E — Epstein–Barr Virus (EBV)
Epstein–Barr virus is a gammaherpesvirus with a double-stranded DNA genome that establishes lifelong latency in B lymphocytes. Transmission occurs via saliva, and primary infection often targets oropharyngeal epithelial cells before infecting B cells via CD21 (CR2).
EBV exhibits distinct latency programs (Latency I, II, III), characterized by expression of specific viral proteins such as EBNA1, EBNA2, LMP1, and LMP2. LMP1 mimics CD40 signaling, activating NF-κB and promoting B-cell survival and proliferation. This ability to drive cellular growth underlies its oncogenic potential.
Infectious mononucleosis results from robust CD8+ T-cell responses against infected B cells. Symptoms (fever, lymphadenopathy, splenomegaly) reflect immune activation rather than direct cytotoxicity. After acute infection, EBV persists in memory B cells in a latent state.
EBV is associated with multiple malignancies, including Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, and certain gastric cancers. Oncogenesis involves viral latency proteins, genomic instability, and host/environmental cofactors.
Research on EBV has illuminated mechanisms of viral latency, oncogenic transformation, immune evasion, and epigenetic regulation. It serves as a model for understanding virus-driven cancers and host–virus coevolution.
Epstein–Barr virus is a gammaherpesvirus with a double-stranded DNA genome that establishes lifelong latency in B lymphocytes. Transmission occurs via saliva, and primary infection often targets oropharyngeal epithelial cells before infecting B cells via CD21 (CR2).
EBV exhibits distinct latency programs (Latency I, II, III), characterized by expression of specific viral proteins such as EBNA1, EBNA2, LMP1, and LMP2. LMP1 mimics CD40 signaling, activating NF-κB and promoting B-cell survival and proliferation. This ability to drive cellular growth underlies its oncogenic potential.
Infectious mononucleosis results from robust CD8+ T-cell responses against infected B cells. Symptoms (fever, lymphadenopathy, splenomegaly) reflect immune activation rather than direct cytotoxicity. After acute infection, EBV persists in memory B cells in a latent state.
EBV is associated with multiple malignancies, including Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, and certain gastric cancers. Oncogenesis involves viral latency proteins, genomic instability, and host/environmental cofactors.
Research on EBV has illuminated mechanisms of viral latency, oncogenic transformation, immune evasion, and epigenetic regulation. It serves as a model for understanding virus-driven cancers and host–virus coevolution.