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Biology Core Idea 2 > Viruses > Flashcards

Viruses Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Characteristics of living organisms based on cell theory (7)

A
  1. Cellular organisation
  2. Metabolic activity
  3. Grow and develop
  4. Reproduce
  5. Common hereditary molecule
  6. Respond to stimuli
  7. Adapt to the environment
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2
Q

Why viruses may be regarded as living organisms

A
  1. Possess genetic material and are capable of propagating their genetic information
  2. Once inside host cell it directs host enzymes to carry out metabolic processes
  3. Once inside host cell it directs its own self-replication → reproduce by creating multiple copies through self-assembly
  4. Undergo mutation and reassortment of genetic material during replication → new viral strains
  5. Can react to environment → respond to stimuli like heat
  6. Able to evolve to adapt to new environment
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3
Q

Why viruses may be regarded as non-living organisms

A
  1. Acellular and lack cellular organelles
  2. Do not carry out metabolism
  3. Lack ability to reproduce on their own independently
  4. Do not grow
  5. Do not respond to stimuli outside host cell
  6. Can only evolve within a host cell
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4
Q

Conclusion

A

Viruses are obligate parasites which requires a living host to support many of their functions like metabolism and replication

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5
Q

Obligate parasite

A

Organism that cannot live independently of its host and depends on host to complete its life cycle

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6
Q

Structure of viruses

A
  1. Genome
  2. Capsid
  3. Envelope
  4. General Morphology
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7
Q
  1. Genome
A
  • Single/segmented
  • Circular/linear
  • DNA/RNA → never both
  • Single/double-stranded
  • Codes for synthesis of viral components and enzymes for replication and assembly of virion
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8
Q
  1. Capsid
A
  • Protein coat
  • Surrounds genome
  • Composed of protein subunits (capsomeres)
  • Protect, attach and introduce genome into host cells
  • Nucleocapsid = Capsid + viral nucleic acid
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9
Q
  1. Envelope
A
  • Surrounds nucleocapsid
  • Lipid bilayer → phospholipids + glycoproteins
  • Derived from host cell membranes via budding
  • Virus incorporates its own glycoprotein spikes
  • Naked/non-enveloped vs enveloped
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10
Q
  1. General Morphology (4)
A
  • Shape
  • Type and structure
  • Presence/absence of viral envelope
  • Mode of replication
  1. Helical (Tobacco mosaic virus)
  2. Icosahedral (Adenoviruses)
  3. Enveloped (Influenza, HIV)
  4. Complex (T4 bacteriophage)
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11
Q

Viral replication

A
  • Virus has specific host, recognised via host cell antigen (Attachment)
  • Virus genetic material injected into host cell or entire virus may enter and disassemble to free genetic material (Penetration)
  • Virus takes over host cell metabolic machinery and resources to synthesise its own nucleic acid
  • Viral genome codes for viral structural components like capsid protein and viral enzymes (Replication)
  • Self-assembly into new virions (Assembly)
  • Exit cell via budding, exocytosis or lysis (Release)
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12
Q

Viral replication steps (5)

A
  1. Attachment → Virus recognises and attaches to host cell
  2. Penetration → Viral genome introduced into host cell
  3. Replication → Synthesis of viral components
  4. Maturation → assembly of complete viruses
  5. Release
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13
Q

Bacteriophages (2)

A
  1. Lytic bacteriophages (T4 phage) → lytic life cycle

2. Temperate bacteriophages (Lambda phage) → lytic + lysogenic cycle (prophage)

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14
Q

T4 Bacteriophage Structure

A

Genome (ds DNA)

Protein coat = Icosahedral capsid head + contractile sheath

Collar core
Tail
Base plate
Tail fibres
Tail pins
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15
Q

Lambda Bacteriophage Structure

A

Genome (ds DNA)

Protein coat = Capsid + Contractile Sheath

Icosahedral head
Tail
Tail fibre

Can replicate by lytic life cycle or incorporate DNA into bacterium’s DNA and become non-infectious prophage

