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MedST IB: Biology of Disease (BoD) > 2.0 Virology > Flashcards

2.0 Virology Flashcards

1
Q

What is the size range of a virus?

A

Most are <b>20-700nm</b><br></br><br></br>(can be smaller)

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2
Q

What is the smallest virus?

A

Foot and mouth disease virus (FMDV) - 20nm

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3
Q

What is the largest virus?

A

Mimivirus - 700nm

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4
Q

What is the structure of virions?

A

<b>1) Nucleic acid (genome)</b><br></br><b>2) Capsid</b><br></br><br></br>Some have:<br></br>3) Lipid membrane (envelope)

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5
Q

Structure of capsids:

A

Composed of <b>capsomers</b> (repeating protein units)<br></br>Symmetrical (can be <b>helical</b> or <b>icosahedral</b>

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6
Q

Structure of lipid membrane:

A

Phosopholipid membrane (aquired from host)<br></br>Embedded viral protein<br></br>May be glycosylated

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7
Q

How do virions increase the coding capacity of their small genomes?

A

1) Densely packed genes<br></br>2) Overlapping reading frames<br></br>3) Splicing<br></br>4) Few non-coding regions

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8
Q

What are the different ways to measure viruses?

A

<b>1) Electron micrograph</b><br></br>- Useful for quantification<br></br>- No info on virulence<br></br><br></br><b>2) Polymerase chain reaction</b><br></br>- Useful for diagnosis<br></br>- No info on virulence<br></br><br></br><b>3) Immunological evidence of infection</b><br></br>- Detection of adaptive immune response<br></br>- Too slow for diagnosis (useful epidemiologically)<br></br>- Can give some info on virulence<br></br><br></br><b>4) Plaque assay</b><br></br>- Preffered method to measure infectivity

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9
Q

What are the stages of viral replication?

A

1) Adsorption and penetration<br></br>2) Eclipse phase<br></br>3) Assembly and release

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10
Q

What is the mean burst size?

A

Average yield of virus particles per cell<br></br>- Varies greatly

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11
Q

How does HIV bind to target cell?

A

<b>gp120</b> (envelope glycoprotein) on HIV binds to <b>CD4</b> + chemokine co-receptor<br></br><br></br>CD4 = only on T-cells

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12
Q

How does influenza bind to target cell?

A

<b>Haemagglutin (HA)</b> (envelope glycoprotein) on influenza binds to <b>sialic acid</b><br></br><br></br>Sialic acid = on most cells

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13
Q

How does EBV bind to target cell?

A

<b>gp340</b> (envelope glycoprotein) on EBV binds to <b>CD21</b>

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14
Q

How does HIV penetrate the target cell?

A

Binding of gp120 to CD4 → conformational change in virus gp120/gp41 → <b>virus envelope fuses with plasma membrane</b>

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15
Q

How does infleunza penetrate the target cell?

A

Binding of HA to sialic acid → <b>endocytosis</b> → endosome is acidified <br></br><br></br>↓ pH → rearrangement of HA → viral envelope is pulled closer to vesicle membrane → disruption → fusion

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16
Q

What happens in the eclipse phase?

A

<b>No virus particle present in host cell</b><br></br><br></br>Virus has disassembled<br></br>Genome is being replicated<br></br>Virus proteins are being made

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17
Q

What are the steps for -ve ssRNA and dsRNA viral replication?

A

<b>OCCURS IN CYTOPLASM</b><br></br><br></br><b>1) Viral genome transcribed to +ve sense RNA</b><br></br>- Enzyme = viral RNA dependent RNA polymerase<br></br><b>2) +ve sense RNA can be used as mRNA or to make new viral genome</b><br></br><br></br>Exception to this is influenza (occurs in nucleus - uses host RNA pol II)

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18
Q

What are the steps for +ve ssRNA viral replication?

