viruses Flashcards

1
Q

Give reasons why viruses are considered living and non-living

A

Living:
1. they contain genetic material

non-living:

1) acellular&lack cellular organelles and they
2) do not carry out metabolism (e.g. respiration).
3) are unable to reproduce independently
4) are unable to respond to stimuli(such as radiation)and
5) are unable to mutate hence adapt to new environments unless in a living host cell.

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2
Q

list 3 definitive characteristics of a virus

A
  1. they are obligate parasites, they are totally dependent on a host cell for replication
  2. the genome is made up of only 1 type of nucleic acid: DNA or RNA but never both
  3. viral components must assemble into complete viruses to be able to infect another cell
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3
Q

Structure of the T4 Phage and Lambda Phage

A
  1. genome: double stranded DNA
  2. capsid: icosahedral capsid head
  3. envelope: absent
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4
Q

Structure of the influenza virus

A
  1. Genome (-) strand RNA
    - -> viral genome is complementary to viral mRNA
    - 8 different segments of ss RNA associated with nucleoproteins
    - Each RNA segment is packed with 3 polymerase proteins which comes together to form an RNA-dependent RNA polymerase enzyme complex which replicates and transcribes the viral genome in the host cell
  2. Capsid: present
  3. envelope: glycoproteins - haemagglutinin (80%) and neuraminidase (20%)
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5
Q

Structure of the HIV virus

A

genome (+) strand RNA
→ viral genome has the same sequence as viral mRNA
▪2 identical copies of single stranded RNA bound to nucleocapsid proteins

capsid: present; conical shaped
enzymes : reverse transcriptase, integrase and protease found in capsid

envelope: glycoproteins - gp120 and gp41 embedded in it

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6
Q

Describe the attachment and penetration stage of the T4 phage/ lambda phage

A
  1. Attachment sites** on tail fibres adsorbs** to complementary** receptor sites on bacterial surface(e.g. E.coli)
  2. Bacteriophage releases lysozyme** which digests bacterial cell wall*
    ▪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**
    ▪When the tip of the hollow core tube reaches the plasma membrane, phage DNA is injected into the bacterial cell
    ▪The empty capsid remains outside
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7
Q

Describe the replication stage of the t4 phage undergo the lytic cycle

A

Host cell macromolecular synthesising machinery** is used to synthesise phage proteins

▪Early phage proteins**: degrade host DNA
▪Phage DNA synthesised using host cell nucleotides and phage proteins

▪Late phage proteins**: are phage enzymes and structural components

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8
Q

Describe the replication stage of the lambda phage undergoing the lysogenic cycle

A

Linear phage DNA circularises** and inserted** into host cell genome** by enzyme integrase**

▪The integrated phage DNA is known as a prophage***

▪Expression of phage genes is repressed by phage repressor proteins***. Hence new phages are not synthesised

▪Prophage replicates along with bacterial chromosome

▪During spontaneous induction*, cellular proteases are activated. They destroy the repressor proteins

▪The prophage is then excised from the bacterial genome

▪The replication phase of lytic cycle then occurs

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9
Q

Describe the maturation stage of lytic/lysogenic cycle and the subsequent release

A

▪Phage DNA and capsid assemble into a DNA-filled head

▪Head, tail and tail fibers assembled independently & join in a specific sequence.

(release)
Phage lysozyme synthesised within the cell breaks down the bacterial cell wall

▪Bacterial cell membrane lyses and release the newly formed virions

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10
Q

Describe the attachment and penetration stage of the influenza life cycle

A
  1. Haemagglutinin recognises and binds* to specific complementary sialic acid receptor on host cell (e.g. epithelial cells in respiratory tract) membrane

(penetration)
2. Virus enters host cell by endocytosis** (which involves invagination** of membrane)
3. Endocytic vesicle fuses with lysosome
➔which lowers the pH
➔causes viral envelope to fuse with lipid bilayer of vesicle
➔nucleocapsid is released into cytosol

(uncoating/ degradation of capsid)

  1. Capsid degraded by cellular enzymes
    - 8 viral RNA segments that are released into cytosol enter the nucleus***
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11
Q

Describe the replication stage of the influenza life cycle

A

Viral RNA-dependent RNA polymerase uses viral genome as a template to synthesise mRNA

mRNA

  1. enters cytosol** ➔ translated into viral structural components **
    - Capsid proteins are made by ribosomes in the cytosol.
    - Envelope glycoproteins are made in the RER & eventually are embedded in host cell membrane

2.can also act as template*
for synthesis of new viral RNA genome
in the nucleus. RNA-dependent RNA polymerase
CATALYSES THIS REACTION. Viral RNA genome then exits nucleus.

