The entry of Epstein-Barr virus into B lymphocytes and epithelial cells during infection.
- Author:
Lie-Lian ZUO
;
Mei-Juan ZHU
;
Shu-Juan DU
;
Jian-Hong LU
;
Gui-Yuan LI
- Publication Type:Journal Article
- MeSH:
Animals;
B-Lymphocytes;
virology;
Epithelial Cells;
virology;
Epstein-Barr Virus Infections;
virology;
Herpesvirus 4, Human;
genetics;
physiology;
Humans;
Viral Proteins;
genetics;
metabolism;
Virus Internalization
- From:
Chinese Journal of Virology
2014;30(4):476-482
- CountryChina
- Language:Chinese
-
Abstract:
Epstein-Barr virus (EBV) is a human herpesvirus associated with important human diseases, including infectious mononucleosis syndrome, malignant lymphoma, and nasopharyngeal carcinoma. The mechanism of EBV entry into host cells remains a subject of intensive research. After decades of study, researchers have identified several key proteins and different patterns of EBV intrusion into host cells. The viral surface glycoproteins, gp350/220, gp42, gB, gH, and gL, are involved in interactions with the CR2 receptor on the surface of B lymphocytes during viral entry. However, the majority of epithelial cells lack CR2 receptor expression, which makes viral invasion much more complex than in B lymphocytes. Three different models have been proposed to explain how EBV enters epithelial cells: (1) "transfer of infection", mediated by B lymphocytes or Langerhans cells; (2) EBV utilizes its own proteins during the process of fusion with the cell membrane; and (3) progeny virions arising from EBV-infected epithelial cells cross lateral membranes into adjacent epithelial cells. This review will discuss the relevant mechanism of viral entry into B lymphocytes and epithelial cells during EBV infection.
