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HIV Infection

Human Immunodeficiency Virus

For medical students2 min readUpdated 2026-10-10

HIV infection is a chronic disease targeting the immune and central nervous systems, leading to profound immunosuppression and acquired immunodeficiency syndrome (AIDS). The pathogen selectively infects cells expressing the CD4+ receptor, causing their gradual destruction and severe opportunistic infections.

PathogenRetrovirus, lentivirus family (HIV-1 and HIV-2)

Main TargetCD4+ T-lymphocytes, macrophages, and dendritic cells

Course DynamicsThree main phases: acute, chronic, and crisis (AIDS)

NeoplasmsKaposi sarcoma and B-cell lymphomas

Etiology and Genetic Forms of the Pathogen

The causative agent is the human immunodeficiency virus (HIV), belonging to the lentivirus family. The virus is genetically heterogeneous and divided into two main forms:

HIV-1: Dominates globally, including Europe, the USA, and Central Africa.
HIV-2: Localized predominantly in West Africa.

The primary targets in the human body are cells of the immune system and the central nervous system. The high viral tropism is driven by the presence of high-affinity CD4+ surface receptors.

Pathogenesis and Immune System Depletion

Profound immunosuppression in HIV infection develops due to the progressive reduction of the CD4+ T-cell pool. Mechanisms of cell destruction include direct and indirect pathways:

Integration of proviral DNA into the genome of dividing lymphocytes, leading to their destruction.
Damage to immature precursors in the thymus and bone marrow.
Syncytium formation—fusion of infected and healthy cells.
Autoimmune destruction and cytokine deficiencies.

Monocytes and macrophages play a specific role: unlike T-lymphocytes, they do not die upon viral replication, serving as a viral reservoir, "factory," and vehicle transporting the pathogen into tissues, especially the CNS.

Stages of the Disease Course

The interaction between the virus and the host proceeds through several clinical stages:

Early Acute Phase (Seroconversion): Accompanied by high viremia peaking in the first weeks, with mononucleosis-like symptoms.
Chronic Phase: A period of relative viral containment where replication occurs primarily within lymphoid tissue, while the immune system remains relatively intact for several years.
Final Phase (AIDS): Characterized by runaway viral replication, a total drop in CD4+ T-cell counts, severe opportunistic infections, nervous system involvement, and malignancies.

Pathological Anatomy and Complications

Morphological changes affect various organs and tissues:

Lymph Nodes: Early stages show marked follicular hyperplasia, whereas the AIDS stage exhibits total depletion.
Central Nervous System: HIV encephalomyelitis develops with microglial nodules, multinucleated giant cells (symplasts), and foci of softening.
Neoplastic Processes: Kaposi sarcoma develops in 40% of patients with generalized skin, lymph node, and internal organ involvement, alongside B-cell lymphomas.
Opportunistic Infections: Caused by opportunistic bacteria, fungi (Candida, Cryptococcus), protozoa, and viruses (cytomegalovirus, herpes simplex) against a backdrop of critical immunosuppression.

Mnemonic

THREE phases of HIV: Acute (viremia), Chronic (lymph node containment), AIDS (crisis and opportunists). Target — CD4+ cells.

Frequently asked questions

What opportunistic infections develop against the background of critical immunosuppression in AIDS?

Severe immunodeficiency in AIDS leads to infections caused by opportunistic microorganisms. Main pathogen groups:

Protozoa — Pneumocystis, Toxoplasma, Cryptosporidia.
Fungi — Candida, Cryptococcus.
Bacteria — Mycobacteria (M. avium, M. intracellulare), Legionella, Salmonella, Enterobacteriaceae.
Viruses — Cytomegaloviruses, herpes viruses, slow-infection viruses.

Opportunistic infections are characterized by severe relapsing courses, a tendency toward generalization, and treatment resistance. Main clinical forms include gastroenteritis, urinary tract infections, sepsis, and opportunistic encephalitis or meningitis.

Besides CD4+, what coreceptors are required for HIV entry into the target cell?

Entry of the human immunodeficiency virus into target cells requires additional binding to chemokine coreceptors. The obligatory coreceptors include:

CCR5 Receptor — A chemokine coreceptor preferred by the virus primarily in early disease stages (expressed on macrophages).
CXCR4 Receptor — A chemokine coreceptor utilized during later disease progression (expressed on T-cell surfaces).

CD4 receptor binding alone is insufficient for infection; coreception with one or both chemokine receptor types is required.

What are the histological features of Kaposi sarcoma in HIV infection?

Microscopic examination of Kaposi sarcoma in HIV shows distinct histological architecture. The tumor consists of:

Thin-walled vascular channels — arranged haphazardly.
Spindle cells — forming intersecting fascicles.
Stroma — containing extravasated erythrocytes and hemosiderin pigment accumulations.

In AIDS, this tumor exhibits malignant behavior with systemic generalization, involving lymph nodes, the gastrointestinal tract, lungs, and other visceral organs.

Which cells serve as the primary HIV reservoir in the body?

The main viral reservoirs are CD4+ T-cells, macrophages, and dendritic cells. Infected macrophages do not die during viral replication and actively transport the virus into tissues.

How do early lymph node changes differ from those in the AIDS stage?

Early stages show marked hyperplasia of lymphoid follicles and their germinal centers, whereas in AIDS, lymphoid tissue is completely depleted and the nodes shrink drastically.

What are the main causes of death in HIV infection?

The prognosis is unfavorable with a nearly 100% mortality rate if untreated. The primary causes of death are severe opportunistic infections and generalized neoplastic processes such as Kaposi sarcoma.

Go deeper

Epidemiology and risk groups for infection
Humoral immunity disorders and hypergammaglobulinemia
Pathogenesis and morphology of herpetic infection
Mechanisms of HIV mutation and immune evasion
Specific CNS manifestations in HIV encephalomyelitis