Epstein-Barr virus induces actin polymerization in human B cells.
The EBV selectively infects human and primate lymphocytes. This selective tropism occurs as a result of live virus infection through permissive membrane receptors. Once EBV has entered the cell, it induces proliferation and immortalization of these cells. The mechanism of EBV infection, however, remains largely unknown. We demonstrate here that a transforming strain, but not a nontransforming strain, of EBV stimulates the conversion of globular actin (G-actin) to filamentous actin (F-actin), a process that has been associated with activation and transformation of other cell types. Preincubation of B cells with botulinum C2 toxin or cytochalasin, which block the conversion of G-actin to F-actin, resulted in the inhibition of EBV-induced proliferation. These findings indicate that actin rearrangement is essential for infection of B cells by EBV.
Melamed
I
I
Division of Immunology/Allergy, Hospital for Sick Children, Toronto, Ontario, Canada.
Stein
L
L
Roifman
C M
CM
D008841:Actin Cytoskeleton / Q000648:ultrastructure*; D000199:Actins / Q000378:metabolism*; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology / Q000648:ultrastructure*; D001905:Botulinum Toxins / Q000494:pharmacology; D015638:Cytochalasin D / Q000494:pharmacology; D006566:Herpesviridae Infections / Q000473:pathology*; D004854:Herpesvirus 4, Human / Q000472:pathogenicity*; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects; D014412:Tumor Virus Infections / Q000473:pathology*
D000199:Actins; D015638:Cytochalasin D; D001905:Botulinum Toxins