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Home/Equine Research Bank/J Virol/Role of dendritic cell targeting in Venezuelan equine enceph...
Journal of virology2000; 74(2); 914-922; doi: 10.1128/jvi.74.2.914-922.2000

Role of dendritic cell targeting in Venezuelan equine encephalitis virus pathogenesis.

Abstract: The initial steps of Venezuelan equine encephalitis virus (VEE) spread from inoculation in the skin to the draining lymph node have been characterized. By using green fluorescent protein and immunocytochemistry, dendritic cells in the draining lymph node were determined to be the primary target of VEE infection in the first 48 h following inoculation. VEE viral replicon particles, which can undergo only one round of infection, identified Langerhans cells to be the initial set of cells infected by VEE directly following inoculation. These cells are resident dendritic cells in the skin, which migrate to the draining lymph node following activation. A point mutation in the E2 glycoprotein gene of VEE that renders the virus avirulent and compromises its ability to spread beyond the draining lymph blocked the appearance of virally infected dendritic cells in the lymph node in vivo. A second-site suppressor mutation that restores viral spread to lymphoid tissues and partially restore virulence likewise restored the ability of VEE to infect dendritic cells in vivo.
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Publication Date: 2000-01-07 PubMed ID: 10623754PubMed Central: PMC111612DOI: 10.1128/jvi.74.2.914-922.2000Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This study explores how Venezuelan equine encephalitis virus (VEE) specifically targets dendritic cells in the early stages of infection and how this impacts the spread and severity of the virus.

Understanding Venezuelan equine encephalitis virus (VEE) spread

VEE infects a type of immune cell known as dendritic cells, which are critical in alerting the rest of the immune system about the presence of invading pathogens. This study maps out the initial steps of how VEE spreads from the infection site, the skin, to the draining lymph node.

  • In the first 48 hours following infection, the virus primarily targets dendritic cells in the draining lymph node.
  • The researchers used green fluorescent protein and immunocytochemistry for this finding, which indicates that the dendritic cells are the first primary targets of the virus.

Role of Langerhans Cells

The study highlights the role of a specific type of dendritic cells, called Langerhans cells, in VEE infection.

  • Langerhans cells are the initial set of cells infected by VEE directly following inoculation.
  • These resident dendritic cells in the skin migrate to the draining lymph node upon activation.
  • VEE viral replicon particles, which can undergo only one round of infection, are used to identify the Langerhans cells as the initial cells being targeted.

Viral Mutations and Their Effects

The research also examined how a mutation in the E2 glycoprotein gene of VEE affects the spread and virulence of the virus.

  • A point mutation rendering the virus avirulent, compromising its ability to spread beyond the draining lymph node, blocked the appearance of virally infected dendritic cells in the lymph node, in vivo.
  • A second-site suppressor mutation, which restores viral spread to lymphoid tissues and partially restores virulence, likewise restored the ability of VEE to infect dendritic cells in vivo.

In conclusion, the findings bring insightful understanding on the role of dendritic cells in VEE infection and how the specific targeting of these cells can influence the initial spread and severity of the virus. Further exploration of viral mutations may contribute to the development of strategies to block VEE spread.

Cite This Article

APA
MacDonald GH, Johnston RE. (2000). Role of dendritic cell targeting in Venezuelan equine encephalitis virus pathogenesis. J Virol, 74(2), 914-922. https://doi.org/10.1128/jvi.74.2.914-922.2000

Publication

Journal of virology
ISSN: 0022-538X
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 74
Issue: 2
Pages: 914-922

Researcher Affiliations

MacDonald, G H
  • Department of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina 27599-7290, USA. gmacd@med.unc.edu
Johnston, R E

    MeSH Terms

    • Animals
    • Cell Line
    • Chemical Fractionation
    • Cricetinae
    • Dendritic Cells / virology
    • Encephalitis Virus, Venezuelan Equine / genetics
    • Encephalitis Virus, Venezuelan Equine / pathogenicity
    • Encephalomyelitis, Venezuelan Equine / pathology
    • Encephalomyelitis, Venezuelan Equine / virology
    • Green Fluorescent Proteins
    • Injections, Subcutaneous
    • Langerhans Cells / virology
    • Luminescent Proteins
    • Lymph Nodes / cytology
    • Mice
    • Viral Envelope Proteins / genetics
    • Viral Envelope Proteins / physiology

    Grant Funding

    • F32 AI009778 / NIAID NIH HHS
    • A122186 / PHS HHS
    • F32-AI09778 / NIAID NIH HHS
    • NS26681 / NINDS NIH HHS

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