A

<b>OCCURS IN CYTOPLASM</b><br></br><br></br><b>1. Translation</b><br></br>- Translated proteins include RNA dependent RNA polymerase<br></br><b>2. Virus genome is replicated into complimentary (-ve sense) RNA </b>(RNA dependent RNA polymerase)<br></br><b>3. Second stage of replication is to copy -ve sense to +ve RNA </b>(RNA dependent RNA polymerase)<br></br><b>4. These can then be packaged into new virions</b>

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19
Q

What are the steps for retrovirus replication?

A

<b>1. Virus genome is copied by reverse transcriptase</b><br></br>- This is an RNA dependent DNA pol<br></br>- Packaged within the virus particle<br></br>- Creates dsDNA intermediate<br></br><b>2. dsDNA intermediate is integrated into host genome</b><br></br>- Provirus<br></br><b>3. mRNA is transcribed by host DNA dependent RNA pol II</b><br></br>- provirus = template<br></br><b>4. Full length transcripts can be translated</b><br></br><b>5. Or packaged into new virus capsids in the cytoplasm</b>

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20
Q

What are the steps for ds DNA viral replication?

A

<b>OCCURS IN NUCLEUS</b><br></br><br></br><b>1. Virus genome is transported into nucleus</b><br></br><b>2. Transcription</b><br></br>- Uses host DNA-dependent RNA pol<br></br><b>3. mRNA translation</b><br></br>- Occurs in cytoplasm<br></br><b>4. Some proteins are transported back to nucleus</b><br></br>- e.g. DNA pol and capsid proteins<br></br><b>5. In nucleus viral DNA is replicated and progeny genomes are packed into new capsids</b>

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21
Q

How are poxviridae virions an exception to ds DNA viral replication?

A

Replication occurs in cytoplasm<br></br><br></br>They carry their own enzymes (DNA dep. RNA pol + capping/polyadenylating enzyme)<br></br><br></br>Viral DNA alone is not infectious

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22
Q

In viral replication, what do early genes code for and what do late genes code for?

A

1) Early genes → nucleic acid replication (+ modification of host cell)<br></br><br></br>2) Late genes → structural proteins of virion<br></br><br></br>(Early proteins = low amounts, late proteins = large amounts)

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23
Q

What are the mechanisms virions use to make different proteins (poly-protein processing)?

A

<b>1) Post-translational cleavage</b> (using specific proteases)<br></br><br></br><b>2) Segemental genome</b> (influenza)<br></br><br></br><b>3) Splicing</b> (e.g. HIV → gp160 → gp120 + gp41)

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24
Q

What are the two mechanisms of viral release from a cell?

A

1) Lysis of cell<br></br>2) Budding of enveloped virus

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25
Q

What viruses show latency?

A

1) Retroviruses<br></br>2) Herpesviruses

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26
Q

What modifications to host cells can viruses induce?

A

1) Subversion of cellular metabolism to make only viral proteins<br></br>2) Cell stimulation <br></br>3) ↑ dNTP pool<br></br>4) Membrane modifications<br></br>5) Cytopathic effect (CPE)<br></br>6) ↓ host cell signalling (↓ innate immunity)<br></br>7) Lytic/non-lytic infections<br></br>8) Cell transformation

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27
Q

What viruses cause lytic infections?

A

1) DNA viruses<br></br>2) Non-enveloped RNA<br></br>3) Viruses that cause host-cell shut off

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28
Q

What viruses cause non-lytic infections?

A

1) Enveloped RNA<br></br>2) Retroviruses

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29
Q

What viruses cause cell transformation?

