Heterotypic immunity against vaccinia virus in an HLA-B*07:02 transgenic mousepox infection model
Clicks: 312
ID: 116600
2020
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
69.6
/100
312 views
202 readers
Trending
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #428 of 1,628 articles by views in Scientific reports
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 1,628 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Vaccination with vaccinia virus (VACV) elicits heterotypic immunity to smallpox, monkeypox, and mousepox, the mechanistic basis for which is poorly understood. It is generally assumed that heterotypic immunity arises from the presentation of a wide array of VACV-derived, CD8+ T cell epitopes that share homology with other poxviruses. Herein this assumption was tested using a large panel of VACV-derived peptides presented by HLA-B*07:02 (B7.2) molecules in a mousepox/ectromelia virus (ECTV)-infection, B7.2 transgenic mouse model. Most dominant epitopes recognized by ECTV- and VACV-reactive CD8+ T cells overlapped significantly without altering immunodominance hierarchy. Further, several epitopes recognized by ECTV-reactive CD8+ T cells were not recognized by VACV-reactive CD8+ T cells, and vice versa. In one instance, the lack of recognition owed to a N72K variation in the ECTV C4R70–78 variant of the dominant VACV B8R70–78 epitope. C4R70–78 does not bind to B7.2 and, hence, it was neither immunogenic nor antigenic. These findings provide a mechanistic basis for VACV vaccination-induced heterotypic immunity which can protect against Variola and Monkeypox disease. The understanding of how cross-reactive responses develop is essential for the rational design of a subunit-based vaccine that would be safe, and effectively protect against heterologous infection.
| Reference Key |
joyce2020scientificheterotypic
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Amrendra Kumar,Naveen Chandra Suryadevara,Kyle J. Wolf,John Tanner Wilson,Richard J. DiPaolo,James Brien,Sebastian Joyce;Amrendra Kumar;Naveen Chandra Suryadevara;Kyle J. Wolf;John Tanner Wilson;Richard J. DiPaolo;James Brien;Sebastian Joyce; |
| Journal | Scientific reports |
| Year | 2020 |
| DOI |
10.1038/s41598-020-69897-w
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.