EBV review Flashcards
EBV virion features
Gammaherpesvirus, large double stranded DNA genome, enveloped, labile in the environment
All herpes viruses, including EBV 2 life cycles (lytic replication/ latency)
Herpesvirus lytic replication
- binding and fusion
- transport of DNA to the nucleus
- Viral vhs degrades host mRNA
- Viral transcription factor VP16 localizes to the nucelus to initiate viral gene transcription
- Viral DNA circulizes
- HSV alpha genes transcribed by host RNAP2
7/8. Some alpha gene products transactivate transcription of beta genes, beta gene products are required for viral DNA syntesis - Viral DNA synthesis triggers expression of gamma viral gene
- Many gamma products are structural components of the virion
- Viral DNA is packaged into capsid
- Filled viral capsid bud thru host membranes to form a mature virion that exits from the cell
Latent EBV
Early alpha and some beta are produced
Only EBNA1 might be expressed
When plasma cells differentiate into plasma cells will cause EBV reactivation
alterations of the immune system (triggers) cause it to reactivte
EBV infection in B cells
EBV encoded RNAS transcribed in all infected cells but never translated into a protein
Infectious EBC is secreted in saliva all the time even in healthy idif=viduals
EBV acquired in the 1st decade of life leads to mild cold like symproms
EBV acquired in adolescence will become an acute infection and is termed infectious mononucleosis-95% of college kids are infected
Infections mono is characterized by a massive expansion of T cells, these T cells are CD8+, Downey cells, higly activated effector cells with many if not most of them being specific for EBV infected B cells
A significant increase in activated B cells leading to increase in production of AB against self Ag
Clinical course of Infectious mononucleosis
Fever lymphadenopathy, malaise and fatigue, vrus in saliva, atypical lymphocytes, heterophile, Anti Ea, Anti VCA IgM, IgG, Anti EBNA
Mechanisms of Viral oncogenesis
Direct transformation (80% or greater of cancer cells have to be virus positive) Hit and run (Virus changes cellular environment, promotes mutagenesis) Bystander effect (virus infected cells secrete a storm of growth factor