Journal
JOURNAL OF VIROLOGY
Volume 74, Issue 2, Pages 914-922Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.2.914-922.2000
Keywords
-
Categories
Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [F32AI009778] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS026681] Funding Source: NIH RePORTER
- NIAID NIH HHS [F32 AI009778, F32-AI09778] Funding Source: Medline
- NINDS NIH HHS [NS26681] Funding Source: Medline
- PHS HHS [A122186] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available