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MICI 2100 > Final > Flashcards

Final Flashcards

1
Q

Restriction Endonuclease (6)

A
  1. Bacterial defense against viral infection
  2. Enzyme
  3. Targets dsDNA
  4. Makes sequence specific incisions
  5. Viral DNA is targeted because it is methylated (unlike host DNA)
  6. Useful in research because each RE has a different target sequence so they can be used to splice DNA in targeted regions.
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2
Q

Why is study of parasites important? (3)

A
  1. Kill million of children a year
  2. Parasitic infection is endemic/epidemic in third world countries
  3. Multicellular parsites weaking the immune response to other disease
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3
Q

Helminths (3)

A

Nematodes (roundworms)

Cestodes (tapeworms)

Trematodes (flukes)

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4
Q
  1. Immune modulation by helminths
  2. Its impact on kidney transplant and pregnancy
A
  • Steer immune response from Type 1 to Type 2 effectors.
  • Induce polyclonal B cell activation and proliferation
  • Directly
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5
Q

Innate immune responses to viral infection (2)

A

Structural protection

IFN a and B

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6
Q

Structural protection against viruses

A

Skin is #1 protection

GI tracts, lungs, upper respiratory tract are major sites of infection and have special structure;

Muscous in intestine from goblet cells;

Epithelial cell packed tightly and bound by tight junctions to prevent virus entry into bloodstream;

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7
Q

IFN a and B response to viral infection

A
  1. Cell infected w virus is stressed; releases IFN a and B
  2. IFN a and B bind to IFN a/B receptor on neighbouring cell;
  3. Activation of Jak Stat pathway
  4. Stimulation of ISGF3 and AAF
  5. Neighbour
    1. inactivates protein translation
    2. induces RNAse activity
  6. Neighbour suicides - prevents spread of virus
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8
Q

Adaptive immune to virus involves (2)

A

antiobody

cytotoxic T cells (CD8+)

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9
Q

Role of antibody in fighting virus

A

Block attachment - beinds to vurs and prevents viral penetration. Neutralizing antibody.

Aggregate for phagocytosis - many viral particles removed by monocytes and myeloid liver cells (after made into immune complexes)

Activate complement and Mac Attack - some viruses are susceptible to complement activation by its classical pathway

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10
Q

Activation and killing by T cells in viral infection

A
  1. Infected cells are killed via IFNa/B and Jak Stat pathway
  2. DCs phagocytose viral antigens from cell lysis; some contents go to cytoplasm;
  3. Viral antigens in cytoplasm are broken down by proteosome, go through Tap and then bind to class 1 MHC
  4. Class 1 MHC takes viral antigen to cell surface - called cross presentation
  5. In the node, CD8+ cells interact with Class 1 MHC; Co-stimulation;
  6. CD8+ cells activated; Proliferate; exit via blood and go to site to produce granules and kill
  7. Recognize infected cells by presentation on class 1 MHC;
  8. Perforin perforates the cell so that granzyme can enter and activate caspases leading to apoptosis
  9. If this doesn’t work, Fas ligand on CTL binds to Fas receptor that activates another caspase pathway leading to death as well.
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11
Q

Cross presentation

A

Can only be done by DCs

taking something on the outside and popping it out onto cell surface

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12
Q

Virus fights back against immune response (2)

A
  1. Downregulate Class 1 MHC expression;
    • allows virus infected cells to hide from CTLs
    • but Natural Killer cells will see cells without MHC1 and kill them
  2. Produce immune regulatory proteins
    • Steal IL-10 gene from cells and incorporate it into viral genome
    • IL-10 downregulates CTS activity and NK cells activity
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13
Q

Major action of HTVL 1 and 2

A

Virus that wants to get into T cells and lymphocytes

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14
Q

What is the worst thing a virus can do to the immune system

A

kill CD4+ T cells.

These produce cytokines that help CD8+ cells function

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15
Q

What vaccine do you get often? Why

A

Tdap because it is a pure protein vaccine and needs to be boosted because it doesn’t have good persistence.

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16
Q

Locus of enterocyte effacement (LEE)

ex:

A

Pathogencity island associated with intestinal cell attachment and diarrheal disease

Infects effectors into hot cells that function to alter cellular activities

STEC e coli get insert long protrusions into microvilli and hold on tight

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17
Q

Listeria

A

Gram +ve bacterium that is common in food-borne illness

  1. Intracellular pathogen; taken up by phagocytes
  2. Gets into cell using Interlanin B; mediated endocytosis using clathrin;
  3. LLO is produced at the perfect time; Generates pores in phagosome so that bacterium can escape
  4. ActA (actin modulating protein); forms a Listerio-pod and pushes bacterium from cell to cell.

