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VirusesEdexcel A-Level Biology B: Revision notes

Section 1

Structure and classification of viruses

A virus is a tiny infectious particle, much smaller than a bacterium. It has a core of nucleic acid (DNA or RNA) surrounded by a protein coat called a capsid. Some viruses have an outer envelope made from host membrane. They have no cell surface membrane, cytoplasm, organelles or ribosomes.

Viruses are classified by their structure (the shape of the capsid, and whether there is an envelope) and the type of nucleic acid they contain.

Key termsviruscapsidenvelopenucleic acid

Section 2

Four example viruses

  • Lambda phage: a bacteriophage with a DNA genome, an icosahedral head and a tail. It infects bacteria such as E. coli.
  • Tobacco mosaic virus (TMV): a rod-shaped (helical) capsid around RNA, with no envelope. It infects plants.
  • Ebola virus: a filamentous, enveloped virus with RNA. It infects humans through contact with body fluids.
  • HIV: a spherical, enveloped RNA retrovirus. It carries the enzyme reverse transcriptase, which makes DNA from the viral RNA. The DNA is inserted into the genome of the helper T cells it infects.
Key termsbacteriophageretrovirusreverse transcriptase
Exam tip

Learn the four viruses as a table: nucleic acid, shape, envelope and host.

Section 3

The lytic cycle and latency

In the lytic cycle:

  1. The virus attaches to a specific receptor on the host cell.
  2. Its nucleic acid enters the cell (a phage injects its DNA).
  3. The host's enzymes and ribosomes replicate the viral nucleic acid and make viral proteins.
  4. New virus particles are assembled.
  5. The host cell lyses, releasing many new virus particles.

In latency the viral nucleic acid becomes part of the host genome (lambda phage DNA in the bacterial chromosome; HIV DNA as a provirus). It is copied every time the host cell divides, but no new virus particles are made. A trigger, such as stress or ultraviolet light, can switch it into the lytic cycle.

Key termslytic cyclelatencylysis
Common mistake

Latency is not the virus being dead. The genome is still present and can reactivate.

Section 4

Viruses are not living cells: antivirals

Viruses are not living cells. They have no cell structure and no metabolism, and they cannot reproduce independently, only inside a host cell. Because they use the host's enzymes and ribosomes, antibiotics that target bacterial cell walls or 70S ribosomes have no effect on them.

Antiviral drugs must therefore inhibit virus replication. Examples are reverse transcriptase inhibitors for HIV (such as zidovudine), which stop viral DNA being made. Drugs have to avoid harming host cells, so antivirals are harder to develop than antibiotics.

Key termsantiviralantibiotic

Section 5

Disease control: Ebola in 2014

Viruses are difficult to treat once infection has occurred, so disease control focuses on preventing spread. In the 2014 outbreak in West Africa, Ebola spread by contact with the body fluids of infected people, including the dead. Control measures were:

  • Isolation of patients
  • Contact tracing and monitoring
  • Protective clothing for health workers
  • Safe burials, with community education

These reduced contact with infectious body fluids. No licensed vaccine or antiviral existed at the time.

Key termscontact tracingisolation

Section 6

Ethics of untested drugs in epidemics

During an epidemic with a high death rate, an experimental drug may be offered before clinical trials are complete. To evaluate:

  • For: patients may die anyway, so potential benefit may outweigh risk; it may help to control the epidemic.
  • Against: safety and effectiveness are unknown; harm is possible; informed consent is hard in an emergency; supplies are limited, so who receives it is a fairness issue; a placebo group may be unethical, but without controls evidence is weak.

A balanced answer reaches a justified judgement, for example that giving the drug is acceptable with consent, under monitoring, as part of a trial.

Key termsinformed consentclinical trial

Must know

  • Viruses are classified by structure and nucleic acid: lambda phage (DNA), TMV and Ebola (RNA), HIV (RNA retrovirus)
  • Lytic cycle: attach, inject, replicate using host machinery, assemble, lyse
  • Latency: viral genome in host genome, no new virus particles
  • Viruses are not living cells; antivirals inhibit replication
  • Control of spread, as in the 2014 Ebola outbreak
  • Evaluate ethics of untested drugs using benefits, risks, consent and fairness

That's the notes covered.

Carry on to the next subtopic.

Exam questions on Viruses

  1. Human immunodeficiency virus (HIV) is an enveloped virus that infects helper T cells. Each virus particle contains two molecules of RNA and the enzyme reverse transcriptase. Zidovudine, an antiviral drug, inhibits reverse transcriptase. Penicillin, an antibiotic, has no effect on HIV.
    Explain how zidovudine reduces the replication of HIV.2 marks
  2. Lambda phage is a virus that infects the bacterium Escherichia coli. After infecting a bacterium, the phage can either destroy the cell within about an hour, releasing around 100 new phages, or have its DNA inserted into the bacterial chromosome and copied each time the bacterium divides. After many generations, exposure of the infected bacteria to ultraviolet light causes many of them to burst and release new phages.
    Suggest two advantages to the virus of latency.2 marks
  3. The 2014 outbreak of Ebola virus disease in West Africa spread rapidly through Guinea, Sierra Leone and Liberia. Ebola is an RNA virus spread by contact with the body fluids of infected people, including people who have died of the disease. At that time no licensed vaccine or antiviral drug existed. The response included isolating patients, tracing their contacts, training health workers to wear protective clothing and organising safe burials with community leaders.
    Explain why control of the outbreak focused on preventing the spread of the virus rather than treating infected people.3 marks
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Written by the Exaim team, led by Shaun Daswani (Head of Upper Secondary, Improve ME Institute; MSc Financial Mathematics, Imperial College London; BSc, UCL) and Jason Daswani (operational lead, Improve ME Institute; LSE).