A

1) HPV → wart/cervical cancer (16 +18)<br></br>2) Rous sarcoma virus → sarcoma in chickens

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30
Q

What viruses have the following portals of entry?<br></br><br></br>Oropharnx:<br></br>Respiratory tract:<br></br>Alimentary canal:<br></br>Conjunctiva:<br></br>Skin:<br></br>Genital tract:<br></br>Blood:<br></br>Insect bite (blood):

A

<b>Oropharnx:</b> HSV, CMV, EBV<br></br><br></br><b>Respiratory tract:</b> Influenza, measles, mumps, rubella, VZV, adenovirus, rhinovirus<br></br><br></br><b>Alimentary canal:</b> Poliovirus, Hep A, rotavirus<br></br><br></br><b>Conjunctiva:</b> HSV<br></br><br></br><b>Skin:</b> HPV, HSV, Rabies<br></br><br></br><b>Genital tract:</b> HIV, HSV, HPV<br></br><br></br><b>Blood:</b> Hep B, HIV<br></br><br></br><b>Insect bite (blood):</b> Yellow fever, dengue

31
Q

How are viral nucleic acids recognised by PRRs?

A

1) Unusual place (cytoplasm)<br></br>2) Unusual structure (RNA 5’ triphosphate)

32
Q

What transcription factors do PRRs activate?

A

1)<b>NFkB</b><br></br>2) <b>IRF</b> (interferon response factors)

33
Q

What are the three types of interferon (IFN)?

A

<b>Type I</b><br></br>TNFα + TNFβ<br></br>Released from infected cells<br></br>↑ antiviral state in adjacent cells<br></br>↑ MHC I<br></br><br></br><b>Type II</b><br></br>TNFγ<br></br>Released by T cells and macrophages<br></br>↑ Th1 responses<br></br>↑ Inflammation<br></br><br></br><b>Type III</b><br></br>TNFλ<br></br>Important for epithelial cells

34
Q

What are the steps of IFN type I action?

A

1) PRR/TLRs recognize virus → NFkB/IRF3<br></br>2) NFkB/IRF3 go to nucleus + ↑ IFNβ transcription<br></br>3) IFNβ secreted → binds to Type I IFN receptor on adjacent cells<br></br>4) This stimulates JAK-STAT pathway<br></br>5) JAK-STAT → + ISGF-3 → + ISRE → ↑ proteins that make cells resistant to viruses

35
Q

How can viruses interfere with interferon action?

A

1) Stop PRR recognition<br></br>2) Releasing IFN binding factors to prevent their effect<br></br>3) Inhibit JAK-STAT pathway<br></br>4) Block Interferon stimulated genes (ISGs) + block action

36
Q

What cell types do the following viruses cause death to:<br></br><br></br>1) Poliovirus<br></br>2) Rotavirus<br></br>3) HIV<br></br>4) Hep B<br></br>5) Rabies

A

<b>1) Poliovirus</b><br></br>Motor neurons → paralysis<br></br><br></br><b>2) Rotavirus</b><br></br>Gut epithlia → diarrhoea<br></br><br></br><b>3) HIV</b><br></br>CD4 cells → immunodeficiency<br></br><br></br><b>4) Hep B</b><br></br>Hepatocytes → acute hepatitis<br></br><br></br><b>5) Rabies</b><br></br>Purkinje cells (cerebellum) → hydrophobia

37
Q

Where do the following viruses remain latent?<br></br><br></br>1) Hep B<br></br>2) Measles<br></br>3) HSV-1/HSV-2<br></br>4) VZV

A

<b>1) Hep B</b><br></br>Hepatocytes → chronic hepatitis<br></br><br></br><b>2) Measles</b><br></br>Neurons <br></br><br></br><b>3) HSV-1/HSV-2</b><br></br>Neurons → cold sore/genital warts<br></br><br></br><b>4) VZV</b><br></br>Neurons → chicken pox/shingles

38
Q

What cancers do the following viruses induce?<br></br><br></br>1) Hep B<br></br>2) HPV 6,11<br></br>3) HPV 16, 18<br></br>4) EBV<br></br>5) RSV

A

1) Hep B → HCC<br></br>2) HPV 6,11 → wart<br></br>3) HPV 16, 18 → cervical/penile cancer<br></br>4) EBV → B cells → Burkitt’s/nasopharyngeal CA<br></br>5) RSV → chicken sarcoma

39
Q

What factors affect outcome of viral infection?

