Viral Immunity Flashcards

1
Q

What receptors on the cell membrane recognize viral infection?

A

Viral capsid proteins : TLR2/6 and TLR4

Viral RNA: TLR3

Cytoplasmic RNA receptors - RIG-I

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2
Q

With a viral infection, what response to you want to produce?

A

Type 1 interferons

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3
Q

What happens after a receptor recognizes viral RNA or the virus capsule?

A

it activates IRF 3/7 which then binds to the DNA and promotes synthesis of the antiviral cytokines, another cascade makes inflammatory cytokines

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4
Q

What is the responsibility of the Type 1 IFNS?

A

they are antiviral cytokines that create a hostile environment for the virus- works on the neighborhood and the infected cells themselves too.

  • it shuts everything down
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5
Q

How does IFN shut down viral replication?

A

Viruses use host machinery to replicate, synthesize genes and make proteins

IFN inhibits the host transcription and translation machinery

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6
Q

Are Interferons the same thing as cytokines?

A

_Cytokines i_s the umbrella term for

interferons

chemokines and

interleukins

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7
Q

What is the effect of type 1 IFN on immune cells?

A

it upregulates the MHC class 1 (so cytotoxic T cells can target the cell)

  • it activates DC and macrophages
  • Activates cytotoxic T cells - directly kill infected cell
  • B cell activation - antibodies
  • Activate NK cells - directly kill infected cells
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8
Q

How does the complement system play a role in fighting viral infections?

A

when an antibody meets and antigen- it causes a cleave of C3- wihch recruits the inflammatory cells, opsonisation of pathogens, and membrane attack complex

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9
Q

How do Viruses avoid our immune response?

A
  • some viruses can antagonize the normallly cellular response to make transcription factors for anti-viral cytokines
  • some viruses express membrane CD59 - which is a protein that our cells express to inhibit complement activation against our own cells
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10
Q

how are antibodies used against viral infections?

A
  1. B cells encounter the virus coating
  2. BCR binds to epitope on viral coating and internalize it
  3. Viral coating segment is degraded into peptides within the B cell
  4. Peptides form the internal protiens of the virus are presented to the T cell- which activates B cells to make antibodies agains viral coat protein
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11
Q

What are the three activities of Antibodies agains the virus?

A

neutralization - prevents viral adherence to cells (IgG, IgA)

opsonization - promotes phagocytosis (IgG)

and complement activation - activates complement which enhances opsonization (IgG, IgM)

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12
Q

What is ADCC- antibody dependent cellular cytotoxicity ?

A

you use antibodies to invoke a process that kills cells that you don’t want - so once you have an antibody/antigen interaction = it will perturb the membrane and make it release the toxic granules into the cytoplasm - driving cell apoptosis

  • Antibody driven
  • Effector cell – Natural Killer Cell, Eosinophil,

Macrophage and Neutrophils

  • Antibody binds virus/bacteria/tumour cell
  • Fc region binds FcR on effector cell
  • Induce cell death
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13
Q

What is the principle mechanism of disposing of virally infected cells?

A

Cytotoxic T cell activation

  • virally infected cell will display viral antigens on MHC class 1 molecule
  • vill be activated to upregulate MHC class 1
  • infected cell decorated with MHC class 1 bound to viral antigens
  • Cytotoxic T cells are pre-programmed to kill if they recognize an antigen on MHC Class 1
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14
Q

How do viruses use MHC class 1 to their advantage?

A
  • The viruses can mutate genes so they aren’t recognized by MHC class 1
  • they can interfere with antigen processing (epstein barr virus does)
  • they can down regulate MHC class 1 and prevent it from getting to the surface- but our body still attacks these cells
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15
Q

What are NK cells?

A

Natural killer cells = lymphoid cells that detect altered self cells -

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16
Q

What do Natural Killer cells do?

A

Innate immune cells – no Ag receptor

  • Key in anti-viral and anti-tumour immunity
  • Recognise altered ‘self’ cells – viruses trigger down regulation of MHC

class I on cells to prevent Tc (CTL) discovery

  • Cytotoxic activity
  • Detected within 2 days of an infection
  • Very active against Herpes viruses and cytomegalovirus
17
Q

How do NK cells work?

A

NK cells have an inhibitory receptor (when bound inhibitis cell lysis) - and an activatory receptor (when bound it activates cel lysis)

  • When the NK cells bind MHC class 1, it inhibits the cell lysis = normal cell, do not attack
  • When the NK cell cannot find an MHC class 1 to bind to = activates itself and kills the cell
18
Q

Do NK cells and cytotoxic T cells kill differently?

A

No, they kill the same way

1) perfornin
2) granzyme
3) cell death/apoptosis

*they also release the cytokine IFN gamma, which drives Th1 responses and CTL activity

19
Q

What causes activation of the NK cell?

A

the lack of MHC class 1 binding activates the NK cell

20
Q

What is RSV and why is it so dangerous?

A

Respiratory Synctial Virus - RSV -

Major cause of lower respiratory tract infections

particularly affects newborns, elderly, immunocompromised

  • virus infects respiratory cells, causes the cells to secrete mediators which accumulate an inflammatory response
  • after that you get the specific immune response - ultimately this leads to an inflammatory status in patients- and brachial swelling making it difficult to breath
  • RSV is sneaky - it can block the antiviral response by blocking interferon response factors blocking their upregulation of interferon transcription
21
Q

What treatment do we have for RSV?

A

antiviral treatment and breathing aids -

antiviral = Ribarvirin

22
Q

How do Cytoxic T cells and Natural Killer cells use MHC class1?

A

Cytotoxic T cells- if MHC 1 presents antigen = cell death

Natural Killer cells = if no MHC 1= cell death

*both are looking for abnormal cells, but both rely on differnt signals*