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12
Q

Describe the maturation stage of the influenza life cycle and its subsequent release

A
  • capsid proteins associate with host cell membrane where viral glycoproteins are inserted
  • nucleoproteins associate with the RNA genome and then interact with the capsid proteins that have associated with the glycoproteins embedded on the plasma membrane
  • this initiates the budding process

(release)
- newly formed viruses bud off * by evagination, acquiring host cell membrane with embedded glycoproteins
- neuraminidase
facilitates the release** of the new virions from the host cell membrane by cleaving sialic acid from the host cell receptor

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13
Q

Describe the attachment and penetration of the HIV life cycle

A
  1. gp120 recognises & binds** to complementary* CD4 receptors on T helper cells*** or (macrophages) with the help of a co-receptor.

(penetration)
2. With the help of gp41, the viral envelope FUSES* with host cell membrane***
➔nucleocapsid is released into cytosol

(uncoating/ degradation of capsid)
Capsid degraded by cellular enzymes➔the 2 viral RNA strands and enzymes are released into the cytosol***

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14
Q

Describe the replication stage of the HIV life cycle

A

▪Reverse transcriptase*** makes DNA strand using viral RNA as template to form a DNA-RNA hybrid.
The RNA is then degraded and the 2nd DNA strand is made
➔double-stranded DNA molecule produced

▪Viral DNA ENTERS NUCLEUS **
➔inserted into host cell genome by integrase

➔Viral DNA known as provirus**
➔can remain latent** for a long time

▪Upon activation, viral DNA transcribed to viral RNA which ENTERS CYTOSOL*
▪Viral RNA can either act as mRNA and be translated into proteins or become part of the genome of the new virions

▪mRNA

  1. is translated to viral polyproteins**
  2. is translated into envelope glycoproteins gp120** and gp 41** in the RER and eventually are embedded in the host cell surface membrane.
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15
Q

Describe the maturation and release of the HIV virus

NOTE: for HIV, maturation is completed only AFTER release of virus

A
  • The viral RNA genome and polyproteins assembles at the cell surface membrane where viral glycoproteins have been inserted.

(Release)
▪Newly formed viruses bud off**** by evagination, acquiring host cell membrane with embedded viral glycoproteins

▪Viral protease** cleaves polyproteins, forming viral enzymes and proteins*
▪The viral RNA genome and enzymes are then encapsulated by a protein coat to form a capsid**.
▪The mature HIV virus (virion) is now able to infect neighbouring cells.

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16
Q

Describe antigenic drift

A

When the influenza virus replicates in its host cell, mutations frequently occur
due to the
1) poor proofreading mechanism*** of the viral RNA-dependent RNA polymerase and

2) the fast replication rate*** of the virus.

Over time, there is an accumulation of mutations* in the viral genome.
Sometimes, these mutations produce viruses with MODIFIEDsurface antigens
(e.g. glycoproteins such as haemagglutinin or neuraminidase) with different conformation**.

If these viruses infect a host that does not have the antibodies that recognise these modified surface antigens, the host becomes susceptible the virus.

17
Q

Describe antigenic shift

(Note: As long as the species barrier is crossed, antigenic shift is said to have occurred. It may or may not involve genetic reassortment.)

A

When a bird strain of influenza A and human strain of influenza A (2 or more different strains) infect a SINGLE CELL** of an INTERMEDIATE HOST** (e.g.a pig), GENETIC REASSORTMENT** can occur. Thus when new viruses are assembled in the host cell, a new combinations of RNA segments can come together.**

Sometimes, genetic reassortment produces viruses with NEWsurface antigens**(e.g. glycoproteins such as haemagglutinin or neuraminidase).

If these viruses infect a human host, the host becomes susceptible to the virus, as the host will not have the antibodies that recognise these NEW*surface antigens,

18
Q

Explain the change that took place to allow the avian virus to adapt to infect human cells [2m]

A
  1. Antigenic shift** occurred with accumulation of mutations** thus enabling a bird strain of influenza A to jump directly from a bird to humans
  2. Mutation in haemagglutinin*** –> changed the structure –> able to bind more effectively to sialic acid receptor
  3. neuraminidase*** –> more precise active site to better cleave sialic acid which facilitates the release of virions
19
Q

How does genetic reassortment occur? [2m]

A
  1. 2 virus (1 avian and 1 human) infected the SAME CELL**;
  2. Antigenic shift* occurred where the RNA segments from the 2 different influenza virus packaged into the same virion/viral particle, giving rise to new combinations of RNA segments* resulting in new combination of glycoproteins in the novel virus
20
Q

State whether the rabies virus is a naked virus or an enveloped virus?

