Taxonomy and epidemiology
The causative agent belongs to the family Retroviridae and the genus Lentivirus (lymphotropic viruses). The infection has a tendency to rapidly spread epidemically. Currently, two main variants of the virus are distinguished, differing in their structural and antigenic characteristics:
- HIV-1: Discovered in 1983 by the French virologist Luc Montagnier. It is the main causative agent of the infection worldwide.
- HIV-2: Discovered in 1985 in West Africa.
Virion ultrastructure
HIV is a complex virus. Its structure is best examined from the center outward to the outer envelopes:
- Nucleocapsid (core): Has a truncated cone shape and is built from approximately 2,000 copies of the p24 protein. Inside the capsid are packaged two molecules of +RNA, nucleoproteins (p7, p6, and p9 proteins), and a crucial enzyme complex comprising reverse transcriptase, integrase, and protease.
- Matrix layer: Located directly on top of the capsid. Formed by the matrix protein p17.
- Supercapsid (outer envelope): A double-layered lipoprotein membrane that the virus acquires from the host cell membrane during budding. The membrane is pierced by exactly 72 glycoprotein spikes (trimers). Each such spike consists of a transmembrane glycoprotein gp41 embedded in the envelope and an outwardly protruding surface glycoprotein gp120.
Genome organization
The HIV genome is represented by two RNA strands. All genetic information is distributed among 3 structural and 7 regulatory genes (tat, rev, nef, vif, vpr, vpu, vpx), which control reproduction processes and pathogenesis.
Key structural genes:
- gag (group antigen): encodes the synthesis of internal structures (matrix, capsid, and nucleocapsid proteins).
- pol: responsible for the production of replication enzymes (reverse transcriptase/revertase, integrase, protease, RNase).
- env: encodes outer envelope proteins—glycoproteins gp120 and gp41.
Antigenic structure and variability
In response to the infection, the human body produces antibodies to all products of the env, gag, and pol genes. The group-specific antigen p24 provokes the most significant immune response.
The main antigenic determinant of the virus is the surface glycoprotein gp120, which contains a domain for binding to the CD4 receptor and coreceptors on the surface of target cells.
Important feature: The region of the env gene encoding gp120 is hypervariable. Due to extremely high mutability, new antigenic variants of gp120 are formed during each replication cycle of the virus. This allows the pathogen to effectively evade the immune system.
HIV variants and classification
The main causative agent (HIV-1) is classified based on the env gene. It is divided into three groups: M, N, and O. Groups N and O are localized primarily in West Africa, whereas group M dominates the rest of the world and includes 10 subtypes (from A to K). Subtype A prevails in the Russian Federation.
HIV-1 and HIV-2 have a number of significant genetic and antigenic differences:
| Structure | HIV-1 | HIV-2 |
|---|---|---|
| Regulatory gene | vpu | vpx |
| Surface glycoprotein | gp120 | gp140 / gp105 |
| Transmembrane glycoprotein | gp41 | gp36 |
| Capsid protein | p24 | p26 |
Cultivation and resistance
HIV cannot grow on standard nutrient media; special cell cultures are required for its propagation.
The virus is quite sensitive to environmental factors. It is destroyed by sunlight, UV radiation, 70% alcohol, and all known disinfectants. Heating to 56 °C causes a sharp decline in infectivity, and a temperature of 70 °C inactivates the virus within 10 minutes.
Nevertheless, the virus can persist in biological fluids for a long time:
- In a frozen state (in semen or serum)—survives for several years.
- In dried plasma at room temperature (23–27 °C)—retains infectious activity for up to 7 days.
Briefly: answers to topical questions
What stages and clinical manifestations are characteristic of HIV infection as it transitions into AIDS?
HIV infection goes through several stages:
- Stage 1 (incubation)—from 3 weeks to 3 months, active HIV replication without clinical manifestations and antibodies.
- Stage 2 (primary manifestations)—acute HIV infection with fever, skin rashes, lymphadenopathy, pharyngitis, diarrhea; mononucleosis- or rubella-like syndrome is possible.
- Stage 3 (early symptomatic)—may last 3–5 years; characterized by fever, night sweats, fatigue, chronic diarrhea, generalized lymphadenopathy, oral candidiasis, leukoplakia, and respiratory tract infections.
- Stage 4 (late symptomatic, pre-AIDS)—progressive decline in CD4+ lymphocytes, moderate immunodeficiency, and increased risk of opportunistic infections.
When the immune system is suppressed, opportunistic infections develop, including Pneumocystis pneumonia, toxoplasmosis, cryptosporidiosis, candidiasis, and histoplasmosis. The final stage of HIV infection is AIDS—acquired immunodeficiency syndrome, characterized by severe damage to the immune system.
What receptors and coreceptors on the surface of target cells does HIV use for entry?
HIV uses the CD4 receptor and chemokine coreceptors CCR5 and CXCR4 to enter the cell. The entry mechanism involves several stages: first, the viral glycoprotein gp120 binds to the CD4 receptor on the surface of the target cell (primary binding), followed by interaction with chemokine coreceptors CCR5 and/or CXCR4, which is necessary for membrane fusion. Afterward, the viral protein gp41 undergoes conformational changes, ensuring the fusion of the viral and cellular membranes. Target cells include T-helper cells, macrophages, follicular dendritic cells, Langerhans islet cells, and brain microglia.
For quick memorization of the three main structural genes, use the phrase GPE (e.g., "Go Play Everywhere"): Gag—packaging (internal proteins), Pol—polymerase/enzymes (assembly tools), Env—envelope (outer shell).
Class and exam questions
Why is it difficult for the immune system to cope with HIV?
This is due to the hypervariability of the env gene region. In each new cycle of viral reproduction, altered variants of the gp120 surface protein are formed, which previously generated antibodies can no longer recognize.
Which HIV enzyme distinguishes it from many other RNA viruses?
Reverse transcriptase (revertase), a product of the pol gene. This enzyme allows DNA synthesis using viral RNA as a template, which is a hallmark of the retrovirus family.
Which protein is responsible for HIV fusion with the human cell membrane?
The transmembrane glycoprotein gp41 is responsible for the fusion of the viral envelope with the target cell membrane.
What else to study on this topic
- Mechanisms of HIV entry into the target cell and the role of CD4 receptors.
- The life cycle of retroviruses: from reverse transcription to budding.
- Functions of regulatory genes (tat, rev, nef, vif) in the pathogenesis of HIV infection.
- Laboratory diagnosis of HIV infection: detection of antibodies and the p24 antigen.
- Features of the pathogenesis of acquired immunodeficiency syndrome (AIDS).
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