Primary EBV infection induces an expression profile distinct from other viruses but similar to hemophagocytic syndromes.
Epstein-Barr Virus (EBV) causes infectious mononucleosis and establishes lifelong infection associated with cancer and autoimmune disease. To better understand immunity to EBV, we performed a prospective study of natural infection in healthy humans. Transcriptome analysis defined a striking and reproducible expression profile during acute infection but no lasting gene changes were apparent during latent infection. Comparing the EBV response profile to multiple other acute viral infections, including influenza A (influenza), respiratory syncytial virus (RSV), human rhinovirus (HRV), attenuated yellow fever virus (YFV), and Dengue fever virus (DENV), revealed similarity only to DENV. The signature shared by EBV and DENV was also present in patients with hemophagocytic syndromes, suggesting these two viruses cause uncontrolled inflammatory responses. Interestingly, while EBV induced a strong type I interferon response, a subset of interferon induced genes, including MX1, HERC5, and OAS1, were not upregulated, suggesting a mechanism by which viral antagonism of immunity results in a profound inflammatory response. These data provide an important first description of the response to a natural herpesvirus infection in humans.
Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Samantha K
SK
Dunmire
Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Oludare A
OA
Odumade
Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Jean L
JL
Porter
Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Juan
J
Reyes-Genere
Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America ; Department of Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
David O
DO
Schmeling
Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Hatice
H
Bilgic
Biostatistics and Bioinformatics Core, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Danhua
D
Fan
Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Emily C
EC
Baechler
Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America ; Department of Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Henry H
HH
Balfour
Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America ; Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Kristin A
KA
Hogquist
D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D003715:Dengue / Q000473:pathology / Q000821:virology; D020031:Epstein-Barr Virus Infections / Q000097:blood / Q000235:genetics*; D020869:Gene Expression Profiling; D004854:Herpesvirus 4, Human / Q000502:physiology*; D006801:Humans; D007244:Infectious Mononucleosis / Q000235:genetics / Q000821:virology; D007249:Inflammation / Q000473:pathology; D007372:Interferons / Q000378:metabolism; D007700:Kinetics; D008180:Lupus Erythematosus, Systemic / Q000235:genetics; D051359:Lymphohistiocytosis, Hemophagocytic / Q000097:blood / Q000235:genetics* / Q000821:virology*; D009000:Monocytes / Q000276:immunology; D015854:Up-Regulation / Q000235:genetics; D017735:Virus Latency; D055815:Young Adult
D007372:Interferons