A

<b>1) Viral dose</b><br></br><b>2) Route of entry</b><br></br><b>3) Age + sex</b><br></br>VZV/EBV/HBV different in different aged people<br></br>HBV = worse prognosis in males<br></br><b>4) Physiological state</b> (of host)

40
Q

What is a superficial viral infection?

A

Viral replication occurs in epithlium at initial infection site<br></br>Does not spread to other tissues<br></br>Outcome = independent of specific immune response

41
Q

Examples of superficial viral infections:

A

1) Common cold<br></br>2) Influenza<br></br>3) Gastroeneritis

42
Q

What is a systemic viral infection?

A

Virus replicates at site of entry but then spreads to other areas<br></br>More severe<br></br>Outcome = dependent on specific immune responses (esp. CTLs)

43
Q

Examples of systemic viral infections:

A

1) Small pox<br></br>2) Chicken pox<br></br>3) Measles<br></br>4) FMDV

44
Q

What are the routes of spread for systemic infections?

A

1) Blood<br></br>2) Lymph<br></br>3) Nerve tracts (rabies)

45
Q

What are the permissive site/cell and latent site for:<br></br><br></br>1) HSV<br></br>2) VZV<br></br>3) CMV<br></br>4) EBV

A

“<div><img></img></div>”

46
Q

What viruses use the following portals of exit:<br></br><br></br>1) Blood<br></br>2) Skin<br></br>3) Alimentary canal<br></br>4) Respiratory system<br></br>5) Saliva<br></br>6) Genital tract<br></br>7) Breast milk<br></br>8) Placenta

A

“<div><img></img></div>”

47
Q

What is more stable, enveloped or non-enveloped virions?

A

Non-enveloped<br></br><br></br>(e.g. picornaviridae spread feco-orally because stable in water)

48
Q

What are the three proteins associated with the lipid membrane of influenza?

A

<b>1) Haemagglutinin (HA)</b><br></br>- Glycoprotein<br></br>- 17 different types<br></br><br></br><br></br><b>2) Neuraminidase (NA)</b><br></br>- Glycoprotein<br></br>- 9 different types<br></br><br></br><b>3) M2</b><br></br>- Ion channel

49
Q

What 3 polypeptides make up the RNA-dependent-RNA polymerase of influenza?

A

1) PB1<br></br>2) PB2<br></br>3) PA

50
Q

How does influenza enter the cell?

A
  1. HA on influenza binds to sialic acid on cell surface<br></br>2. Virion is internalised by endocytosis<br></br>3. Vesicle with virion is acidified ⟶ conformational change in HA ⟶ fusion of virus membrane with endosomal membrane<br></br>4. Nucleocapsid enters the cytosol and is transported to nucleus (where replication takes place)
51
Q

What is the structure of HA?

A

<b>HA = trimeric molecule</b><br></br><b>Each monomer is composed of HA1 + HA2 subunits</b><br></br><br></br><b>H1</b> <br></br>- Globular head<br></br>- Binds to sialic acid<br></br><br></br><b>H2</b><br></br>- Stalk between head and viral membrane<br></br>- Has fusion peptide at N-terminal<br></br><br></br><b>↓pH → H1 moves → exposure of fusion peptide</b>

52
Q

What is NA needed for during new influenza virion release?

A

<b>NA cleaves sialic acid residues from proteins</b><br></br>∵ sialic acid is present over the cell surface, if there was no NA, the virus would just bind back to the cell and be unable to escape<br></br>The NA also removes sialic acid residues from the HA and NA proteins on virions, to <b>prevent aggregation of virions</b><br></br>Drugs that inhibit NA have developed and marketed (tamiflu and Relenza)

53
Q

Anitgenic drift vs antigenic shift:

A

<b>Antigenic drift</b><br></br>- Gradual amino acid mutations in HA<br></br><br></br><b>Antigenic shift</b><br></br>- Radical change to HA<br></br>- Caused by acquiring new HA from another virus<br></br>- Due to reassortment in cell infected by two different viruses

54
Q

What is the Hep B virus surface protein that allows the virus to enter the cell?

