Etiology and genetic forms of the pathogen
The causative agent of the disease is the human immunodeficiency virus (HIV), which belongs to the family Lentiviridae. The virus is genetically heterogeneous and divided into two main forms:
- HIV-1: dominates in most regions of the world, including Europe, the USA, and Central Africa.
- HIV-2: localized predominantly in West Africa.
The primary targets of the virus in the human body are cells of the immune system and the central nervous system. The high tropism of the virus is due to the presence of the high-affinity CD4+ receptor on the cell surface.
Pathogenesis and immune system depletion
Profound immunodepression in HIV infection develops due to the progressive depletion of the CD4+ T-cell pool. The mechanisms of their destruction are divided into direct and indirect:
- Integration of proviral DNA into the genome of dividing lymphocytes leads to their death.
- Damage to immature precursors in the thymus and bone marrow.
- Syncytium formation—fusion of infected and healthy cells.
- Autoimmune destruction and deficiency of essential cytokines.
Monocytes and macrophages play a special role: unlike T-lymphocytes, they do not die upon viral replication, serving as its reservoir, "factory," and vehicle, delivering the pathogen to tissues, especially the central nervous system.
Stages of disease progression
The interaction between the virus and the organism goes through several clinical stages:
- Early acute phase (seroconversion): accompanied by pronounced viremia, peaking in the first weeks, and symptoms resembling mononucleosis.
- Chronic phase: a period of relative viral containment, where replication occurs predominantly in lymphoid tissue, and the immune system remains intact for several years.
- Final phase (AIDS): characterized by runaway viral replication, a total drop in CD4+ T-cell levels, severe opportunistic infections, nervous system damage, and tumors.
Pathological anatomy and complications
Morphological changes affect various organs and tissues:
- Lymph nodes: marked hyperplasia of lymphoid follicles is noted in the early stages, whereas in the AIDS stage, their complete depletion is observed.
- Central nervous system: HIV encephalomyelitis develops with microglial nodules, multinucleated symplasts, and foci of softening.
- Tumor processes: 40% of patients develop Kaposi sarcoma with generalized involvement of the skin, lymph nodes, and internal organs, as well as B-cell lymphomas.
- Opportunistic infections: caused by opportunistic bacteria, fungi (Candida, Cryptococcus), protozoa, and viruses (cytomegalovirus, herpes simplex) against the background of critical immunosuppression.
Briefly: answers to topical questions
Which opportunistic infections develop against the background of critical immune depletion in AIDS?
Against the background of severe immunodeficiency in AIDS, infections caused by opportunistic microorganisms develop. The main groups of pathogens:
- Protozoa — Pneumocystis, Toxoplasma, Cryptosporidium.
- Fungi — Candida, Cryptococcus.
- Bacteria — mycobacteria (M. avium, M. intracellulare), Legionella, Salmonella, enterobacteria.
- Viruses — cytomegaloviruses, herpes viruses, slow virus infections.
Opportunistic infections are characterized by a severe relapsing course, a tendency to generalize, and resistance to ongoing treatment. The main clinical forms include gastroenteritis, urinary tract infections, sepsis; encephalitis and meningitis due to opportunistic infection are possible.
Which coreceptors, in addition to CD4+, are necessary for HIV entry into the target cell?
For the human immunodeficiency virus to enter the target cell, additional binding to chemokine coreceptors is required. A prerequisite for viral entry is the presence of the following coreceptors on the cell:
- CCR5 receptor — a chemokine coreceptor to which the virus shows tropism predominantly in the early stages of the disease (located on macrophages).
- CXCR4 receptor — a chemokine coreceptor, binding to which occurs during the further development of the infection (located on the surface of T cells).
The presence of the CD4 receptor alone is not sufficient for infection; co-reception with one or both types of these chemokine receptors is required.
What are the histological features of the structure of Kaposi sarcoma in HIV infection?
Upon microscopic examination, Kaposi sarcoma in the setting of HIV infection has a characteristic histological structure. The tumor consists of the following elements:
- Thin-walled blood vessels — arranged haphazardly.
- Spindle cells — form fascicles.
- Stroma — contains hemorrhages and deposits of hemosiderin pigment.
In AIDS, this tumor acquires a malignant character with generalization of the process and involvement of lymph nodes, the gastrointestinal tract, lungs, and other internal organs.
THREE phases of HIV: Acute (viremia), Chronic (latency in lymph nodes), AIDS (crisis and opportunists). Target — CD4+ cells.
Class and exam questions
Which cells are the main reservoir of HIV in the body?
The main reservoirs of the virus are CD4+ T-cells, macrophages, and dendritic cells, wherein infected macrophages do not die upon viral replication and actively transport it into tissues.
How do early lymph node changes differ from changes in the AIDS stage?
In the early stages, pronounced hyperplasia of lymphoid follicles and their germinal centers is observed, whereas in the AIDS stage, complete depletion of lymphoid tissue occurs and the nodes become drastically reduced in size.
What are the main causes of death in HIV infection?
The prognosis of the disease is unfavorable, with a mortality rate of 100%. The main causes of death are severe opportunistic infections and generalized tumor processes, such as Kaposi sarcoma.
What else to study on this topic
- Epidemiology and risk groups for infection
- Humoral immunity disorders and hypergammaglobulinemia
- Pathogenesis and morphology of herpetic infection
- Mechanisms of HIV mutation and evasion of immune control
- Features of CNS involvement in HIV encephalomyelitis
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