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Foundations of Medicine > TBL 12 Viruses > Flashcards

TBL 12 Viruses Flashcards

1
Q

Viruses are ______, ______________.

A

small obligate intracellular parasites

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2
Q

The following viruses have ______ genome.

Herpes, Pox, Adeno, Papilloma

A

dsDNA

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3
Q

The following viruses have _______ genome.

Corona (e.g. Covid-19, SARS), Picorna (E.g. Polio virus, rhinovirus), Flavi (E.g. Dengue virus)

A

(+)ssRNA

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4
Q

HIV (_____virus) has _____ genome.

A

HIV (Retrovirus): (+)ssRNA

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5
Q

Orthomyxo (e.g. _______) has a ____ genome.

A

Orthomyxo (e.g. Influenza) has a (-) ssRNA.

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6
Q

Viruses (have/have no) metabolism.

A

Viruses have no metabolism. They rely entirely on processes and machinery in the host cell.

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7
Q

How do viruses replicate?

A

NOT by division.

By the production of components and subsequent assembly.

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8
Q

How does HIV enter the host cell?

Recognition: ____ on HIV binds to ___ on the host cell

Fusion:
____ on HIV binds to ___ on the host cell, facilitating the fusion of the viral envelope with the host cell membrane.

A

Recognition: gp120 on HIV binds to CD4 on host cell

Fusion: gp41 on HIV binds to CCR5/CXCR4 on host cell

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9
Q

Once HIV genome and materials enter the host cell upon fusion, HIV RNA is ________ to form HIV ____. This process occurs in the _______.

HIV DNA is then translocated to the nucleus, where _______ will integrate HIV DNA into the host cell genome, for evasion of immune response.

A

Once HIV genome and materials enter the host cell upon fusion, HIV RNA is reverse transcribed to form HIV DNA. This process occurs in the cytoplasm.

HIV DNA is then translocated to the nucleus, where Integrasewill integrate HIV DNA into the host cell genome, for evasion of immune response.

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10
Q

The ________ effect (change in appearance of the host cells) is usually a result of viral lysis of the cell.

A

cytopathic effect

This is characterised by rounding of the cells and detachment from the plate for in vitro analysis.

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11
Q

Viruses can cause the formation of ______, by mediating the fusion of an infected cell with neighbouring cells.

A

syncytia

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12
Q

Viruses are observed to grow with single step growth kinetics, with 3 main phases.

  1. Eclipse phase
  2. Log phase
  3. Cell death
A
  1. Eclipse phase: Initial addition followed by a drop (due to viruses entering the host cell)
  2. Log phase:
    Viruses are released from cells=> Exponential increase
  3. Cell death: Host cells die, cannot be infected again => plateau and eventual fall in virus titre
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13
Q

Diagnosis of viral infection:

  1. To detect viral genome: _____
  2. To detect viral antigens: _____
  3. To detect viral particles:
    Use electron microscopy and __________ of RBCs.
A
  1. To detect viral genome: PCR
  2. To detect viral antigens: ELISA test
  3. To detect viral particles:
    Use electron microscopy and haemagglutination of RBCs.
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14
Q

How does the ELISA test work to detect the presence of specific viral antigen?

A
  1. Immobilise antibody on a solid support to capture viral antigen that binds to it
  2. The viral antigen is detected using a second antibody which is labelled fluorescently.

(Think of the viral antigen as a sandwich)

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15
Q

How does influenza virus enter the host cell?

________ on influenza recognises and binds to ________ receptors on the host cell membrane. This causes the influenza virus to be taken up by ____________.

H+ ions are pumped into the lumen of the endosome, resulting in a pH-dependent conformational change which allows the viral membrane to fuse with the endocytic membrane, releasing the viral genome into the host cell.

A

How does influenza virus enter the host cell?

Haemagglutinin (HA) on influenza recognises and binds to sialic acid receptors on the host cell membrane. This causes the influenza virus to be taken up by receptor-mediated endocytosis.

H+ ions are pumped into the lumen of the endosome, resulting in a pH-dependent conformational change which allows the viral membrane to fuse with the endocytic membrane, releasing the viral genome into the host cell.

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16
Q

Once internalised, the viral genome is released.

All DNA viruses (Except ______) will be transported to the ______ for transcription.

