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THE STRUCTURAL CHANGES OF MACROPHAGES INFECTED WITH TICK-BORNE ENCEPHALITIS VIRUS
Abstract:
Macrophages belong to the innate immune cells and play a key role in the pathogenesis of viral infections. The results of ultrastructural study of macrophages infected with tick-borne encephalitis virus (TBEV), the Flavivirus family, pathogens of human infections, affecting the nervous system, were presented. With the assistance of virological methods was found that the TBEV are absorbed by macrophages and replication in them. An ultrastructural study has shown that the virus enters into the cytoplasm by local destruction of plasmalemma and newly synthesized virus particles exited from the cell by same. Simultaneously there is a seal of perinuclear cytoplasm space, where found in a large number of ribosomes, microfilaments, ribonucleoprotein fibers and viral special structure: nucleocapsids, tubular formations and viral layers (fabrics). On the surface of last structures the newly synthesized virus particles were visualized. Thus, the evidence shows that macrophages play a role in the spread of TBEV, being for their the target cell. As active antigen presenting cells the macrophages can modulate the protective response of the body and influence on the pathogenesis of tick-borne encephalitis.
Insights
Macrophages are key innate immune cells in viral infections. This study shows tick-borne encephalitis virus (TBEV) infects and replicates within macrophages, aiding its spread and influencing disease pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages are crucial innate immune cells involved in host defense against viral pathogens.
- Tick-borne encephalitis virus (TBEV), a Flavivirus, causes significant human infections, particularly affecting the nervous system.
Purpose of the Study:
- To investigate the role of macrophages in the pathogenesis of tick-borne encephalitis virus (TBEV) infection.
- To elucidate the cellular mechanisms of TBEV entry, replication, and exit from macrophages.
Main Methods:
- Ultrastructural electron microscopy was employed to study macrophages infected with TBEV.
- Virological methods were used to confirm TBEV absorption and replication within macrophages.
Main Results:
- TBEV is absorbed and replicates within macrophages.
- Virus entry into macrophages occurs via local plasmalemma destruction, with new virus particles exiting similarly.
- Accumulation of ribosomes, microfilaments, and viral structures (nucleocapsids, tubular formations, viral layers) observed in the perinuclear cytoplasm.
Conclusions:
- Macrophages serve as target cells for TBEV, playing a role in viral spread.
- As antigen-presenting cells, macrophages can modulate the host's protective response and influence tick-borne encephalitis pathogenesis.
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