PuSH - Publikationsserver des Helmholtz Zentrums München

Möhl, B.S. ; Chen, J.* ; Longnecker, R.*

Gammaherpesvirus entry and fusion: A tale how two human pathogenic viruses enter their host cells.

In:. New York, NY [u.a.]: Elsevier, 2019. 313-343 (Adv. Virus Res. ; 104)
Postprint DOI
Open Access Green
The prototypical human.-herpesviruses Epstein-Barr virus (EBV) and Kaposi Sarcoma-associated herpesvirus (KSHV) are involved in the development of malignancies. Like all herpesviruses, they share the establishment of latency, the typical architecture, and the conserved fusion machinery to initiate infection. The fusion machinery reflects virus-specific adaptations due to the requirements of the respective herpesvirus. For example, EBV evolved a tropism switch involving either the B-or epithelial cell-tropism complexes to activate fusion driven by gB. Most of the EBV entry proteins and their cellular receptors have been crystallized providing molecular details of the initial steps of infection. For KSHV, a variety of entry and binding receptors has also been reported but the mechanism how receptor binding activates gB-driven fusion is not as well understood as that for EBV. However, the downstream signaling pathways that promote the early steps of KSHV entry are well described. This review summarizes the current knowledge of the key players involved in EBV and KSHV entry and the cell-type specific mechanisms that allow infection of a wide variety of cell types.
Altmetric
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Sammelbandbeitrag/Buchkapitel
Korrespondenzautor
Schlagwörter Epstein-barr Virus (ebv) ; Gammaherpesvirus Entry And Fusion ; Glycoprotein Gb And Gh/gl ; Kaposi Sarcoma-associated Herpesvirus (kshv) ; Viral Fusion ; Virus Entry; Epstein-barr-virus; Sarcoma-associated Herpesvirus; Kaposis-sarcoma; Glycoprotein-b; Crystal-structure; Target-cells; Pseudorabies Virus; Cellular Receptor; Surface-receptors; Epithelial-cells
ISSN (print) / ISBN 0065-3527
e-ISSN 1557-8399
Quellenangaben Band: 104, Heft: , Seiten: 313-343 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort New York, NY [u.a.]
Nichtpatentliteratur Publikationen