All RNA viruses (except _______) will remain in the _______ for translation to occur.

A

All DNA viruses (Except poxvirus) will be transported to the nucleus for transcription.

All RNA viruses (except influenza) will remain in the cytoplasm for translation to occur.

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17
Q

DNA viruses are more stable than RNA viruses because…

A

Because DNA viruses uses cellular proof-reading mechanism => less susceptible to mutations, whereas RNA genome replication is dependent on RDRP which lacks proof-reading ability.

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18
Q

RNA replication for RNA viruses occurs in the ________ of the host cell.
(except for orthomyxo viruses)

Therefore, RNA viruses (have/do not have) RNA splicing.

A

RNA replication occurs in the cytoplasm, except for orthomyxo viruses (e.g. influenza)

RNA viruses do not have RNA splicing.

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19
Q

For (+) ssRNA e.g. ____virus:

In the cytoplasm - immediately translate into protein product, which includes the viral _________ (enzyme).

This enzyme will then be used for subsequent production of (-)ssRNA strand for replication purposes.

ALL processes for RNA viruses occur in the _______.

A

For (+) ssRNA e.g. poliovirus:

In the cytoplasm - immediately translate into protein product, which includes the viral RDRP (enzyme).

This enzyme will then be used for subsequent production of (-)ssRNA strand for replication purposes.

All processes for RNA viruses occur in the Cytoplasm.

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20
Q

For (-)ssRNA strand, the RDRP must be together with the virus as transcription must occur before translation of protein products.

A

(-)RNA –> (+)RNA

–> protein

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21
Q

Viral _________ are specialised proteins which establish transient intermediate structures.

Viral proteases which are packaged into these structures are later activated to remove scaffold and allow for final assembly.

A

Viral scaffolding proteins

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22
Q

Viral genome packing must be specific (to distinguish host cell genome from viral genome). This is achieved by the presence of __________ on the genome which are recognised by structural proteins.

Might also be achieved by coupling the packing with RNA synthesis

A

packaging signals on viral genome

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23
Q

For enveloped viruses, viral membrane proteins are translated on the __________, where it will be transported out to the plasma membrane.

A

ER membrane

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24
Q

Most viruses will undergo _________, which refers to the processing of virion components for the production of infectious particles.

A

Maturation

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25
Q

Poliovirus is transmitted by the ________ route, normally causing a localised infection of the _______.
But neurovirulent virus may infect _______ instead, causing paralysis (poliomyelitis).

A

Poliovirus:

transmitted by the faeco-oral route

localised infection of small intestine

infect motor neurons (accidental pathogenesis)

26
Q

Zika virus usually causes acute infection that is normally asymptomatic.

However, pregnant women can pass the virus to her developing fetus and cause serious birth defects. (accidental pathogenesis)

A

-

27
Q

______ infections occur with low level of replication in viruses in tissues, whereas _______ infections are where viral genomes are maintained, but no virus is seen until reactivation when the host is immunocompromised.

A

Chronic (e.g. Hep B and Hep C viruses which replicate in the liver)

Latent infections (e.g. Herpes virus)

28
Q

How do viruses evade immune response?

  1. Viruses may downregulate ____ molecules, avoiding detection by T-cells.
  2. Compensation by making a _______ of MHC molecules to avoid detection by NK cells.
  3. Antigen variants
  4. Infect tissues with reduced immune surveillance at _________ sites like the CNS or skin.
A
  1. Downregulate MHC molecules to avoid detection by T-cells.
  2. Compensate by producing viral analogue of MHC molecules to avoid killing by NK cells.
  3. Antigen variant
  4. Immunoprivileged sites
29
Q

The herpes simplex virus has a _____ phase in its life cycle, where there are no virions detected (only __________).

HSV infects _________ (secondary site of infection) from epithelial cells and can be reactivated when the host is immunocompromised to reinfect the skin epithelial cells and neuroinvasion of the CNS causing encephalitis.

A

latent phase

only latency associated transcripts (LATs)

primary site: epithelial cells on skin
secondary site: sensory neurons where they shift into latent phase

30
Q

_________ can cause cancer as it encodes inhibitors of tumor suppressor p53, known as ___ and ___ genes, which forces the cell to enter the S phase indiscriminately.

