Alternate replication in B cells and epithelial cells switches tropism of Epstein-Barr virus.

Abstract:

:Epstein-Barr virus is ubiquitous and is causally implicated in lymphoid and epithelial malignancies. Virus invades oropharyngeal mucosa and establishes latency in B lymphocytes. Reactivating lymphocytes shed virus into saliva for spread to new hosts. A complex of three virus glycoproteins, gH, gL and gp42, is essential for entry. B-cell entry requires binding of gp42 to human leukocyte antigen (HLA) class II whereas entry into epithelial cells lacking HLA class II requires complexes without gp42. To accommodate infection of each, the virus carries both three-part and two-part complexes. We show here that HLA class II in the virus-producing cell alters the ratio of three-part to two-part complexes. As a consequence, virus originating in epithelial cells efficiently infects B cells whereas B-cell derived virus better infects epithelial cells. This molecular switch is a novel strategy that could alter tropism of virus from epithelium to B cells and then back to epithelium in a new host.

journal_name

Nat Med

journal_title

Nature medicine

authors

Borza CM,Hutt-Fletcher LM

doi

10.1038/nm0602-594

keywords:

subject

Has Abstract

pub_date

2002-06-01 00:00:00

pages

594-9

issue

6

eissn

1078-8956

issn

1546-170X

pii

nm0602-594

journal_volume

8

pub_type

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