Viral entry and intracellular processing
To initiate the infectious process, a virus must attach to a target cell using its membrane molecules as receptors. For example, Epstein–Barr virus binds to the complement receptor CD21, measles virus binds to CD150 and CD46, and HIV uses the CD4 molecule and CXCR4/CCR5 coreceptors.
Upon attachment, the viral envelope fuses with the cell membrane, and its contents enter the interior. Next, nucleic acid transcription and its integration into the cell genome occur with the participation of the integrase enzyme.
Presentation of viral antigens to the immune system follows the endogenous pathway:
- Viral DNA is translated, and viral proteins are synthesized in the cytosol.
- Some of the proteins are cleaved in proteasomes.
- Peptide fragments are transported into the endoplasmic reticulum.
- Peptides are loaded into major histocompatibility complex class I (MHC-I) molecules.
- The MHC-I–peptide complex is translocated to the membrane for recognition by cytotoxic CD8+ T lymphocytes.
Innate immunity responses
Infected cells often die due to the cytopathogenic effect of the virus. Their fragments are phagocytosed by macrophages and dendritic cells. Inside phagolysosomes, viral nucleic acids act as pathogen-associated molecular patterns (PAMPs). They are recognized by Toll-like receptors (TLRs), which activates the transcription factor NF-κB. This triggers the production of pro-inflammatory factors and interferons.
Interferon system (Defense factor 1) Type I interferons (α and β) are most actively synthesized by plasmacytoid dendritic cells. Interferons directly inhibit pathogen replication and induce viral RNA degradation.
Role of NKT and NK cells (Defense factor 2) The infected cell begins to express stress proteins (MICA, MICB, ULBP). They are recognized by the NKG2D receptor present on NKT and NK cells.
- NKT cells secrete interferon-gamma (IFNγ) in response.
- NK cells (natural killers) perform cytolysis in the presence of stress proteins and an additional condition—the loss of MHC-I molecules by the target cell.
Triggering of adaptive cellular response
Myeloid dendritic cells capture soluble components of dead cells and present them in the regional lymph node. Viral peptides in the context of MHC-II are presented to CD4+ T cells, and in the context of MHC-I to CD8+ T cells.
Activated CD4+ T helpers differentiate into two subpopulations:
- Th1 cells: secrete IL-2 (for CD8+ cell proliferation) and IFNγ (for the activation of NK cells and macrophages).
- Th2 cells: stimulate B lymphocytes using interleukins (e.g., IL-4), assisting the humoral response.
Cytotoxic T lymphocytes (Defense factor 3) Under the influence of IL-2, CD8+ T cells actively proliferate and differentiate into specific killers. They locate infected cells that retain MHC-I expression with the viral peptide and destroy them.
Humoral immunity and immunological memory
Free viral particles are recognized by B-cell receptors (BCRs). Having received stimulating signals from Th2 lymphocytes, B cells proliferate and differentiate into antibody-secreting plasma cells.
Neutralizing antibodies (Defense factor 4) bind to the surface of extracellular viruses. This prevents the infection of new cells and helps macrophages eliminate the pathogen more rapidly.
The outcome of adaptive immunity activation is the formation of memory T and B cells. Upon re-exposure to the same virus, they provide a robust secondary response: T-killer generation is accelerated, antibody secretion is enhanced, and NK-cell activity is stimulated. This establishes reliable protective immunity.
Briefly: answers to topical questions
What are the morphological features and surface markers of plasmacytoid dendritic cells?
The surface markers of plasmacytoid dendritic cells include various receptors, although their morphological features are not described in the text. These cells express the following on their membrane:
- Toll-like receptors — TLR1, TLR6, TLR7, TLR9, and TLR10.
- Lectin receptors — DEC-205 (CD205) and Dectin-1.
- Other markers — CD45RA.
What stages do B lymphocytes undergo during differentiation into plasma cells in germinal centers?
The differentiation of B cells in the germinal center involves the following stages and zones:
- Centroblasts — mutating cells in the dark zone of the follicle.
- Centrocytes — cells of the light basal zone where selection takes place.
- B-immunoblasts — proliferating cells of the light apical zone.
- Plasmablasts — generated in the apical part of the germinal center, retain proliferative capacity, lose CXCR5, acquire CXCR4, and migrate to other zones where they differentiate into mature plasma cells.
Memory B cells derived from mature B centrocytes complete somatic hypermutation, isotype switching, and affinity maturation.
Which signaling pathways are activated by Toll-like receptors upon recognition of viral PAMPs?
Upon recognition of viral PAMPs by Toll-like receptors, intracellular signaling pathways involving kinases and adaptor proteins are activated:
- MyD88-dependent pathway participates in signal transduction from TLRs.
- Activation of NF-κB leads to the activation of pro-inflammatory cytokine genes.
- Induction of type I interferons (α and β) promotes viral RNA degradation and prevents viral replication.
Which immunoglobulin isotypes participate in the neutralization of viruses on mucosal surfaces?
The neutralization of viruses on mucosal surfaces is primarily mediated by secretory IgA (sIgA). It binds to pathogens, blocking their adhesion and motility, and serves as the main factor of specific mucosal immunity.
The 4 main factors of antiviral defense can be remembered by the acronym INKA: Interferons (type I), Neutralizing antibodies, Killers (natural killer cells), Antigen-specific killers (T lymphocytes).
Class and exam questions
What is the main condition for the activation of natural killer (NK) cells?
NK cells are activated and kill the infected target cell provided that it has lost normal surface expression of MHC-I molecules.
Which cells synthesize the highest amount of interferons during a viral infection?
The most intense synthesis of type I interferons (α and β) is carried out by plasmacytoid dendritic cells.
Why does a virus need the integrase enzyme?
Integrase is a specialized viral enzyme required for the insertion (integration) of viral nucleic acid into the genome of the infected cell.
What else to study on this topic
- Processing of viral antigens in proteasomes
- Mechanisms of intracellular signaling via NF-κB
- Cell surface stress proteins (MICA, MICB, ULBP)
- Features of antiprotozoal immunity using malaria as an example
- Antigenic variation in plasmodia (variant surface antigens, VSAs)
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Other topics in the section "Immunity in defense and damage of the organism. Pathology of immunity"
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