the antigen to neutralize it, making it lose its infectivity, but HIV antigens have many structures Mutations, often making it difficult for antibodies to recognize

[0005] Judging from the current AIDS treatment methods that have been used clinically, the effect is not so ideal: (1) HIV reverse transcriptase inhibitors: can only prevent the infection of susceptible cells that have not been infected with HIV, and have no therapeutic effect on infected cells, and are toxic There are many side effects, including mitochondrial toxicity, myelosuppression, erythrocytic anemia, neutropenia and thrombocytopenia, pancreatitis, and the generation of cross-drug resistance. Drug-resistant variants, resulting in decreased clinical efficacy or failure

(2) HIV protease inhibitors: prone to drug-induced liver injury, lipid metabolism disorders and other side effects and drug resistance

(4) Inhibiting HIV virus entry inhibitors: including blocking the binding of gp120 to CD4, blocking the binding of HIV to coreceptors, acting on gp41 membrane subunits, and acting on CC chemokine receptor 5 (CCR5) on the surface of T lymphocytes to block HIV from entering host cells, but has side effects on the liver and heart

(6) HIV vaccine treatment: Due to the particularity of HIV, such as innate immunity is not enough to resist HIV and its targeted destruction of the immune system, and the virus mutates rapidly, so far no truly safe and effective vaccine has been developed

(7) Gene therapy: HIV gene therapy research has never stopped, including antisense technology, RNA decoy, RNA interference, intracellular antibodies, dominant negative mutants, suicide genes, etc., but gene therapy that has entered phase II clinical trials hardly

[0008] In short, various drugs and biological products cannot effectively kill HIV in the body, and they are expensive and have severe side effects. So far, there is no effective method for the treatment of AIDS, which has become a worldwide problem that cannot be overcome for a long time.

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