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*B33VPI - Biology & Physiology > Viruses; Structure, Classification, Replication > Flashcards

Viruses; Structure, Classification, Replication Flashcards

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1
Q

What are viruses?

A
  • Small, subcellular (smaller than cells) organisms with an obligate parasitic intracellular lifestyle (can’t survive outside cells for long)
  • Composed of proteins, nucleic acids (DNA or RNA) and sometimes lipids (stealing cell membrane from host)
  • From Latin; ‘poison/slime/vermin’
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2
Q

Are viruses alive?

A
  • Cannot reproduce on their own (non-living criteria), but can do so in living cells and can also affect behaviour of host profoundly
  • Plays a major role in shaping evolution, including humans (not just negative)
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3
Q

How large are viruses?

A

Small af:

  • Viruses: 20-100 nm (Smallpox is big at 300nm)
  • Bacteria: 1 - 10 μm (10,000nm = 10μm)
  • Animal cells: 1 - 100 μm
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4
Q

Where are viruses found?

A
  • Ubiquitous; everywhere (every living organism can host viruses; bacteria, fungi, animals, plants etc.), even other viruses (e.g. mamavirus infected with Sputnik virus)
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5
Q

How many viruses are humans on average infected with?

A
  • At least two different viruses e.g. HSV-1/2, EBV, CMV
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6
Q

Can viruses be transmitted to future generations?

A

Yes, they can become part of the host genome and be transmitted to future generations

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7
Q

Are viruses always bad?

A

1) They play a key role in cycle of life in aquatic environments; maintaining equilibrium
2) Can be used to treat bacterial infections (bacteriophage therapy; confers no resistance)
3) 8% of human genome is of viral origin (retroviruses); shaped our evolution and made us into us (but the 8% has no activity)

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8
Q

WHat are the common features of viruses?

A
  • Viral genomes (DNA or RNA) are packaged into particles (not stable on their own), necessary for transmission between hosts
  • Viral genome contains information needed for replication within permissive host cell (one that allows viral replication)
  • Viral survival esnured by establishing its genome in host cell population
  • All viruses are obligate parasites; they NEED the cellular machinery (ribosomes, tRNA etc.) to replicate themselves
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9
Q

What is one way of classifying viruses? (Shapes)

A

Classified according to their structure and morphology, using the criteria:

  • Absence OR presence of an envelope (enveloped vs. naked viruses; arising from hijacking cell membranes)
  • Shape of the capsid; protein containing viral DNA or RNA, which is either helical or icosahedral
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10
Q

How many faces does an icosahedron have? Why is this shape preferred?

A
  • 20 identical sides; nearest geometrical shape to sphere
  • Spheres have the highest volume/surface ratio; can pack bare nucleic acids w/o too much protein for ‘packaging’
  • Structure can be built from multiple repetitions of a single protein (only one gene required; gene economy, utilising space inside icosahedron capsid)
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11
Q

What are the rules for viral capsid self-assembly?

A

Capsids can self-assemble w/o need for additional proteins if:

1) Each subunit has identical bonding contacts w/its neighbouring proteins; usually achieved by symmetrical assemblies of oligomers (mainly pentamers/hexamers/dimers of a single protein)
2) Proteins are linked together by non-covalent bonds; allowing rapid assembly and disassembly of capsid to release nucleic acid

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12
Q

Why is the capsid needed?

A

1) Provides protection for nucleic acid outside the cell (BUT; needs to be released after entry to host cell too)
> Capsid made from multiple subunits non-covanlently linked (symmetry provides maximal contact between subunits)
> Capsid is metastable ‘spring-loaded’ during assembly; unfolds in cells like ‘bakugan’/Jack in the Box vibes, as conditions change (e.g pH/salt concentration)
2) Provides specific attachment to cell receptors (for naked viruses)

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13
Q

How does the enveloped/non-enveloped nature of viruses affect transmission?

A

Enveloped:
- Sensitive to: dryness, heat, detergents, acids (must stay wet to be transmitted); does not survive in GIT (thus not transmitted by food) e.g. HIV-1

Non-enveloped (much tougher/easier to transmit):
- Resistant to: dryness, heat, detergents, acids, proteases (can remain infective upon drying, transmitted on fomites, survive GIT, and in environment on surfaces) e.g. Adenovirus (cold), Rotavirus (stomach upset)

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14
Q

Define: capsid.

A

Protein shell containing the viral genome (RNA or DNA)

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15
Q

Define: nucleocapsid

A

Capsid containing nucleic acid

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16
Q

Define: capsomer

A

Individual protein molecules which together form the capsid (monomer of capsid)

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17
Q

Define: envelope

A

Lipid bilayer derived from host cells which surrounds the capsid

18
Q

Define: tegument

A

Additional protein layer located between capsid and envelope in some viruses; same as matrix

19
Q

Define: virion

A

A complete, mature infective viral particle outside the cell.

20
Q

What are the distinct steps of the animal virus life cycle?

A
  • Attachment (docking)
  • Penetration
  • Uncoating
  • Transcription (or reverse transcription; generate copies)
  • Biosynthesis
  • Release & Maturation
21
Q

How do viruses attach to host cells?

A

Bind to specific receptors on host cells:

  • HIV-1 to CD4 and CXCR4 (co-receptor) on T-cells and macrophages
  • Rhinovirus to ICAM-1 on nasal epithelium (Intracellular Adhesion Molecule 1)
  • Influenza to sialic acid on respiratory epithelium (hence lung symptoms)
22
Q

What is cell tropism?

