EBV Infection

Frage	Antworten
Age of host	Determines the effect of primary infection
EBV Carriers at Risk of Cancer	Immunocompromised & genetically unlucky
Virus Integration	Doesn't happen- remains an extrachromosomal episome
Genome Size & Type	Large DNA virus
Genome Stability	High- rarely mutates
Latency	Enters this phase in some hosts- the form that causes cancers
Avoiding Immune Surveillance- Avoid Cytotoxic T-Cell	Blocking antigen processing/presenting by phagocytes
Avoiding Immune Surveillance- Latency	Suppression of viral gene expression that makes immune detection impossible
Avoiding Immune Surveillance- Response Modification	EBV can modify the immune response to its detection, causing the release of inflammatory cytokines
Source of Infection	Usually through saliva
Site of Infection	Most commonly B cells
CD21	Together with CD19, it forms the B cell receptor- EBV binds to it to enter the cell
GP350	Used by EBV to bind to CD21, which allows it to enter the cell by endocytosis
Viral Replication Cycle	Lytic
Characteristic Of Lytic Replication	IgG's against viral capsid proteins
Exit From Cell	Endocytosis, so cell isn't killed
Viral DNA Polymerase	Responsible for copying the genome in the lytic cycle
Products of Latency Stage	Doesn't result in EB virons, allowing it to avoid the immune system
Length of Infection Before Latency is Activated	3 to 6 weeks
Host DNA Polymerase	Responsible for copying the genome in the latent phase

Zusammenfassung der Ressource

	Erstellt von gina_evans0312 vor etwa 10 Jahre