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Virology > Host Response to Viral Infection > Flashcards

Host Response to Viral Infection Flashcards

1
Q

Physical barriers are part of which type of immunity?

A

innate

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2
Q

Which cells produce the mucociliary blanket and what does it do?

A

goblet cells; innate physical defense that traps larger particles so they can be swallowed or coughed out

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3
Q

What 2 things do cytoplasmic granules of NK cells contain?

A

perforin: produce pores in plasma membranes
granzymes: initiate apoptosis

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4
Q

What activates NK cells?

A

in virus infected cells, MHC I expression reduced so inhibitory receptors aren’t engaged and ligands for activating receptors are expressed

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5
Q

PAMPs

A

macromolecules present in viruses and other microbes but not host cells -> recognized by PRRs

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6
Q

PRR

A

expressed on a variety of cells including macs, DC, neutrophils, NK cells, endothelial cells, mucosal epithelial cells

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7
Q

Binding of PAMP to a TLR on a macrophage results in what?

A

phagocytosis
chemotaxis
inflammatory mediators
IFN

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8
Q

Which important interleukins are relased when PRRs are ligated by PAMPs?

A

IL1 and IL12

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9
Q

Do interferons show virus specificity?

A

NAH

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10
Q

T/F RNA viruses are stronger inducers of IFN than DNAviruses

A

troooo

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11
Q

How should interferons be administered to a patient?

A

parenteral route (injection) since they are orally inactive

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12
Q

Type 1 IFN

A

IFN a

IFN B

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13
Q

IFN a

A

leukocyte interferon

  • produced in large quantities by plasmacytoid DC
  • produced in smaller amounts by macs, monocytes and lymphocytes
  • not host specific
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14
Q

IFN B

A
  • fibroblast interferon secreted by virus-infected fibroblast
  • generally host species specific
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15
Q

roles of type 1 IFNs

A
  • inhibit virus replication
  • activate NK cells
  • increase MHC I expression
  • stimulate differentiation of monocytes into DC
  • maturation of DC
  • stimulates memory T cell proliferation
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16
Q

How do Type I IFNs inhibit virus replication?

A
  • activate RNAse L -> degrades viral RNA
  • induce synthesis of MX proteins that bind and trap viral nucleocapsid and inhibit virus assembly
  • induce synthesis of PKR which prevents initiation of translation of viral RNA
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17
Q

Type II IFN

A
  • IFN gamma
  • mostly immunoregulatory
  • produced by antigen-stimulated T cells and NK cells
  • labile at pH 2
  • host specific
18
Q

functions of IFN gamma

A
  • increased MHC expression
  • mac activation
  • TH1 effector cells
  • isotype switching to opsonizing and complement-fixing antibodies
19
Q

Type III IFN

A
  • IFN lambda1, IFN lambda2, IFN lambda3
  • expressed in response to viral infections and activation of TLR
  • mainly immunoregulator
  • recently discovered
20
Q

gene silencing

A

RNAi-endonuclease complex binds to mRNA complementary to RNAi and chops off viral mRNA into small pieces
*can disrupt viral replication

21
Q

granulocytosis

A

presence in peripheral blood of an increased # of granulocytes (neutrophils, eosinophils, basophils, mast cells)
*usually not provoked by viral infections

22
Q

T/F antibodies may be directed against viral proteins on free virions (capsid or envelope) or against viral proteins expressed on surface of infected cells

A

T

23
Q

virus neutralization

A

neutralizing antibodies prevent virus attachment and entry into host cells; bind to viral capsid or host envelope

24
Q

opsonization

A

coating of virions with antibodies so its more easily recognized and phagocytosed by macs and sometimes neutrophils

25
Q

IC formation

A

clumping of viruses; reduced # of viral particles available for cell invasion

26
Q

chemotaxis

A

attracting macs and neutrophils

27
Q

lysis

A

rupturing membranes of foreign cells/pathogens

28
Q

agglutination

A

clustering and binding of pathogens together

29
Q

ADCC

A
  • antibodies bind antigens on target cells
  • NK cell CD16 Fc receptors recognize cell-bound antibodies
  • cross-linking of CD16 triggers degranulation into lytic synapse
  • infected cells die by apoptosis
30
Q

antigenic plasticity

A

rapid changes in structure of viral antigen that may be the result of mutation, reassortment or recombination -> virus may become resistant to immunity generated by previous infection

31
Q

antigenic multiplicity

A

antigenic variants with little or no cross-reactivity -> immunity against one serotype may not work against other variants

32
Q

negative cytokine regulation

A
  • blocking IFN receptor signal
  • virokines
  • viroreceptors
33
Q

virokines

A

some viruses synthesize proteins which are homologs of cytokines
e.g. E-B has vIL10 which suppresses cytokine production by TH1 CD4 cells

34
Q

viroreceptors

A

some viruses encode proteins that are homologous to receptors for cytokines; secreted cytokine receptor homologs bind to cytokines and serve as competitive agonist (poxviruses)

35
Q

down-regulation of MHC I pathway

A

interfere with expression of MHC I molecules and inhibit antigen presentation
*form of evasion

36
Q

inhibition of complement activation

A
  • vaccinia virus has VAP which binds C4b to inhibit classical complement pathway
  • glycoprotein of herpes simplex virus binds C3b inhibiting both classical and alternative complement pathways
37
Q

evasion of neutralizing antibodies

A
  • soluble proteinsthat soak up antibody
  • variation in viral antigens
  • antibodies incapable of neutralization (caprine arthritis-encephalitis of goats)
  • slow production of antibodies compared to fast infection of cells by virus
38
Q

latency

A
  • transcription of viral genes that encode antigenic proteins are blocked
  • integration of viral genome in host cell genome (retroviruses)
39
Q

cell-to-cell spread

A

not exposed to host immune mediators

40
Q

inhibition of apoptosis

A

poxvirus and herpesvirus produce caspase inhibitors that protect infected cells against death and allow completion of viral replication

Virology (16 decks)

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