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Epstein-Barr Virus Infects and Induces Apoptosis in Human Neutrophils
Bernard Larochelle,
Louis Flamand,
Pierrette Gourde,
Denis Beauchamp, and
Jean Gosselin
From the Laboratory of Viral Immunology, Laboratory of Virology,
Centre de recherche en Rhumatologie et Immunologie, Laboratory of
Infectiology, Centre de Recherche du CHUL, Université Laval,
Québec, Canada.
The role of neutrophils during Epstein-Barr virus (EBV) infection is
not known. Disruption of the initial and nonspecific immune response
may favor the spread of EBV infection. We have previously shown that
EBV interacts with human neutrophils and modulates protein expression.
In this study we have investigated the ability of EBV to infect
neutrophils. Electron microscopy studies showed penetration of virus
and its subsequent localization to the nucleus. The presence of viral
genomes in isolated nuclei from neutrophils was also shown by
polymerase chain reaction (PCR). Expression of viral transcripts like
EBNA-2 (Epstein-Barr nuclear antigen-2) and ZEBRA (BamHI Z EBV
replication activator) was not detected by reverse transcriptase
(RT)-PCR, suggesting that EBV does not seem to establish a latent or a
lytic infection in neutrophils. However, at 20 hours post-EBV
infection, 77% of cells were apoptotic as compared to 22% in
uninfected cell cultures, as evaluated by flow cytometry. This
EBV-induced apoptosis was prevented by the addition of
granulocyte-macrophage colony-stimulating factor to the cell cultures.
Apoptotic cell death seems to implicate the Fas/Fas ligand (L) pathway,
as reflected by an increase of Fas/Fas L expression on neutrophils
treated with EBV and an increase of soluble Fas L, which may function
in an autocrine/paracrine pathway to mediate cell death. Lastly, EBV
genome was detected from neutrophils of infectious mononucleosis (IM)
patients in contrast to neutrophils obtained from healthy
EBV-seropositive donors. Our findings on the interactions of EBV with
neutrophils will then provide new insights on the immunosuppressive
effects associated with EBV infection.
Blood, Vol. 92 No. 1 (July 1), 1998:
pp. 291-299
© 1998 by The American Society of Hematology.
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