May lead to gastroenteritis, encephalitis

Mother to fetus transmission

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18
Q

Prions

A

Proteins that adopt novel conformations that inhibit normal protein function and cause degredation of neural tissue

Mad cow disease

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19
Q

HIV capsid maturation requires

A

Viral proteases

Pre proteins are cleaved into vital forms this way

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20
Q

Egress of naked icosahedral viruses typically requires

virus ex

A

apoptosis

poliovirus

21
Q

Enveloped viruses can escape the cell by (2)

A

Budding into an internal membrane, followed by exocytosis

Budding directly from plasma membrane

22
Q

Poliovirus preparation and egress

A
  • 2 protease steps: when cleaving polyproteins and when scultping capsid
  • genome replicates quickly in cytoplasm
  • VP0, VP3 and VP1 capsid proteins; 60 copies each for icosahedron
  • +ssRNA genome associates with capsid proteins when forming capsid
  • VP0 undergoes autocatalytic cleavage to bcm VP2 and VP4 after assembly - no viral particle is infectious
  • timing of apoptosis precisely timed to completion of the capsid
23
Q

herpes virus egress

A

via exocytosis - 2 models

  1. Virus picks up envelopes from internal structures and uses them to get out by natural mechanisms
  2. herpes capsids are enveloped inside the cell and use the normal protein secretory pathway for egress
24
Q

Egress via budding from plasma membrane

A
  1. virion proteins assemble at the plasma membrane
  2. virions bud out of cell, acquiring host plasma membrane (and some host cell surface proteins)

Ex: Influenza, HIV

25
Q

HIV egress

A

Egree via budding from plasma membrane

  1. Virus proteins gather at PM and recruit 2 copies of HIV genome
  2. Once virus buds, proteases cleave components of gag proteins to complete maturation
26
Q

Influenza:

route of transmission

target cells

cell receptor

A

person-to-person contact or aerosols

targets epithelial cells of respiratory tract/alveolar macrophages

sialic acid

27
Q

Influenza entry into the cell

A

via endocytosis

  1. Initial attachment of HA envelope glycoprotein to cell curface sialic acid
  2. Receptor mediated endocytosis
  3. pH drops in endosomes inducing conformational chnage in HA; exposes hydrophobic fusion peptide
  4. Fusion; viral and cell membranes mix
  5. flu genome delivered to host cell
  6. -ssRNA viral genome migrates to nucleus
28
Q

Influenza genome replication

A

-ssRNA genome is segmented

8 segments encode 11 proteins

virus encoded RNA-dependent-RNA-polymerase makes +ssRNA from -ssRNA template which is then exported to cytoplasm and translated and used as template for progeny -ssRNA genome.

29
Q

cause of antigenic drift in influenza

A

RNA-dependent-RNA-polymerase is error prone. Used to transcribe the -ssRNA genome to +ssRNA.

Leads to mutations that lead to evasion of host immune recognition -> Antigenic Drift

30
Q

Antigenic Shift

A

common influenza

target cells con-infected with 2 different strains of influenza.

Allows for reassortment of genome segments in viral progeny

A dramatic single step

Often the cause of pandemics

31
Q

Influenza virus assembly and egress

A
  • HA and NA proteins have hydrophobic signal sequences so they are translocated into the ER and proceed through golgi apparatus and then become embedded in PM
  • The glycoproteins must be properly processed
    • glycosylated in ER and golgi so they resemble host protein
    • cleaved by proteases in golgi
  • HA and NA proteins cluster on PM
  • Viral proteins and genome ‘home in’ on this cluster and assembly takes place
  • virions bud from PM, taking some host proteins with them
  • NA has sialic acid cleaving ability; allows virus to leave cell
32
Q

Some cells lack the enzyme required to cleave HA into its active form. Are virus particles produced by these cells infectious?

A

No protease = no HA modification = HA can no longer bind to allow membrane fusion bt progeny virus and next host cell

33
Q

Influenza drugs

A

ANtivirals: tamiflu and relenza

NA inhibitors - influenza virus stays tethered to surface

34
Q

HIV assembly and egress

A
  1. Reverse transcriptase makes dsDNA from +ssRNA in cytoplasm
  2. dsDNA is taken to nucleus to integrate into host genome
    1. Has to inegrate to replicate
  3. Once viral genome is in context of host DNA, transcription occurs using host machinery
  4. ENV is the HIV envolope protein;
    • N terminal signal sequence removed by signal peptidase
    • Cleavage in golgi to gp160 to gp120 and gp41
    • Transported to PM
  5. gp41 fusion peptide buried in viral membrane
  6. Gag recruits HIV +ssRNA to budding site
  7. HIV escapes host cell by budding from PM, acquiring some host PM as they do
35
Q

Vpu

A

HIV-1 egress is inefficient in some cell types due to tetherin inhibiting the retrovirus release

Vpu is an accessory protein that antagonizes tetherin and allows these HIVs to escape host cell.

