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21 Cards in this Set

  • Front
  • Back
What are the two stages of EBV infection?
Lytic phase in which the virus replicates and makes viral capsid and antigens. The second stage is the latent phase of EBV infection
How does the immune system react to initial EBV infection?
Lytically infected B-cells are largely eliminated by EBV specific cytotoxic T-cells, NK cells, and INF mediated processes, ADCC.
What occurs in the latency period that allows immune evasion for EBV?
During the latency period, latent membrane proteins signaled via CD40 are expressed. CTL are directed to most of these except for EBNA 1 which is blocked from protesome degradation. EBNA 1 binds origin of replication and initiates replication and is a transcriptional enhancer.
Why do we not recognize the EBNA1 molecule?
It has a Gly-Ala-Gly-Ala repeat that is not able to be degraded by the proteosome machinery. Thus it is not presented.
What are the typical markers of immunoblastic lymphoma?
low affinity Fc receptors and adhesion molecules. LFA-1, CDA 11, LFA-3, ICAM, etc. This causes big clumps of cells to form.
Burkitt's lymphoma
Has a latency phase as well. With EBNA 1 transcription. CALA is expresssed but no adhesion molecules so get dispersed cells in culture. Occurs often in immunostimulated individuals
Frequency Dependent Selection
occurs when a virus adapts to the most common HLA type and becomes more pathogenic. Example HLA11 (EBNA 3 presenting) and EBV. Pt. mutation at anchor proteins will lead to lack of presentation of the virus
What are the important regions of the EBV virus?
Long terminal repeats, GAG region(packaging of viral nucleic acids), POL (reverse transcriptase and processing enzymes), and evelope region.
What are the steps in pathogenesis of HIV
CD4 positive cell invasion (monocytes, macrophages, Th cells, and memory T-cells). Pre-integration complex formation. Insertion of DNA into human genome
Immune response to HIV
biphasic. Initial response is mediated by CD8T cell destruction of CD4+ T-cells and macrophages. However virus infected monocytes and memory CD4+ T-cells remain. This phase is follwed by clinical asymptomatic phase which precedes viral escape via mutation which allows naive T-cells to be infected. --> AIDS
What determines the tropism of HIV?
The virus envelope has a counter receptor which binds a cellular receptor. The distribution of the cellular receptor determines the tropism of the virus. CCR5 and CXR4 chemokine receptors that determine tropism
What are the ligands for CCR5? What is the role of CCR5
RANTES, MIP-alpha, MIP-beta. These are produced in large quantities by activated T-cells. CCR5 is responsible for telling the cell to go inot a site of peripheral inflammation
How is CCR5 distributed amond CD4+ cells?
Found on monocytes, dendritic cells, and both effector and memory T-cells, but not naive T-cells.
What does the delta-32 polymorphism do?
renders CCR5 unexpressed and therefore incapable of binding HIV R5 strains.
CXER4 receptor
binds stromal derived GF CXER4 which directs cells to the lymphnode. Seen in naive CD4 cells.
Which is the sexually transmittable form of the disease?
R5 which mainly replicates in macrophages and moncytes and can infect memory T-cells but at a lower rate.
What causes the switch to X4 tropic strain?
Selective pressure of chemokines progressively causes mutation to X4 tropic strain
Diffuse infiltrative lymphocytic syndrome. occurs when there is a exuberant CD8 T-cell response with cytokine release. Patients show enlarged parotid glands, submandibular glands, and lacrimal glands.
Sjorgen's syndrome
An autoimmune disease with dry eyes, dye mouth from CD4 T-cell inflammation.
Long term non progressors
HLAB-27+ individuals that have strong CD8 T-cell response. Release high levels of cytokines which compete for the CCR5 receptor. Their HLA type also recognizes the most number of immunodominat peptides.
In addition to viral pathogenesis why are CD4 T-cells lost ?
physiological apoptosis occurs and viral proliferation is linked to cell activation. When a T-cell becomes active the viral LTR resconds and activates replication. The responding T-cell expresses HIV and is killed by CD8