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Immunology > L9 Immunity to Viruses > Flashcards

L9 Immunity to Viruses Flashcards

1
Q

composition of viruses (DNA/RNA, ss/ds)

A

can be composed of either ss or ds DNA (mostly dsDNA), ss or ds RNA (mostly ssRNA)

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2
Q

How does the virus enter the body?

A

Via mucosal surfaces usually

Mainly infects epithelial cells as a primary site

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3
Q

What is viraemia?

A

Presence of the virus in the blood stream - can cause secondary infections at distant site. E.g. polio can affect neurons.

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4
Q

viruses that have an envelope

A

HIV and Influenza A virus have the lipid bilayer envelope

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5
Q

Is EBV a DNA or RNA virus?

A

DNA

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6
Q

what is infection with EBV called during adolescence/young adulthood?

A

infectious mononucleosis

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7
Q

symptoms of EBV

A

fever, sore throat, swollen lymph nodes, can have swollen liver/spleen.

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8
Q

diagnostic tests for mononucleosis

A

white blood cell count elevated

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9
Q

Why is WBC count elevated in EBV infection?

A

EBV infects B cells and can lead to proliferation of B cells during the acute stage.

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10
Q

lifelong dormant infection of EBV can increase risk of developing?

A 
Burkitt's lymphoma (Sub-saharan Africa, malaria may also play role)
Nasopharyngeal carcinoma (South-east Asia)
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11
Q

give bullet point explanation for virus cellular infection life-cycle

A

virus enters cell, interacts with specific receptor, uncoats (sheds capsid), interacts with endosome, replication of itself, translation of its mRNA into proteins, long polyproteins processed by proteases.

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12
Q

describe assembly of virus after replication

A

Capsids around nucleic acids form - released by (i) cytolysis if no envelope, or (ii) budding if it has an envelope

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13
Q

does a cell need to be receptor positive or receptor negative to allow infection via a virus in most cases?

A

cell needs to be receptor positive for a successful infection

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14
Q

receptor for SARS COVID-19 and their locations

A

ACE2 (lungs, heart, kidneys, GI)

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15
Q

EBV receptor and cell type infected?

A

Receptor: CR2

Cell type: B cells

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16
Q

are viral infections more commonly acute or chronic?

A

most commonly acute

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17
Q

types of acute viral infections

A

can be acute with recovery and viral elimination (infleunza)
can be latent infection reactivated (herpes simplex virus)
can persist with continuance or intermittent shedding (hepatitis B)

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18
Q

which branch of the immune system detects the virus?

A

the innate immune system

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19
Q

what is released by the innate immune system as a result of detection of a virus?

A

interferons (type 1)

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20
Q

which immune cell detects viral infected cells?

A

natural killer cells

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21
Q

which immune cell drives the adaptive immune response?

A

B cells

22
Q

what triggers B cells to produce antibodies?

A

viral antigens

23
Q

Briefly describe the two methods of action of antibodies (direct and indirect)

A

Direct action: neutralisation of the infected cell

Indirect: recruit other cells, like CTLs, to kill the virus-infected cell

24
Q

what do early-responding B cells do?

A

they release IgM antibody which is viral-specific

25
Q

what cells comprise the memory cells of the viral infection?

A

IgG/IgA B and T cells remain and can be rapidly reactivated if reinfection occurs.

26
Q

aim of vaccination against viruses

A

achieve adaptive immune memory without the need for the primary infection.

27
Q

TLRs and what they recognise:

A

TLR3: dsRNA (rotavirus)
TLR7: ssRNA (norovirus, poliovirus)
TLR9: CpG dsDNA (Herpes)

28
Q

What mediators activate antiviral response in neighbouring cells?

A

IFNs

29
Q

effect of plasmacytoid dendritic cells interacting with TLR7 and TLR9

A

stimulates the production of a large amount of type 1 interferons IFNalpha and IFNbeta.

30
Q

what do INF alpha and beta target?

A

virus infected cells.

31
Q

What do IFN alpha and INF beta stimulate?

A

An anti-viral response in neighbouring cells, which prevents viral replication

32
Q

how long does it take for antiviral response to activate?

A

develops within a few hours, last 1-2 days

33
Q

what does ribonuclease L do?

A

degrades viral mRNA

34
Q

What happens when INFα & IFNβ bind to IFN receptors on virus-infected cells?

A

Viral mRNA degradation occurs (mediated by ribonuclease L).
Inhibition of protein synthesis mediated by protein kinase and phosphorylated initiation factor (elF-2).
Induction of 2’5’ oligoA synthase, which plays a role in ribonuclease L activity.

35
Q

How does the immune system eliminate a ‘free’ virus?

A
  • Via antibodies alone: blocks binding to the cell, blocks entry, blocks virus un-coating
  • Via antibody + complement: damage to virus envelope, blockade of virus receptor
  • Neutralisation
36
Q

How can virus-infected cells be eliminated by the immune system?

A
  • Antibody + complement: lysis of infected cell, opsonisation of coated virus or infected cells for phagocytosis
  • Antibody bound to infected cell: antibody-dependent cellular cytotoxicity via NK cells, macrophages and neutrophils
37
Q

how do CTL’s recognise and kill virus infected cells?

A 
recognize virus peptides bound to MHC class I on surface of infected cell
kill by apoptotic cell death
38
Q

how do NK cells recognize and kill virus-infected cells?

A 
recognize loss of MHC class I on cell surface 
kill by apoptotic cell death.
39
Q

what immune cell removes apoptotic bodies due to apoptosis of virus-infected cells?

A

macrophages

40
Q

how do viruses associated with persistent infection prevent their detection and destruction by CTL’s?

A

they downregulate MHC class I on the surface of cells as CTL’s recognize and kill cells that do not express MHC class I receptors on their surface.

41
Q

MHC Class I + foreign antigen is killed by which immune cell?

A

Cytotoxic T cell (CTL)

42
Q

No MHC Class I - killed by which immune cell?

A

Natural killer cell

43
Q

what enzymes degrade chromosomal DNA?

A

nucleases

44
Q

how do phagocytes, like macrophages, recognize apoptotic bodies?

A

phosphatidylserine residues are displayed on the outer surface of the apoptotic bodies.

45
Q

What is perforin?

A

a granule protein which creates pores on the surface of the target cell via polymerising itself

46
Q

what can enter the target cell once the pore has formed?

A

granzyme B and DNase.

47
Q

What does Granzyme B do?

A

It activates apoptosis via activation of caspase-3, which cleaves substrates, including DNase which will degrade the cell’s DNA.

48
Q

Mechanisms of evading the immune system:

A
  • Alteration of the surface antigen, so as to not be recognised by the memory immunity.
  • Changes in protein coat
49
Q

Mechanisms of viruses inhibiting the MHC Class I-mediated presentation of cytosolic proteins?

A
  • Blockade of TAP transporter

- Removal of MHC Class I molecules from the ER

50
Q

Example of viruses which have acquired homologs of cellular cytokines or their receptors to limit host immune recognition:

A
  1. The E3 product of adenovirus blocks transport of MHC to the surface
  2. EBV produces an IL-10 homolog which reduces IFNγ function
51
Q

IL-10 effect?

A

Pleiotropic, immunosuppressive mainly.

Immunology (10 decks)

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