36
Q

HIV protease

A

Cleaves viral proteins into their final products

allows for virus maturation

Cleaves Gag into functional products leading to huge morphological changes in escaped capsid

37
Q

Host defenses against HIV (2)

A

Pattern recognition receptors recognize +ssRNA genome

Toll Like Receptors 7 and 8

Host protein, TRMalpha can recognize uncoming HIV capsids and

  1. cause their degredation
  2. trigger an innate immune response
38
Q

emergent

A

diseases that suddenly become prevalent

39
Q

zoonitc infections

A

Animal diseases that are trasnmissible to humans

wild animals that interact with humans/domestic animals are often the source

we can use sequencing technology to find out which viruses are present in which animals

40
Q

zoonotic HIV

A
  • HIV is from a large family of primate retroviruses that are natural in African nonhuman primates
  • Our immune systems weren’t prepared for HIV bc it was a primate retrovirus
  • Don’t cause severe issues in the primates they come from
  • Closes virus to HIV-1 is SIVcpzPtt
  • HIV-1 groups M, N and O each resulted from independed cross-infections of SIVcpzPtt
    • Probably transmitted locally then south to congo river where the group M pandemic probably spawned
41
Q

Co-evolution

A
  • Explains why many pathogens aren’t harmful in their primary host organisms
  • Innate and addaptive arms of our immune system evolve to defeat a virus and virus simultaneous evolves to beat our immune system
  • Escalating warfare
  • The Red Queen Hypothesis = for an evolutionary system, continuing development is needed just in order to maintain fitness relative to the system it is co-evolving with
42
Q

genetic armed race

A

Viruses promote fitness by hijacking host genes

Strong natural selection for non-synonymous substitutions in coding regions for both viral and host genomes.

Substitutions can weaken or strengthen interactions

43
Q

Poxvirus morphology

resevoir hosts

interaction with host

A

Enveloped, core capside ancases genome

many different resevoir hosts

Numerous poxvirus genes that target host defense and multiple nodes of interaction

44
Q

Poxvirus

Antigenic drift experiment

A
  • PKR is a pattern recognition receptor that sees foreign viral structures and initiates immune response
    • Recognizes dsRNA, a viral PAMP and phosphorylates to block host translation of the viral genome
  • Poxvirus has proteins, E3L and K3L that are involved in antagonizing the action of PKR
  • Delete E3L
    • Virus either does not persist, or persists very well
    • When it persists very well, that is because poxvirus makes a second copy of K3L, which is amplified
    • Mistakes are made and within amplification there is an advantageous variation of K3L
    • Genome collapses to just the advantageous new copy of K3L
  • Poxvirus can rapidly evolve under selective pressure even in the absense of an error-prone polymerase (influenza)
45
Q

Influenza Antigenic Drift

A

Host antibodies can neutralize influenza viruses

RNA-dependent-RNA polymerase is error prone

Gradual viral evolution that leads to evasion of antibodies

Antigens that drift are mostly on HA (where blocking attachment would occur)

Mutated amino acids are clustered on receptor binding region

46
Q

Model of antigenic shift in the lab

serial passage in mice

A
  • Use reference strain called PR8 (non-pathogenic H1N1)
  • generate 3 identicle virus stocks
  • Innoculate each stock into a naive mouse and a vaccinated mouse
  • Harvest/homogenize lungs, harvest virus and infect next mouse
  • After serial passage HA and NA are sequenced
  • HA protein mutated in vaccinated mice, not naive mice because it is under massive selective pressure from vaccine
47
Q

What happens when HA mutant viruses infect a naive host?

A

There is no circulating antibody to provide selective pressure

New mutations lowered receptor binding avidity to optimal range

Illustrates important of binding avidity - strong enough to enter, but not so strong as to impede the release of progeny viruses

48
Q

impact of serial passage/antigenic shift experiment?

A

Antigenic drift is accelerated by sequential passage of IAV between immune and non-immune individuals.

Non immune are mostly children

Decreaseing naive population by increasing vaccination will likely slow antigenic drift.

MICI 2100 (3 decks)

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