inteferons and how viruses evade them Flashcards

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1
Q

CpG and ZAP

A

viruses that have a high level of CPG are detected in the body by a ZAP protein in our body, which cuts the CPG- CPG needed for replication, so they can’t replicate

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2
Q

type 1 interferons- what they are and functions

A

polypeptides released from infected cells- cause an antiviral state in infected and neighbouring cells (ie they produce interferon stimulated genes), and enhanced innate and adaptive response

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3
Q

types of type 1 interferons- cells that produces them, what triggers them, and how many types

A

IFN beta produced by all cells, triggered by IRF-3, IFN alpha produced by dendritic cells, triggered by IR-F7: only 1 type of IFN beta, 13 types of IFNalpha

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4
Q

type 2 interferons

A

INF gamma- produced by T cells and NK cells, which affect adaptive immune response

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5
Q

type 3 interferons

A

interferon lamda (upside down Y)- important at epithelial cells

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6
Q

how innate immune system senses pathogens and types of PRR’S

A

PAMPS (pathogen associated molecular patterns), detected PRR’S (pattern recognition receptors), such as RLRS (RIG like receptors), TLRS (toll like receptors), which sense foreign RNA in cytoplasm, as well as cGAS (senses foreign DNA)

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7
Q

how RLRS work

A

sense foreign RNA, and activates MAVS, which phosphorylates IRF3, which goes from cytoplasm into nucleus to switch on INF beta gene ie IRF3 acts as a T.F

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8
Q

how TLRS work

A

they work in ENDOSOMES (viruses can enter via endosomes)- when they sense viral RNA, TLR3 activates IRF3, TLR7 activates IRF7, which produces both INF beta and alpha gene

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9
Q

DNA sensor- CGAS

A

senses foreign DNA, which activates IRF3 via STING pathway= switches on INFalpha/beta

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10
Q

effect of type 1 IFN

A

bind to IFNAR (IFN alpha) receptors on both its OWN cell (autocrine signalling) and neighbouring cells (paracrine), switching on MANY IFN stimulated genes

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11
Q

what occurs in herpes simplex encephalitis

A

lack of INF alpha/beta within CNS in response to HSV

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12
Q

inteferon stimulated genes-

A

protein kinase R- inhibits translation (thus virus can’t replicate), serpine (activates proteases), IFITM3 (inhibits viruses entering via ENDOSOMES)

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13
Q

issue with IFN stimulated genes and solution

A

these genes are toxic to the cell, but MORE toxic to virus- SOCS gene turns off these genes

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14
Q

how viruses evade IFN response with examples of INF induction blockage

A

hide their PAMP, activate SOCS, affect protein synthesis (ie can’t produce INF stimulated gene proteins), stop INF production eg Hep C cleaves MAVS using NS3 protease, influenza binds to RLR using NS1 protease

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15
Q

POX viruses

A

large DNA viruses which have accessory genes that modify immune response- they do this by producing cytokine receptors, which bind to cytokines like IFN, preventing them from working

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16
Q

cytokine storm- mediators particularly produced

A

effect of IFNs not preventing viral replication- body continues producing more IFNS,IL-6, and TNF alpha particularly

17
Q

IFN as treatment- IFN alpha/beta vs IFN lambda

A

IFN alpha/beta cause bad side effects due to cell toxicity, and may cause immune cells be overactive= AUTOIMMUNITY, where IFN lambda is not on all cells (only epithelial), so less toxic, thus may be beneficial

18
Q

viruses and vaccines

A

viruses that can’t control inteferon ie don’t have proteases can be used as LIVE ATTENUATED vaccine

19
Q

oncolytic viruses

A

cancer cells don’t produce INF, thus these viruses can damage cancer cells without immune system clearing them, without damaging healthy cells