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16 Cards in this Set
- Front
- Back
- 3rd side (hint)
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ICAM-1
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Adhesion to other cells
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rhinovirus
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the most effective defense against viral reinfection because it is the longest lasting
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serum IgG
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the three earliest immune responses to viral infection leading to recovery:
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1. cytotoxic T cell mediated cytolysis
2. NK cell activation 3. direct activation of complement. |
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viruses that cross the placenta to reach the fetal circulation
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smallpox, rubella, cytomegalovirus
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antigenic drift due to
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point mutations
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mechanism for antigenic drift
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genetic reassortment between human and avian influenza viruses. nfluenza B and C viruses do not exhibit antigenic shift because few related viruses exist in animals.
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Tat-responsive element (TAR)
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binding site for Tat (Trans-activator of transcription protein)
recruits host RNA polymerase machinery to the LTR for viral transcription. |
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HIV-1 long terminal repeat (LTR)
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promoters for viral RNA transcription that is mediated by host RNA polymerase.
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Rev-responsive element (RRE)
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binding sites for the Rev protein.
Rev transports nuclear RNA to the cytoplasm for translation. |
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Inhibitory/Instability sequences (INS)
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Work to inhibit viral protein expression and decrease the efficiency of viral replication.
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coreceptors for CD4
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CXCR4 and CCR5
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Vif (viral infectivity factor):
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promotes infectivity of HIV
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Vpr (viral protein R):
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nuclear import of the viral pre-integration complex, growth arrest of target cells in G2, apoptosis of infected cells
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Vpu (viral protein U):
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degradation of CD4 in the ER and enhancement of virion release from plasma membrane of infected cells (only in HIV-1 and SIVcpz)
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Nef (negative factor):
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one of the first HIV proteins to be produced in the viral life cycle, down- regulates CD4 to have a “negative impact” on HIV replication levels
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Steps of viral DNA transcription into RNA
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RNA polymerase II binds to LTR --> formation of TAR sequence on RNA
Tat + cyclinT1 --> + CDk9 --> phosphorylates RNA polymerase II --> elongation of viral RNA transcript |
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