A

Where the specific viral attachment to host cells results in a preference for specific cell types/tissues (as well as a specific host range)

23
Q

What is host range? Give examples.

A

The ability of a virus to infect different species:

  • Rabies; wide host range, can infect all mammals
  • HIV; narrow host range, can only infect humans
24
Q

What are zoonotic infections?

A

Diseases which normally affect animals but CAN infect humans; e.g. swine/bird flu, viral haemorrhagic fever.

25
Q

Do viruses have preferred routes of entry? Give examples if so.

A

Yes:

  • Rhinovirus + Influenza = via respiratory tract
  • Rotavirus = via GIT
  • HIV = via genital tract
26
Q

What are meant by non-natural routes of entry?

A

Other routes of entry for virus possible e.g. skin trauma, transplants, blood transfusions/blood products.

27
Q

Where is a common site for viral attachment, and why?

A

Lipid rafts:

  • Special regions of cell membrane rich in cholesterol and sphingolipids
  • More densely packed, rigid regions that are more suitable for stable attachment to cell surface; allowing mechanism of penetration
28
Q

How does penetration and uncoating occur for enveloped viruses?

A
  • Fusion of viral envelope w/host cell plasma membrane
  • Followed by capsid disassembly (uncoating)
    »> Fusion of cell membranes (host - host as envelope is stolen)
29
Q

How does penetration and uncoating occur for non-enveloped viruses?

A
  • Attachment onto specific receptors of cell surface membrane
  • Virus is then endocytosed (in vesicles), and taken into the cell (virus in an endosome - vesicle ting)
  • Protein pumps (ATPase?; ATP > ADP) on endosome pump H+ from cytosol into endosome, dropping pH to 4.5
  • pH-triggered release of capsid (uncoating)
30
Q

What steps are involved in the replication (biosynthesis) of viruses?

A

Hijacking cellular machinery to:

1) Make many copies of nucleic acid
2) Produce viral proteins and enzymes (new capsids etc)
3) Assembly and release of new viral particles

31
Q

How can the virus rely entirely on host cell machinery to replicate itself and reproduce?

A
  • Virus only has small amount of genes

- Thus host cell machinery is adequate

32
Q

What is the eclipse phase of viral infection?

A
  • Where viruses replicate their nucleic acid using host cell machinery to be packaged into new capsids and released
  • Phase begins immediately after virus enters host cell; no signs of the virus can be sign at this phase as no virus present extracellularly at this point (thus no symptoms yet either, viruses busy replicating in host cell)
33
Q

What does the Baltimore scheme of virus classification entail?

A

Classification according to the type of viral nucleic acid transcribed to mRNA:
• Group I - dsDNA (+/-)
• Group II - ssDNA (+; one strand)
• Group III - dsRNA (+/-; RNA can be double strand too)
• Group IV - ssRNA (+)
• Group V - ssRNA (-)
• Group VI - ssRNA (+)
• Group VII - ss/dsDNA (+/-; mixture - complicated)

34
Q

How does assembly occur?

A
  • Happens after production of viral proteins and nucleic acids; need to be assembled into new virions
  • At specific points in the cell (depending on virus)
  • Packaging of nucleic acids into capsid occurs through spontaneous self-assembly process
35
Q

Why is there a maturation stage give assembly’s happened?

A
  • Virus may still be non-infectious at this stage
  • Maturation may involve proteolytic cleavage by viral or cellular processes:
    • HIV gag polyprotein, by HIV protease (viral protease, good target)
    • Influenza A haemagglutinin by transmembrane protease serine 2 (cellular protease; more difficult target)
36
Q

What is budding? Examples of viruses?

A
  • The process where newly assembled viruses are released by the infected cells
    E.g. HIV, influenza, measles
37
Q

Do all cells undergo budding? If not, what do they? Examples?

A

Lytic viruses
- Much more radical than budding off; viruses released when the cell bursts open (and dies in the process)
- ‘Bursters’
E.g. Polio

38
Q

How are viruses spread in the body?

A
  • Via the apical side of the cell (virions exit from the top)
  • From cell-to-cell; via the baso-lateral side (ish) moving between cells e.g. Herpes virus (don’t have to be released; barrier to developing vaccination)
39
Q

How do viruses cause cellular damage?

A

They can cause direct damage to infected cells; cytopathic effects:

  • Cell lysis; cell bursts open to release new virions
  • Cell fusion; several cells are fused together as viruses move from one cell to the neighbouring, resulting in multi-nucleated syncytia (fusion of plasma membranes)
  • Transformation; DNA or RNA tumour viruses may mediate multiple changes that convert a normal cell into a malignant one (oncogenic viruses e.g. leukaemia)
  • DNA damage; following viral infection, breakage, fragmentation, rearrangement (detach and reattach elsewhere) and/or changes in the number of chromosomes may occur (genotoxic effects)
40
Q

What else helps a virus survive?

A

Strength in numbers:
- E.g. typical viral load of HIV is 10^4 virions per mL of blood, with 5L of blood per person, 35 million individuals infected
»> 10^15 HIV genomes in total; there are resistant strains to any of the 20 antiretroviral drugs availible
> Selection occurs w/selection pressure

*B33VPI - Biology & Physiology (8 decks)

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