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16
Q
  1. Attachment (Lytic) (1)
A
  1. Attachment sites on tail fibres adsorbs to complementary receptor sites on bacterial surface (e.g. E.coli), via weak bonds → viral specificity
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17
Q
  1. Penetration (Lytic) (4)
A
  1. Bacteriophage releases lysozyme which digests bacterial cell wall
  2. This allows the release of molecules from the bacterium which triggers a change in shape of the proteins in the base plate which causes the contraction of tail sheath which will drive the hollow core tube through cell wall
  3. When the tip of the hollow core tube reaches the plasma membrane, phage DNA is injected into the bacterial cell
  4. The empty capsid remains outside
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18
Q
  1. Replication (Lytic) (5)
A
  1. DNA is immediately transcribed to synthesise mRNA using host RNA polymerase
  2. Host cell macromolecular synthesising machinery is used to synthesise phage proteins
  3. Early phage proteins: degrade host DNA
  4. Phage DNA synthesised using host cell nucleotides and early proteins
  5. Late phage proteins: are phage enzymes and structural components
19
Q
  1. Replication (Lysogenic) (7)
A
  1. Linear phage DNA circularises and inserted into host cell genome by enzyme integrase
  2. Integrated phage DNA is known as a prophage
  3. Expression of phage genes is repressed by phage repressor proteins → new phages are not synthesised
  4. Prophage replicates along with bacterial chromosome (latent)
  5. During spontaneous induction, cellular proteases are → destroy repressor proteins
  6. Prophage excised from bacterial genome
  7. The replication phase of lytic cycle then occurs
20
Q
  1. Maturation (Lytic) (2)
A
  1. Phage DNA and capsid assemble into a DNA-filled head
  2. Head, tail and tail fibres assembled independently and join in a specific sequence.

(Tail fibres + tail) + (DNA + capsid)/DNA-filled head

21
Q
  1. Release (Lytic)
A
  1. Phage lysozyme synthesised within the cell breaks down the bacterial cell wall
  2. Bacterial cell membrane lyses and release the newly formed virions
22
Q

Animal viruses (2)

A
  1. Influenza virus

2. HIV (Retrovirus)

23
Q

Influenza virus Structure (3)

A
  1. Genome
  2. Capsid
  3. Envelope → glycoproteins (haemagglutinin - 80% and neuraminidase - 20%)
24
Q

Influenza genome (4)

A
  1. (-) strand RNA → complementary to mRNA
  2. 8 different segments of ssRNA associated with helical nucleoproteins
  3. Each with 3 polymerase proteins → RNA-dependent RNA polymerase → replicates and transcribes viral genome
  4. Other 5 segments code for haemagglutinin, neuraminidase, nucleoprotein, matrix protein M1 and non-structural proteins
25
Q
  1. Attachment (Influenza) (1)
A
  1. Haemagglutinin binds to complementary sialic acid receptor on host cell (e.g. epithelial cells in respiratory tract) membrane
26
Q
  1. Penetration (Influenza) (3)
A
  1. Virus enters host cell by endocytosis (the process involves invagination of membrane)
  2. Endocytic vesicle/endosome fuses with lysosome → lowers the pH → causes viral envelope to fuse with lipid bilayer of vesicle → nucleocapsid released into cytosol
  3. Capsid degraded by cellular enzymes and the 8 viral RNA segments released into cytosol and enter the nucleus
27
Q
  1. Replication (Influenza) (3)
A
  1. Viral RNA-dependent RNA polymerase uses viral genome as a template to synthesise mRNA
  2. mRNA enters cytosol → translated into viral structural components → capsid proteins (cytosol), envelope glycoproteins (RER) eventually embedded in host cell membrane
  3. mRNA can also act as template for synthesis of new viral RNA genome in the nucleus. Viral RNA genome then exits nucleus
28
Q
  1. Maturation (Influenza) (3)
A
  1. Capsid proteins associate with host cell membrane where viral glycoproteins are inserted
  2. Nucleoproteins associate with the RNA genome and then interact with capsid proteins that have associated with the glycoproteins embedded on the plasma membrane
  3. This initiates the budding process
29
Q
  1. Release (Influenza) (2)
A
  1. Newly formed viruses bud off by evagination, acquiring host cell membrane with embedded viral glycoproteins
  2. Neuraminidase facilitates the release of the new virions from the host cell membrane by cleaving sialic acid from the host cell receptor
30
Q

HIV Structure (3)

A
  1. Genome
  2. Capsid
  3. Envelope → glycoproteins (gp120 attached to gp41)
31
Q

HIV Genome

A
  1. (+) strand RNA → same sequence as mRNA
  2. 2 identical copies of ssRNA bound to nucleocapsid proteins
  3. Gag → structural proteins, Pol → viral enzymes, Env → glycoproteins
32
Q

