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Technical scheme for the treatment of AIDS with Nano-tea

    1. What is the pathogenesis of AIDS?
    AIDS is caused by HIV infection, and HIV belongs to chronic virus sub-family of retrovirus family. At present, two types of HIV are discovered, namely, HIV-1 and HIV-2. HIV-1, which has spread all over the world, is stronger than HIV-2 in aspects of pathogenicity and transmission, and HIV-2 is limited in Western Coast of Africa.
    After HIV having infected human body, virus cyst membrane adsorbs on the CD4 receptor of host cell and fuses with it, and the core of virus enters the cell. Under the action of Reverse transcriptase, the virus translate its RNA into DNA, and when the host cell splits, the virus DNA is integrated into the gene of the? cell. Virus nucleic acid may be transmitted to the filial generation of the cell and hide for a long time, and the patient may live with virus.
    In the course of infection, HIV exists in host cell in two different states, e.g. active state and static state. Once the cell that contains virus in static state is stimulated, such as by karyokinesis gene, antigen, allogene or various infectious factors, the virus DNA integrated into the host cell will begin to transcribe its DNA into RNA and translate the RNA into proteins and enzymes of viral structure, which, after being assembled with a RNA nucleus, will get a envelope from cell membrane in the form of budding when they are released and become a nature HIV. The mature HIV will infect other cells. Along with the duplication and reproduction of the virus, the infected cells are continuously damaged, new cell are continuously infected and the cell count that plays an important role in the immune system of organism is progressively reduced. Although there is a long-term incubation period after being infected and the patient seems to be in a healthy state, the slight changes are undergoing day and day, with immune system continuously damaged and worsen, resulting in the failure of immune functions.
    2. How to recognize the immunologic injury of HIV infection
    After entering the organism, HIV mainly infects the T lymphocyte that contains T4 receptor and rich in proteins, and also invades the cells that have a few receptor proteins or no receptor protein, influencing the special and non-special immune response of immune system and leading to immune deficiency.
    2.1 Accessory T lymphocyte (T4)
    HIV mainly infects T4 cell, which is the central link of immune system and forms the immune network together with other Immunological competent cells including monomacrophage, cytotoxic T cell, NK cell and B cell. The mechanism of T4 cell decrease caused by HIV infection is shown in Figure 3-1.

    Mechanism of T4 cell injury caused by HIV infectionauto

    Virus duplication in T cell that directly leads to the death of cell

    Formation of syncytium that results in the death of a large number of T4 cells not infected by HIV?

    T4 cell dysfunction and interleukin-2 generation reduction that lead to the lowering of?? immunocompetence of regulation net and the dysfunction of cells

