08 EBV Refresher Flashcards
EBNA1
Usually the only EBV protein expressed in latent life cycle
- poorly immunogenic
- maintains episome matinence
EBV classification
Enveloped Gammaherpesvirus
Single Stranded DS +- DNA Genome
EBV proteins causing cell cycle
EBNA 2,3
LMP1,2
BARF1
EBV pathogenesis
Infectious EBV always in saliva
>95% in DEVELOPING infected by 3 years old- mild cold symptoms
in DEVELOPED countries 70% 12 y.o. positive
*EBV during adolescence causes MONONUCLEOSIS >95% infected before finishing college
MONONUCLEOSIS
- Massive CD8(+) T cell reaction “Downy cells”
* B cell expansion with heterophile antibodies
Clinical course of mono
*up to 2 month incubation (usually 2 weeks)
* 3 week syndrome:
Fever, Lymphadenopathy, splenomegaly, pharyngitis, malaise and fatigue, virus in saliva, ATYPICAL LYMPHOCYTES AND HETEROPHILE ANTIBODIES
*Anti EA at around 7 days
* Anti VCA IGM 7 days- 1 month, After that Anti VCA IgG
*Anti EBNA1 after a few months
EBV oncogenesis mechanisms
Direct transformation, Hit-and-run, Bystander effect, Chronic inflammation
EBV direct transformation
Possibly:
^EBV monos =^Bcells
Latency II, and IIIproteins oncogenic in mouse
Not probable:
Oncogenes weren’t necessary for transformation
Only select individuals acquire lymphomas
EBV Hit and run
EBV causes replication and genomic instability which probably leads to endemic Burkitts t(8;22) translocation
Chronic inflammation
Hodgkins lymphoma is associated with EBV and lots of non-transformed inflammatory cells
Bystander effect
Do the EBV replicating cells release cytokines and GFs leading to transformation of nearby cells?