HIV Capsid

A
  • Conical shape
  • 2 molecules of reverse transcriptase
  • Integrase and protease
  • Forms virus core with viral genome
33
Q
  1. Attachment (HIV) (1)
A
  1. gp120 binds to complementary CD4 receptors on T helper cells or (macrophages) with the help of a co-receptor
34
Q
  1. Penetration (HIV) (2)
A
  1. With the help of gp41, the viral envelope fuses with host cell membrane → nucleocapsid is released into cytosol

But can also enter via endocytosis

  1. Capsid degraded by cellular enzymes → the 2 viral RNA strands and enzymes released into the cytosol
35
Q
  1. Replication (HIV) (5)
A
  1. Reverse transcriptase makes DNA strand using viral RNA as template to form a DNA-RNA hybrid → RNA is then degraded and the 2nd DNA strand is made → double-stranded DNA molecule produced
  2. Viral DNA enters nucleus → inserted into host cell genome by integrase → Viral DNA known as provirus → can remain latent for a long time
  3. Upon activation, viral DNA transcribed to viral RNA which enters cytosol
  4. Viral RNA can either act as mRNA and be translated into proteins or become part of the genome of the new virions
  5. mRNA is translated to viral polyproteins or envelope glycoproteins gp120 and gp41 in the RER and eventually are embedded in the host cell surface membrane.
36
Q
  1. Maturation (HIV) (1)
A

For HIV, maturation is completed only after release of virus

  1. viral RNA genome and polyprotein assembles at the cell surface membrane where viral glycoproteins have been inserted
37
Q
  1. Release (HIV) (4)
A
  1. Newly formed viruses bud off by evagination, acquiring host cell membrane with embedded viral glycoproteins
  2. Viral protease cleaves polyproteins, forming viral enzymes and proteins
  3. The viral RNA genome and enzymes are then encapsulated by a protein coat to form a capsid
  4. The mature HIV virus (virion) is now able to infect neighbouring cells
38
Q

Antigenic Drift

A
  • Minor antigenic change → new strain
  • New strains of viruses are formed as a result of accumulation of point mutations of the genome leading to the changes in the ribonucleotide sequence
  • As a result of the lack of proof reading ability of RNA-dependent RNA polymerase in influenza and fast/high rate of replication of the virus
  • Viral RNA is single stranded thus does not have backup copy to carry out repair mechanism
  • Gives rise to changes in the conformations of the glycoproteins/modified surface antigens
39
Q

Antigenic Shift

A
  • Major antigenic change → new subtype
  • a) change in host species (e.g. bird to human), b) genome reassortment between different subtypes.
    a) could result from accumulation of mutations or genome reassortment
    b) when two or more strains of influenza viruses infect a common/same host cell where:
  • Reassortment of the different RNA segments occur resulting in recombination of genetic material in a virion
  • New combination of haemagglutinin an neuraminidase at the viral envelope
40
Q

Pathogenecity of Influenza

A
  • Bind to sialic acid receptors on epithelial cells of respiratory tract
  • Replicates within it and then buds off → infected epithelial cells eventually lyse
  • Build up of dead epithelial cells results in inflammation and symptoms of influenza appear → runny nose and scratchy throat
  • Epithelial layer weakens and the individual is more susceptible to bacterial infections like pneumonia
41
Q

Treatment of Influenza

A
  1. Antibiotics for bacterial infections
  2. Antiviral drugs which target viral enzymes i.e enzyme inhibitors

e.g: Tamiflu for some strains of influenza

42
Q

Pathogenecity of HIV

A
  • Binds to CD4 receptor on a T helper cell, a type of T lymphocyte
  • Replicates within it and then buds off → infected T helper cells eventually lyse.
  • With fewer T helper cells, immune system is depressed and individuals are more susceptible to opportunistic infections
  • When infections become unmanageable → AIDS → death
  • Virus able to avoid detection by immune system as it mutates at a high rate during replication → surface proteins altered → prevent recognition and elimination by immune system
43
Q

Treatment of HIV

A

Drug cocktail that targets:

  1. Enzymes (RIP) i.e. enzyme inhibitors
  2. Glycoproteins (gp120) i.e. entry inhibitors

Biology Core Idea 2 (9 decks)

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