期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 4, 页码 2056-2060出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.4.2056
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- NIAID NIH HHS [R01 AI 14910] Funding Source: Medline
- NIDDK NIH HHS [P30 DK 34928] Funding Source: Medline
EBV, a ubiquitous human herpesvirus, is the causative agent of infectious mononucleosis and is associated with many carcinomas. We have previously shown that the EBV latent genes LMP-1 and LMP-2A (for latent membrane proteins 1 and 2A), transactivate a human endogenous retrovirus (HERV), HERV-K18, in infected B lymphocytes. The envelope (Env) protein of HERV-K18 encodes a superantigen that strongly stimulates a large number of T cells. In this study we report that HERV-K18 env is transactivated even earlier in the infection process, before the establishment of latency; namely, we found at EBV, through its interaction with its cellular receptor CD21, induces the HERV-K18 env gene in resting B lymphocytes. This transactivation is direct and immediate, as up-regulation of transcripts can be detected within 30 min after EBV exposure. Thus, EBV binding to human CD21 on resting B cells triggers the expression of an endogenous superantigen. The biological significance of this superantigen expression for the EBV life cycle is discussed.
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