A

Papillomaviruses encode E6 and E7 genes (inhibitors of p53).

E7 binds to and destabilises Rb protein (tumor suppressor for G1/S phase checkpoint) –> no longer bound to E2F –> E2F is released and promotes S phase.

31
Q

3 factors affecting the virulence of a virus:

A
  1. Viral sequence
  2. Viral load
  3. Co-infections (e.g. secondary bacterial infections)
32
Q

Co-infections which increase virulence of virus:

Secondary ___________ infection following influenza virus can lead to fatal pneumonia.

A

Streptococcus pneumoniae

33
Q

_______ (cancer) is caused by HHV8.

(Co-infection) Immunodeficiency caused by HIV makes patients more susceptible to severe HHV8 infection.

A

Kaposi’s sarcoma (oncogenesis)

34
Q

Some hosts are less susceptible to HIV-1 infection due to a mutation on _________.

A

CCR5 receptors on macrophages

=> unable to recognise and bind gp41 of HIV

35
Q

Name the 2 PRRs that recognises viral PAMPs.

A
  1. RIG-I: Recognises the uncapped 5’ ssRNA and short dsRNA

2. MDA-5: Recognises longer dsRNA

36
Q

Upon PAMP recognition by PRRs (_____/_____), MAVS will be activated.

MAVS mediates both ______ and ______ (Transcription factors) activation to upregulate the transcription of interferon (IFN) genes.

A

PRRs: RIG-I/MDA-5

Activates MAVS

which activates IRF-3 and NF-KB to upregulate transcription of IFN genes.

37
Q

Overall interferon activation:

PAMPs recognised by PRRs (____/______) –> _____ protein activated —> Activates _____ and _______ (TFs) => Upregulates the transcription of interferon genes

A

PAMPs recognised by PRRs (RIG-I/MDA-5) –> MAVS protein activated —> Activates IRF-3 and NFKB (TFs) => Upregulates the transcription of interferon genes

38
Q

How does Influenza virus block host cell interferon release?

A

Influenza virus NS1 sequesters dsRNA and blocks its recognition by RIG-1/MDA-5 (PRRs).

39
Q

How does the Hep C virus block host cell interferon release?

A

Hep C virus protease cleaves MAVS in infected cells to suppress interferon response.

40
Q

Which three viruses can block interferon release?

A
  1. Influenza - blocks recognition by RIG-I/MDA-5
  2. Hep C - protease cleaves MAVS protein
  3. Rotavirus - promotes proteasomal degradation of IRF-3 (TF) in infected cells.
41
Q

There are 3 types of interferons.

Type 1: secreted by ____ cells

Type 2 (IFN-__): secreted by ______

Type 3 (IFN-__): important for controlling viruses transmitted via _______.

A

There are 3 types of interferons.

Type 1 (IFN-B and IFN-a): secreted by ALL cells

Type 2 (IFN-y): secreted by immune cells

Type 3 (IFN-lambda): important for controlling viruses transmitted via epithelial surfaces.

42
Q

How is NFKB transcription factor activated by MAVS?

NFKB is always in the (activated/inactivated) state, bound to ___ (A).
MAVS activate ____ (A kinase), which phosphorylates (A) which is then degraded by proteasome.

=> NFKB is then activated upon the removal of (A) and translocates to the nucleus to bind to the recognition sequence, the promoter of IFN-B.

A

NFKB is always in the inactivated state, bound to IKB.
MAVS activate IKK (IKB kinase), which phosphorylates IKB which is then degraded by proteasome.

=> NFKB is then activated upon the removal of IKB and translocates to the nucleus to bind to the recognition sequence, the promoter of IFN-B.

43
Q

Binding of interferons to IFN receptors results in ____ and ____ phosphorylation, which dimerise and translocate into the nucleus, acting as a transcription factor which upregulates many antiviral mediator genes.

A

STAT1 and STAT2 phosphorylation

44
Q

Protein Kinase R (PKR) is an antiviral mediator gene that has 2 dsRNA binding motifs and 1 kinase motif.

It functions to:

A

Phosphorylate the a-subunit of eukaryotic initiation factor to prevent translation of the viral proteins

45
Q

________ is an important antiviral mediator involved in innate immune response to virus using reverse transcriptase.

It functions to deaminate dC to dU in viral cDNA during reverse transcription, causing a __ to __ hypermutation.

