Viruses lectures Flashcards

1
Q

Size of virus?

A

0.1-0.3 micrometers

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2
Q

What is viral tropism?

A

Each virus affects only 1/ a few cell types

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3
Q

Outside the host cell what are viral particles named?

A

Virons

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4
Q

Draw bacteriophage basic diagram

A

See notes for diagram

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5
Q

What is a lytic virus?

A

It destroys the host cell in its life cycle

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6
Q

What are stages of bacteriophage attack?

A

1) Phage attaches to E. Coli and injects chromosome
2) Bacterial chromosome breaks down
3) Expression of phage genes produces phage structural components
4) Progeny phage assemble
5) Bacterial wall lyses, phage progeny released

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7
Q

Draw HIV

A

See notes for diagram

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8
Q

How does HIV use host PM

A

It bursts out of cell with incorporated receptors for host infection in its viral envelope

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9
Q

What does HIV infect?

A

Lymphocytes (T helper cells) and macrophages with CD4 molecule on surface

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10
Q

What does viral genome code for?

A

Capsid and genome replication and viral protein synthesis in the host cell

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11
Q

How does viral translation work?

A

From RNA sense strand engaging host ribosomal machinery for protein synthesis

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12
Q

How do bacteriphages with double stranded DNA replicate their genome?

A

bacteriophages with ds DNA can replicate genome separately to the host genome, destroying the host genome in the process (bacteriophage can be ss or ds DNA or RNA)

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13
Q

What is the lysogenic cycle? (different to lytic)

A

Bacteriophage viral genome incorporated in the host genome and replicated with the host genome, ensures viral genome propagated by healthy host cell
ssRNA –> dsDNA (via reverse transcriptase) –> genome integrated into host cell (NB reverse transcriptase uses host tRNA as primer)

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14
Q

How are viral genomes economical?

A

HIV encodes many proteins on a single gene transcribed by a single RNA
Translated by host ribosomes as polyproteins which are then broken down by HIV protease into single proteins
Only need 1 promoter
Expression of a few HIV proteins requires alternate splicing of mRNA

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15
Q

How can viral genomes evolve so rapidly?

A

Polymerases and reverse transcriptases for viruses are very low fidelity so virus still replicated even after lots of mutation

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16
Q

What happens in influenza?

A

There is recombination between strands: 8 RNA strands can be shuffled between coinfecting species

17
Q

What are 3 strategies to get the host ribosome to translate sense viral RNA?

A

1) EIF cleavage
2) Cap stealing
3) IRES use
(see notes for details)

18
Q

How many reading frames can viral RNAs have?

A

Many, can promote ribosome skipping between alternate start AUG codons

19
Q

What is HAART?

A

High activity anti-retroviral therapy, in 1990s transformed HIV to a managable chronic disease
Targets HIV reverse transcriptase and HIV protease
Prevents replication, transcription and assembly of the viral genome

20
Q

How can HIV escape therapy?

A

Long phases of molecular quiescence

HIV infected lymphocytes (T helper cells specifically) are quiescent

21
Q

Draw diagram of how HIV gains entry into cell

A

(see notes for diagram)

22
Q

What enzyme allows HIV genetic material to be integrated into the DNA of the infected cell?

A

Integrase

23
Q

How are virons released?

A

Budding from the cell membrane without cell lysis, viral genome in the host cell can be preserved for many years due to quiescence

24
Q

How does HIV cause immunodeficiency?

A

Via continued apoptosis of infected and non-infected T-cells due to immune reaction
(or direct toxicity of viral proteins)

25
Q

Draw diagram of HIV transition between states

A

(see notes for diagram)

26
Q

What are new therapies for HIV trying to do?

A

Transcription of viral genome by host RNA pol 11 depends on HIV protein TAT (Trans-Activator of Transcription)
TAT above threshold= replication cycle
TAT below threshold= latency
New therapies either try to increase TAT variability and get it above threshold
Or dampen