• The causative agents are human immunodeficiency viruses (HIV) of the Retrovirus genus of the Lentivirinae subfamily of the Retroviridae family. HIV die at 56°C within 30 minutes, but are resistant to low temperatures; quickly die under the influence of ethanol, ether, acetone and conventional disinfectants. In blood and other biological media, under normal conditions, they remain viable for several days. 2 types of virus are known.

    • HIV-1 (HIV-1) is the main causative agent of HIV infection and AIDS (formerly known as HTLV-III or LAV) in the Americas, Europe, Asia, Central, South and East Africa.
    • HIV-2 (HIV-2) is a less virulent virus; does not often cause typical manifestations of AIDS; main causative agent of AIDS in West Africa.

EPIDEMIOLOGY. The source of infection is a person at any stage of the infectious process. The virus is isolated from blood, semen, vaginal secretions, mother’s milk (these fluids determine the route of transmission of the virus), saliva. Ways of transmission – sexual, parenteral, transplacental, through mother’s milk. AT-RISK GROUPS

    • Homosexual and bisexual men (43%)
    • IV drug addicts (31%)
    • Heterosexuals (10%)
    • Recipients of blood and its components, transplanted organs (2%)
    • Patients with hemophilia (1%). PATHOGENESIS
    • Cell populations affected by HIV
    • HIV infects activated CO4
    • -cells (monocytes, macrophages and related cells expressing CO4-like molecules) using the CD4 molecule as a receptor; these cells recognize antigen and act as T-helper/amplifiers
    • Infection is likely due to phagocytosis of immune complexes containing HIV and AT. Infection of monocytes and macrophages is not accompanied by a cytopathic effect, and the cells become a peristaltic system for the pathogen.
    • Reservoirs of HIV in the body of an infected individual
    • The main reservoir is lymphoid tissues. The causative agent reproduces constantly, even in the early stages
    • In the CNS, microglia
    • The intestinal epithelium.
    • Early viremic stage
    • The virus replicates over varying periods of time in small numbers
    • A temporary decrease in the total number of CD4+ cells and an increase in the number of circulating HIV-infected CD4+ T lymphocytes
    • The circulation of HIV in the blood is detected in various periods; virusemia reaches a peak by 10-20 days after infection and continues until the appearance of specific antibodies (until the period of seroconversion).
    • Asymptomatic stage. For various periods of time (up to 10-15 years), HIV-infected people have no symptoms of the disease. During this period, the body’s defense systems effectively restrain the reproduction of the pathogen.
    • Humoral reactions – the synthesis of AT of various types that are not able to have a protective effect and do not protect against further infection
    • Cellular immune responses are capable of either blocking the reproduction of the pathogen, or preventing the manifestations of infection. Probably, cytotoxic reactions dominate in HIV-infected patients with a long absence of clinical manifestations.
    • Immunosuppression
    • Reducing the number of circulating CD4+ cells
    • Reducing the number of circulating CD4+T cells, which is essential for the replication of integrated HIV. Replication of integrated HIV in vitro is activated by mitotic or antigenic stimulation of infected T cells or concomitant herpes infection
    • A possible root cause of the decrease in the number of T cells is the manifestation of a cytopathic effect caused by viral replication. Infection of T cells in vitro is not always productive; the viral genome in an integrated state can remain unexpressed for a long period of time, while the number of T cells is constantly decreasing
    • The appearance of viral glycoproteins in the membrane of infected T-cells is a trigger mechanism for launching immune mechanisms directed against such cells. Implementation Mechanisms – Activation of Cytotoxic T Cells and AT-Dependent Cytotoxicity Response
    • Accumulation of non-integrated viral DNA in the cytoplasm of infected cells causes rapid HIV replication and cell death
    • HIV infects progenitor cells in the thymus and bone marrow, resulting in a lack of regeneration and a decrease in the CO pool
    • -lymphocytes
    • Reducing the amount of CO4
    • -lymphocytes is accompanied by a decrease in the activity of the THt subpopulation of T cells (however, there is no evidence that the activity of TH2 cells increases). An imbalance between TH and TH2 cell subpopulations precedes the development of AIDS. The activity of cytotoxic T cells and natural killer cells decreases, which is associated with a lack of helper cells. The response of B cells also weakens as the TH2 subpopulation decreases in numbers.
    • Defects in humoral reactions to all kinds of Ag o0 are due to a lack of T-helpers. B-lymphocytes are in a state of constant polyclonal activation.
    • Due to polyclonal activation and a defect in regulatory mechanisms, B cells produce antibodies to HIV Ag with low specificity, cross-reacting with nuclear, platelet, and lymphocytic auto-Ag.
    • Mechanisms that allow HIV to avoid the action of immunosurveillance factors
    • Increased humoral anti-HIV response, even more pronounced in AIDS
    • Integration of the HIV genome into host DNA with minimal expression of viral genes
    • HIV mutations in the gp120 epitope. HIV mutates much more frequently than most other viruses because HIV reverse transcriptase works with errors and is devoid of corrective activity
    • Cellular immune responses.

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