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What are viruses, and how do they replicate inside host cells?

The structure of viruses, why they are non-cellular, the lytic and lysogenic cycles, the replication of HIV as a retrovirus, and how viruses cause disease.

A CCEA A-Level Biology answer on the structure of viruses, why they are non-cellular, the lytic and lysogenic replication cycles, the replication of HIV as a retrovirus, and how viruses cause disease.

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  1. What this dot point is asking
  2. Virus structure
  3. Replication cycles
  4. HIV as a retrovirus
  5. Examples in context
  6. Try this

What this dot point is asking

CCEA wants you to describe the structure of a virus, explain why viruses are not classed as living cells, describe the lytic and lysogenic cycles, outline how HIV replicates as a retrovirus, and explain how viruses cause disease.

Virus structure

Viruses are extremely small, typically 2020 to 300 nm300\ \text{nm}, so they can only be seen with an electron microscope. They are not classed as living because they cannot carry out metabolism or reproduce on their own; they are obligate intracellular parasites that must hijack a host cell's enzymes, ribosomes and energy. Because they lack their own metabolism, antibiotics (which target bacterial processes) have no effect on viruses, which is why viral infections need antiviral drugs or vaccines instead.

Replication cycles

The lytic cycle is fast and immediately destructive, producing symptoms quickly. The lysogenic cycle allows the virus to hide for long periods, which is why some viral infections (such as cold sores caused by herpes simplex) can recur, flaring up only when the latent provirus is reactivated.

HIV as a retrovirus

HIV is a retrovirus: its genetic material is RNA, and it carries the enzyme reverse transcriptase. After its attachment proteins bind to CD4 receptors on a helper T cell, the virus enters and reverse transcriptase makes a DNA copy of the viral RNA. This DNA integrates into the host genome and may stay latent. When activated, the host cell transcribes and translates the viral genes, making new virus particles that bud off, destroying helper T cells over time. As helper T cell numbers fall, the immune system can no longer coordinate a response, and the person develops AIDS, becoming vulnerable to opportunistic infections such as tuberculosis and rare cancers.

Examples in context

Example 1. Why flu vaccines change each year. Influenza is an RNA virus whose surface proteins mutate rapidly (antigenic drift), because RNA replication has no proofreading. Each year the surface antigens differ enough that memory cells from last year's infection or vaccine no longer recognise them, so a new vaccine must be made. This illustrates how a virus's simple, error-prone replication shapes public health strategy.

Example 2. Bacteriophages and the lysogenic cycle in cholera. Some bacteria become dangerous only because a virus has integrated into their genome. The cholera toxin gene is carried by a bacteriophage that, in the lysogenic cycle, integrates into Vibrio cholerae as a provirus. The bacterium then produces the toxin that causes severe diarrhoea. This shows the lysogenic cycle in action and how a virus can change the properties of its host.

Try this

Q1. Give two reasons why viruses are not classed as living cells. [2 marks]

  • Cue. No cytoplasm, organelles or metabolism; cannot reproduce without a host cell.

Q2. Explain the role of reverse transcriptase in HIV replication. [2 marks]

  • Cue. It catalyses the synthesis of DNA from the viral RNA template so the genome can integrate into host DNA.

Q3. Suggest why antibiotics are not effective against viral infections. [2 marks]

  • Cue. Antibiotics target bacterial structures and metabolism (cell walls, ribosomes); viruses are non-cellular and use the host's machinery, so there is no such target.

Exam-style practice questions

Practice questions written in the style of CCEA exam questions on this dot point, with worked answer explainers. The year tag is the paper they imitate, not the source.

CCEA 20196 marksDescribe the structure of HIV and explain how it replicates inside a host helper T cell.
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A 6-mark answer needs the structure and the ordered replication steps including reverse transcriptase.

Structure: HIV has two single strands of RNA, the enzyme reverse transcriptase, a protein capsid, and a lipid envelope studded with attachment proteins (such as gp120).

Attachment: the attachment proteins bind to receptors (CD4) on a helper T cell, and the virus enters the cell.

Reverse transcription: reverse transcriptase makes a single strand of DNA from the viral RNA, then a complementary strand, giving double-stranded DNA.

Integration: this viral DNA is inserted into the host genome (as a provirus), where it may stay latent.

Replication and assembly: the host cell transcribes and translates the viral genes, making new viral RNA and proteins, which assemble into new virus particles that bud off, taking some host membrane as their envelope.

Markers reward the named structure, the role of reverse transcriptase, integration, and budding of new viruses.

CCEA 20214 marksCompare the lytic cycle and the lysogenic cycle of a virus.
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A 4-mark compare answer needs matched points of difference and a similarity.

In the lytic cycle, the virus immediately takes over the host: it injects its nucleic acid, the host makes many new viruses, and the cell bursts (lyses) to release them, killing the host cell.

In the lysogenic cycle, the viral nucleic acid integrates into the host DNA as a provirus and is copied silently each time the host cell divides, without killing it, until a trigger later switches it to the lytic cycle.

Similarity: both ultimately use the host cell's machinery to make new virus particles.

Markers reward the immediate destruction in the lytic cycle, integration and dormancy in the lysogenic cycle, and the shared dependence on the host.

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