Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Mar 23;12:640918. doi: 10.3389/fimmu.2021.640918

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2021 Schuhmachers and Münz

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Changes in Epstein Barr virus (EBV) infection, pathogenesis and immune control as revealed by infection of humanized mice with mutant viruses. Elimination of EBNA3C (ΔEBNA3C) allows establishment of persistent EBV infection without transformation. Loss of EBNA3B (ΔEBNA3B) increases and loss of BZLF1 (ΔBZLF1) decreases EBV associated lymphomagenesis. Loss of viral miRNAs (ΔmiRNA) leads to increased expression of the antigen processing machinery for MHC class I presentation, allowing for improved immune control by CD8⁺ T cells. Deficiency in LMP1 (ΔLMP1) causes dependency on CD4⁺ T cell help for EBV induced B cell transformation.