However, HIV has a ___ protein that can degrade APOBEC3G.

A

APOBEC3G

G to A hypermutation

Vif protein

46
Q

________ is hypercytokinemia. Replication of virus with particularly efficient cytokine evasion mechanisms will replicate and induce uncontrolled cytokine response, leading to cellular pathology.

A

Cytokine storms

47
Q

3 mechanisms in which virus can evade antibody response:

A
  1. Antigenic drift
  2. Antigenic shift
  3. Existing as many different genetically stable serotypes
48
Q

________ is when there is continued rapid evolution driven by antigenic pressures from host. This is common in _______ virus.

A

Antigenic drift

Influenza virus

49
Q

Why is antigenic drift common in influenza virus?

hypermutable

A

Influenza virus (-) RNA

uses RDRP which is prone to error
=> induce mutations in the gene coding for surface antigens HA and NA
=> Selection pressure of the new antigen

50
Q

________ mainly results from reassortment of the combination of HA and NA molecules expressed on the surface envelope. Co-infection of the SAME cell will lead to reshuffling of the viral nucleocapsid components.

A

Antigenic shift

51
Q

There are 2 types of antibodies which humans make against HA of influenza:

  1. Head region which binds to _________
  2. Binds to lower down in the conserved regions (Stalk domain)
A
  1. Head region which binds to sialic acid receptors (highly variable)
  2. Stalk domain (more conserved)
52
Q

_________ cause the common cold, and exist sas more than 120 antigenically distinct serotypes which co-circulate simultaneously.

Immense variation exists between antigens, but all still use the same ______ receptor on respiratory epithelial cells, which binds to a region of the rhinovirus capsid called the _____.

A

Human rhinoviruses (HRV)

ICAM-1 receptor on respiratory epithelial cells, which binds to the canyon of the viral capsid

53
Q

How do the immense variation of HRV help with the evasion of recognition by antibodies?

A

Antibodies are not against the highly conversed sequences at the bottom of the canyons, as Fab is too wide to fit within it.
Those at the edges are varied (antigen diversity).

54
Q

Explain the mechanism behind dengue hemorrhagic fever.

A

Antibody from previous infection binds to the new serotype of dengue virus, but is unable to neutralise it.

Instead, it causes antibody-dependent enhancement, allowing it to bind to and invade other immune cells, causing DHF => increased viral load and enhanced cytokine production.

55
Q

Normally. the infected cell will take up viral antigens and:

  1. Process the viral proteins by the action of ________
  2. Load into the ___ complex in the ________, which then passes the peptides to the MHC molecule.
A
  1. Cleave into smaller peptides by proteasomes
  2. Load into TAP complex on the ER membrane, which then passes the peptides to the MHC molecule for it to present it to the cytotoxic T cells
56
Q

There are 3 viruses that can evade antigen loading to TAP transporter:

  1. EBV
  2. Herpes simplex virus
  3. Cytomegalovirus
A
  1. EBV: Produces EBNA1/2 which cannot be processed by proteasomes
  2. Herpes simplex virus: Encodes ICP47 protein which binds to TAP and blocks access of peptide to TAP
  3. Cytomegalovirus: US6 stops ATP binding to TAP, preventing peptides from translocating into the ER lumen
57
Q

There are 2 viruses which modulates tapasin function:

  1. Cytomegalovirus
  2. Adenovirus
A
  1. Cytomegalovirus US3 binds to tapasin to prevent it from loading peptides to MHC class I molecules.
  2. Adenovirus E3-19K prevents the recruitment of TAP to tapasin,
58
Q

______ functions to bind and stabilise the TAP complex and recruit the MHC class molecules. i.e. it is the bridge between MHC and TAP.

A

Tapasin

59
Q

Kaposi sarcoma herpes virus ___ protein induces ubiquitinylation and internalisation of MHC molecules.

A

kk3 protein

60
Q

What are the 2 ways in which viruses evade NK cell killing? (compensate MHC)

A
  1. Encode MHC analogues (e.g. CMV gpUL40)

2. Upregulate MHC on the surface which presents self-peptides

Foundations of Medicine (21 decks)

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