Dengue fever || Dengue virus and pathophysiology

Animated biology With arpan
4 Apr 201616:12

Summary

TLDRThis video explains the replication and pathophysiology of the dengue virus, primarily transmitted by *Aedes aegypti* mosquitoes in tropical regions. It details how the virus infects dendritic cells and macrophages, utilizing specific receptors to enter these immune cells. The video describes the virus's single-stranded RNA structure and its replication process within host cells, leading to the production of new viral particles. Symptoms of dengue fever, including severe joint pain, are highlighted, emphasizing the disease's impact in warm climates where the mosquito vector is prevalent.

Takeaways

  • 😀 Dengue virus is primarily transmitted through the bite of the Aedes aegypti mosquito, prevalent in tropical regions.
  • 😀 Infection occurs when the mosquito injects dengue virus particles into the skin, targeting immune cells like dendritic cells and macrophages.
  • 😀 The dengue virus uses specific receptors, including DC-SIGN and mannose receptors, to enter immune cells via clathrin-mediated endocytosis.
  • 😀 Once inside the cell, the virus's acidic environment triggers conformational changes, releasing its RNA genome into the cytoplasm.
  • 😀 The viral RNA is positive-sense, allowing it to be directly translated into viral proteins by the host's ribosomes.
  • 😀 Infected immune cells migrate to the lymphatic system, secreting interferons that activate other immune responses.
  • 😀 The inflammatory response caused by the immune system contributes to the severe symptoms of dengue fever, including intense joint pain.
  • 😀 Dengue virus is part of the Flaviviridae family and has a single-stranded RNA genome with specific structural proteins.
  • 😀 The virus can utilize multiple receptors to infect a variety of host cells, making it highly adaptable.
  • 😀 The lifecycle of the dengue virus involves replication in host cells and subsequent release to infect additional cells or be transmitted by mosquitoes.

Q & A

  • What is the primary vector responsible for dengue virus transmission?

    -The primary vector for dengue virus transmission is the *Aedes aegypti* mosquito.

  • How does the dengue virus enter the human body?

    -The dengue virus enters the human body when an infected mosquito bites and injects the virus through its saliva.

  • Which immune cells are primarily infected by the dengue virus?

    -The dengue virus primarily infects dendritic cells and macrophages in the dermis.

  • What receptors do dendritic cells and macrophages use to facilitate dengue virus entry?

    -Dendritic cells use the DC-SIGN receptor, while macrophages use mannose-type receptors to facilitate dengue virus entry.

  • What process does the dengue virus utilize to enter immune cells?

    -The dengue virus utilizes clathrin-mediated endocytosis to enter immune cells.

  • What triggers the release of the viral RNA from the dengue virus inside the host cell?

    -An acidic environment within the endocytic vesicle triggers conformational changes in the virus's surface proteins, releasing the RNA into the cytoplasm.

  • What happens to the viral RNA once it enters the host cell?

    -Once inside the host cell, the viral RNA is replicated and translated into proteins, which assemble into new viral particles.

  • How are new dengue virus particles packaged and released from the host cell?

    -New dengue virus particles are packaged in the Golgi apparatus and then released from the host cell to infect other cells.

  • What are some common symptoms associated with dengue fever?

    -Common symptoms of dengue fever include severe joint pain, high fever, and rash, which is why it is sometimes called 'breakbone fever.'

  • What is the genomic structure of the dengue virus?

    -The dengue virus has a linear single-stranded RNA genome that is positive-sense, allowing it to be directly used by the host cell for protein production.

Outlines

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Mindmap

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Keywords

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Highlights

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Transcripts

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Étiquettes Connexes
Dengue VirusReplicationPathophysiologyTropical DiseaseImmune ResponseViral InfectionHealth EducationBiologyPublic HealthVector-Borne
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