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21 Cards in this Set
- Front
- Back
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What are the two stages of EBV infection?
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Lytic phase in which the virus replicates and makes viral capsid and antigens. The second stage is the latent phase of EBV infection
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How does the immune system react to initial EBV infection?
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Lytically infected B-cells are largely eliminated by EBV specific cytotoxic T-cells, NK cells, and INF mediated processes, ADCC.
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What occurs in the latency period that allows immune evasion for EBV?
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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.
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Why do we not recognize the EBNA1 molecule?
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It has a Gly-Ala-Gly-Ala repeat that is not able to be degraded by the proteosome machinery. Thus it is not presented.
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What are the typical markers of immunoblastic lymphoma?
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low affinity Fc receptors and adhesion molecules. LFA-1, CDA 11, LFA-3, ICAM, etc. This causes big clumps of cells to form.
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Burkitt's lymphoma
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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
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Frequency Dependent Selection
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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
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What are the important regions of the EBV virus?
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Long terminal repeats, GAG region(packaging of viral nucleic acids), POL (reverse transcriptase and processing enzymes), and evelope region.
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What are the steps in pathogenesis of HIV
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CD4 positive cell invasion (monocytes, macrophages, Th cells, and memory T-cells). Pre-integration complex formation. Insertion of DNA into human genome
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Immune response to HIV
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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
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What determines the tropism of HIV?
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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
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What are the ligands for CCR5? What is the role of CCR5
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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
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How is CCR5 distributed amond CD4+ cells?
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Found on monocytes, dendritic cells, and both effector and memory T-cells, but not naive T-cells.
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What does the delta-32 polymorphism do?
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renders CCR5 unexpressed and therefore incapable of binding HIV R5 strains.
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CXER4 receptor
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binds stromal derived GF CXER4 which directs cells to the lymphnode. Seen in naive CD4 cells.
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Which is the sexually transmittable form of the disease?
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R5 which mainly replicates in macrophages and moncytes and can infect memory T-cells but at a lower rate.
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What causes the switch to X4 tropic strain?
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Selective pressure of chemokines progressively causes mutation to X4 tropic strain
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DILS
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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.
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Sjorgen's syndrome
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An autoimmune disease with dry eyes, dye mouth from CD4 T-cell inflammation.
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Long term non progressors
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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.
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In addition to viral pathogenesis why are CD4 T-cells lost ?
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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
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