    Death of programmed cell that leads to dramatically decrease of cell count

    Fig. 3-1 Mechanism of T4 cell injury caused by HIV infection

    The course of virus replication in T4 cell is the course of cell death. Experimental observation shows the death of T4 cell infected by HIV usually happens 7-10 days after the cell is stipulated by karyokinesis gene, and following numerous replication and rapid hyperplasia of HIV, infected T4 cells die in great number.
    On the surface of T4 cell infected by HIV, there are capsule proteins left after HIV invasion. capsule protein can fuse with the CD4 receptor on the surface of T4 cell not infected by HIV and form a giant multinuclear syncytium, which will be killed along with T4 cell, thus quickening the decrease of T4 cell count.
    HIV infection can also lead to the dysfunction of T4 cell and the low generation of interleukin-2, leading further dysfunction of the immunological competent cell in the interleukin-2 regulation net.
    Programmed cell death (PCD) that involves cell death as planned is also called active cell suicide. After HIV has infected T4 cell, the glycoprotein GP120 of the virus, together with CD4 molecule, can cross start PCD to make T4 cell (including the one not infected) dead in great number, leading to dramatically decreasing of T4 cell count 2.2 Cytotoxic lymphocyte
    Cytotoxic lymphocyte (CTL) has an effect on killing some antigen matters such as virus and tumor cells, and together with natural killer cells, constitutes an important immune defense line of the organism against virus and tumor. However, the immunoreaction of CTL needs the cooperation of T4 cells. For AIDS patient, the decrease of T4 cells may cause the dysfunction of CTL, and this is one of the important reasons of clinical appearance of multiple infection and tumors.
    2.3 Natural killer cell
    Natural killer cell (NK) has the effect of anti-tumor and anti-virus infection. But if its function is lowered, it can not release its toxic factors and its function become abnormal, leading to the decrease of immune supervision function of mechanism and the likelihood of opportunistic infection and tumors.
    2.4 B lymphocyte
    B lymphocyte is the major immunological competent cell, with which the mechanism can produce antibodies and form humoral immunity. If the component of B lymphocyte changes, the activated polyclonal cells will be increased and finally differentiated into plasma cells that can excrete immune globulin, and thus the serum immune globulin and immune compound will increase, and autoimmunity appears. At the same time, static cells are consumed; number reduced and endogenous deficiency appeared. The immature B cell count increases for compensation, and the increase is related with the likelihood of AIDS patient getting B cell tumors.
    2.5 Mononuclear-macrophage
    Mononuclear-macrophage has a few T4 protein molecules on its surface, and can be infected by HIV. However, infected mononuclear-macrophage is not likely to form syncytium and die from damage. However, the infected mononuclear-macrophage, in the course of dealing with and processing of antigen, may further lead to the decrease of T4 cell function in excreting interleukin and the decrease of the function of immune system. Mononuclear-macrophage, after being infected by HIV and through wandering function, may carry causative agent to various tissues of the organism and cause damage to various viscera. Infection of mononuclear-macrophage by HIV may be one of the reasons for AIDS patient to get pneumocystis carinii pneumonis (PCP). HIV infected mononuclear-macrophage, if wandering into skin cell on guts, persistent diarrhea may happen, and if wandering into nervous system, intracerebral HIV infection may appear, and adopting immune enzymatic mark technology, HIV can be detected in cerebral tissue and separated from cerebrospinal fluid, and DNA and RNA of HIV can also be found in cerebral tissue. This can explain the pathogenesis of the diseases in nervous system such as encephalon and dementia suffered by AIDS patients.
    The basic pathologic change caused by HIV infection is organism immune deficiency, which leads to various kinds of opportunistic infection that endanger the life of patients.?
    3. What is the attack course of AIDS?
    After HIV has infected human body, a dynamic course inclusive of different stages appears, and most of which may develop into AIDS. The attack course is shown in the following figure:


    Stage D


    Stage C


    Stage B

    infection stage
    Acute infection stage

    Stage A

    3.1 HIV acute infection stage (Stage A)
    2-6 weeks after primary HIV infection, in part of patients appear symptoms including slight fever, angina, skin rash and lymphadenectasis, all of which are considered to be common infection and disappear soon. This is the rapid reaction of immune system to the rapid and broad spread of HIV in human body. For some patients, self-constrained neural symptoms may appear, such as atypical suppurative encephalitis and acute encephalitis, and for some patients, systemic lymphadenectasis (lymphadenopathy). These acute reactions of immune system to HIV infection can sustain for several weeks. In some cases, the symptoms of acute infection stage are not significant, but through serologic test the following results can be obtained:
    Hyperplasma viremia
    Number reduction and hypofunction of leucocytes
    Decrease of leucocytes (less than 5x109/L)
    Classified leucocyte count is normal at early stage
    Stage of antibody positive (stage B) 3-6 months after HIV infection, serologic test shows HIV antibody positive and no clinical symptoms. This situation may last a long time, even several years. This stage can be divided into two sub-stages.
    (1) Asymptomatic infection stage (stage B-1) After being infected, many people may have not clinical symptoms for a long time, but for some people, several items of laboratory examination typical of the disease may appear. Along with further infection, leucocyte count may significantly decrease. The duration of asymptomatic infection stage varies greatly with each case. About 30% of the infected people are ill within 2-5 years, with each year longer, the percentage increases 17%, and about 50% of the infected will develop into AIDS within 10 years after being infected. For a few infected, they may have HIV hidden lifelong.
    (2) Persistent generalized lymphadenopathy (stage B-2) Many HIV infected people may suffer from persistent generalized lymphadenopathy (also called PGL or LAS-lymphadenopathy syndrome). By definition, PGL is the enlargement of two or more lymph glands at the outside of the groin (also often at the armpit and neck) sustained over 3 months and caused by no other reason than HIV. If the PGL disease is accompanied by herpes zoster, its outlook tends to be poor. Now it is considered that PGL exists simultaneously with asymptomatic infection stage, but it is an important character of HIV infection.