A

HBsAg

55
Q

What are prions?

A

Infectious proteins

56
Q

What disease do prions cause?

A

Transmissible spongiform encephalopathies (TSEs)

57
Q

Features of normal PrP :

A

GPI anchored<br></br><b>α helix</b><br></br>Highly conserved<br></br>Binds <b>copper</b><br></br>Glycosylated<br></br>High levels in CNS

58
Q

Features of PrPsc :

A

Very stable<br></br><b>β</b> sheet<br></br>Resistant to protease degradation<br></br>↑ misfolding of normal protein (acts as template for PrP to misfold)

59
Q

What causes conversion of PrP to PrPsc?

A

1) Can occur <b>sponaneously</b> (rare)<br></br>2) Misfolded protein causes normal protein to misfold<br></br>3) Amino acid sequence of protein can influence ease of conversion to misfolded form

60
Q

What are the methods of transmission of prion disease?

A

<b>1) Ingestion of infected material</b><br></br>Cannibal → Kuru<br></br>Infected animal food → BSE in cattle<br></br>Eating infected animals → nvCJD<br></br><b>2) Sporadic cases</b><br></br><b>3) Familial cases</b>

61
Q

What is the natural reservoir for Ebola?

A

Bats

62
Q

What are the different viral proteins in Ebola?

A

“<div><img></img></div>”

63
Q

What is the purpose of soluble glycoprotein in ebola?

A

Soaks up antibodies (has an immunomodulatory effect)

64
Q

What is the subfamily of HIV?

A

Lentivirus

65
Q

What protein forms the capsid of HIV?

A

gag p24

66
Q

What proteins are found in the envelope of HIV?

A

gp120 and gp41

67
Q

How does HIV bind to t cells?

A

gp120 binds to CD4<br></br><br></br>Co-receptors are needed (CCR5 + CXCR4)

68
Q

What are the drugs used for HIV?

A

<b>1) AZT (zidovuline)</b><br></br>- Nucleoside analogue<br></br>- Used by reverse transcriptase → chain termination<br></br><br></br><b>2) Protease inhibitors</b><br></br>Target HIV aspartate protease (needed to cleave gag capsid proteins to mature forms)

69
Q

What is a disadvantage of dead vaccines?

A

Only induce antibody response (no cellular immunity)

70
Q

Mode of action of AZT (Azidothymidine):

A

Thymidine analogue<br></br>Anti-HIV<br></br>Contains no 3’hydroxyl<br></br>Selective to HIV reverse transcriptase

71
Q

Mode of action of acyclovir:

A

• Not phosphorylated by cellular kinases<br></br>• But is phosphorylated by HSV thymidine kinase<br></br>• The nucleotide triphosphate is incorporated into newly synthesised viral DNA by the HSV DNA polymerase<br></br>• Incorporation terminates chain growth

72
Q

Mode of action of oseltamivir phosphate (Tamiflu):

A

• Tamiflu and is an analogue of sialic acid and is active against influenza virus<br></br>• It <b>inhibits the neuraminidase</b> so that influenza virus cannot be released from the infected cell<br></br>• The virus also clumps to itself because HA and NA are glycoproteins.

73
Q

Mode of action of HIV protease inhibitors:

A

• The gag (capsid protein) and pol (reverse transcriptase) genes of HIV are transcribed as a single mRNA and translated to give a single polypeptide chain (polyprotein)<br></br>• During virion assembly the polyprotein is cleaved by the virus-specific protease to yield the capsid protein and the reverse transcriptase<br></br>• Several protease inhibitors have been designed that inhibit the HIV protease, but not host proteases<br></br>• These drugs prevent the completion of virus assembly

MedST IB: Biology of Disease (BoD) (9 decks)

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