A

take note of the keyword

  1. Enveloped, presence of HOST-DERIVED** lipid bilayer envelope around the virus
21
Q

Explain why it is necessary for the viral RNA to enter the host cell nucleus? [3m]

take note of point 2

A

1.For transcription** where the viral genome RNA** is used as a template(!!!!!) to synthesise the mRNA strands catalysed by the viral RNA dependent RNA polymerase**

*****2. Using the host cell’s ribonucleotides (and ATP), which is abundant in nucleus, for its synthesis

  1. mRNA can be transported into cytosol as a template***for translation of viral proteins
  2. which in turn acts as a template** for the replication of new viral RNA genome
22
Q

Describe the role of viral DNA in the infection process of the T4 bacteriophage

A
  1. viral DNA codes for enzymes and structural components of phage which are important for infection of bacterial cell
  2. enzyme hydrolyse the DNA at host cell to nucleotides which can be used by host DNA polymerase to replicate viral DNA
  3. enzyme lysozyme which is released by phage to digest bacterial cell wall –> triggers lysis of host cell for release of new virions/ infection of viral DNA
  4. phage proteins–> form tail fibres –> recognises and bind to complementary receptors on surface of bacterial cells
  5. phage proteins –> form the base plate –> change shape in response to molecule released upon contraction
23
Q

Why is HIV described as a retrovirus?

A
  1. A retrovirus is a RNA virus that duplicate via reverse transcription in the host cell;
  2. using the RNA genome as a template, reverse transcriptase** produce DNA from its RNA genome by complementary base pairing;
24
Q

Viruses such as influenza rapidly accumulate gene mutations.

Explain the advantage of this to the virus. [2]

A
  1. Rapid mutations results in antigens like haemagglutinin and neuraminidase having a different conformation;
  2. Thus cannot be recognised by memory** T and B cells of the immune system immune cells;
  3. So it takes a longer time to remove the virus from the body allowing them opportunity to replicate;
25
suggest why it is sufficient for bacteriophages to contain only DNA for their reproductive cycle?
1. host cells have RNA pol which transcribes phage DNA into phage mRNA 2. host cells have ribosomes for translation of phage mRNA into phage proteins required for maturation
26
common qn: with ref to the reproductive cycle of temperate phages, explain why the number of phages increased after a brief UV irradiation
1. induction triggered by the uv irradiation which activates proteases which destroy the repressor protein 2. and this cause a switch from lysogenic cycle to lytic cycle causing the prophage to be excised from the bacterial chromosome DNA 3. since the phage genome is no longer repressed, phage components are produced using the host cell machinery such as DNA pol to transcribe viral DNA 4. lysis** of host cells occur to release bacteriophages resulting in the increase in the number of phages
27
common qn: explain why bacteriophage infection may be beneficial to bacteria population [3m]
1. a small segment of bacterial DNA may be excised together with the prophage 2. Transduction** occurs when the resulting transducing phages infect other bacteria and the newly infected cell acquires the original bacterial DNA 3. transduction increases genetic variation which will increase the adaptability of the bacteria to changes in environment
28
Qn: describe the role of viral DNA in the infection process of the T4 Bacteriophage [3m]
1. Viral DNA codes* for / is transcribed and translated* to produce enzymes *and structural components* of phage which are important for infection of bacterial cell. 2. Enzymes hydrolyse the DNA of host cell to nucleotides* which can be used by host DNA polymerase to replicate viral DNA*. 3. Enzyme lysozyme*** which is released by phage to digest bacterial cell wall to trigger lysis of host cell for release of newly formed virions / to trigger injection of viral DNA into host cell 4. phage proteins which form tail fibres*** which can recognise and bind to receptors on surface of bacterial cell 5. phage proteins which form base plate*** which can change shape in response to molecules released from bacterial cell to cause contraction of contractile sheath for injection of viral DNA.
29
Qn: Suggest the advantages of the lysogenic pathway to the lambda phage virus [2]
1. Via the lysogenic pathway, the lambda phage DNA is integrated into the bacterial DNA forming a prophage* 2. every time the host cell’s machinery replicates the bacterial chromosome, it also replicates the prophage DNA along with it 3. This allows continuous replication of the lambda phage DNA/prophage without killing the host bacteria.