Key Idea: Topic A2.3 is the HL-only study of viruses — tiny, non-cellular infectious particles. A virus is essentially a nucleic-acid genome inside a protein coat, with no cytoplasm, no ribosomes and no metabolism of its own. Because it cannot make copies of itself, every virus is an obligate intracellular parasite: it must get inside a living host cell and hijack that cell's machinery to replicate. The topic builds from structure (1.5.1) to the two ways a virus can replicate — the lytic cycle (1.5.2) and the lysogenic cycle (1.5.3) — then to the special case of retroviruses like HIV that run their genetic information backwards (1.5.4), and finally to where viruses came from and why they evolve so fast (1.5.5). It is tested on Paper 1 (label-the-virus and identify-the-step MCQs) and on Paper 2 (the 'outline the lytic cycle' / 'explain how HIV replicates' extended-response questions).
🦠 Structure & diversity of viruses (1.5.1)
Every virus shares the same minimum plan: a genome of nucleic acid wrapped in a protein capsid made of repeating capsomere sub-units. Some viruses add a lipid envelope (taken from a host membrane) studded with glycoprotein spikes that let them attach to host cells. Within that plan the variety is enormous — the genome can be DNA or RNA, single- or double-stranded, and the capsid can be helical, icosahedral, or complex like a bacteriophage. What never varies: a virus has no cytoplasm, no ribosomes and no metabolism, so it is non-cellular and can only replicate inside a host — an obligate intracellular parasite.
The shared body plan of this whole topic. Every virus is just a nucleic acid GENOME (DNA or RNA) packed inside a protein CAPSID built from repeating capsomere sub-units. A bacteriophage (left) has a polyhedral head and a tail with fibres that anchor to a bacterium; an enveloped virus (right) wraps its capsid in a lipid ENVELOPE stolen from the host membrane and studded with glycoprotein SPIKES for attaching to host cells. No cytoplasm, no ribosomes, no metabolism — non-cellular.
🔒 Interactive diagram
Explore the labelled diagram, charts and maps for this topic in study mode.
| Part | Made of | What it does |
|---|---|---|
| Genome | Nucleic acid — DNA or RNA, single- or double-stranded | Carries the viral genes; only this is needed to take over a host |
| Capsid | Protein sub-units called capsomeres | Protects the genome and helps attach to a host cell |
| Envelope (some viruses) | Lipid membrane taken from the host cell | An extra outer coat around the capsid |
| Spikes (enveloped viruses) | Glycoproteins set in the envelope | Bind specific receptors so the virus can attach to and enter a host |
| Way viruses differ | Examples of the range |
|---|---|
| Genome chemistry | DNA viruses vs RNA viruses; single-stranded vs double-stranded |
| Capsid shape | Helical (rod), icosahedral (20-sided ball), complex (bacteriophage with head + tail) |
| Envelope | Naked (capsid only) vs enveloped (lipid coat from the host) |
| Size | From tiny (~20 nm) to large (~300 nm) — all far smaller than a bacterium |
Every virus = G-C at minimum: a Genome in a Capsid. Add an envelope + spikes and you get the 'enveloped' type. The spikes are the key that fits the host's lock (receptor) — they decide which cells a virus can infect.
💥 The lytic cycle (1.5.2)
The lytic cycle is the fast, destructive way a virulent phage replicates: it gets in, makes lots of copies straight away, and bursts the host open to release them. The five steps — attachment, entry, replication/synthesis, assembly, lysis & release — are a classic Paper 2 'outline the cycle' question, so learn them in order. The key idea is hijacking: the virus brings only its genome (and sometimes a few enzymes); everything else — ribosomes, nucleotides, enzymes, ATP — is borrowed from the host.
The lytic cycle in five steps
- Attachment — the virus binds a specific receptor on the host surface; this specificity sets the virus's host range.
- Entry — the viral genome enters the cell (a phage injects its DNA through its tail).
- Replication & synthesis — the host's machinery (enzymes, ribosomes, nucleotides, ATP) is hijacked to copy the genome and make capsid proteins.
- Assembly — the copied genomes and new capsids self-assemble into many complete virions.
- Lysis & release — the cell bursts open, killing it and freeing the new viruses to infect more cells.
Attachment only works if the virus's spikes (or tail fibres) match a specific receptor on the host. That lock-and-key fit is why a virus can only infect certain cells or species — its host range. It is also why a mutation in the spike can let a virus jump to a new host.
😶🌫️ The lysogenic cycle & temperate phages (1.5.3)
A temperate phage has a second option: instead of lysing the cell at once it can enter the lysogenic cycle. Its DNA integrates into the host chromosome as a prophage and simply hides there. Now it is copied passively every time the host divides, so it is inherited by every daughter cell — but no new virus is made and the host is not harmed. The prophage stays dormant until induction (stress, UV, DNA damage), when it excises and switches to the lytic cycle. So lysogeny is a latent strategy that can turn destructive later.
The lysogenic cycle of a temperate phage
- A temperate phage infects but does not lyse the cell straight away.
- Its DNA integrates into the host chromosome as a prophage.
- The prophage is copied passively every time the host divides, so it ends up in all daughter cells — no new virus is made, no host is killed.
- It stays dormant until induction by stress (UV light, DNA damage, chemicals).
- On induction the prophage excises from the chromosome and switches to the lytic cycle, killing the host and releasing virions.
| Feature | Lytic cycle | Lysogenic cycle |
|---|---|---|
| What happens to the genome | Copied immediately to make new viruses | Integrates into the host chromosome as a prophage and lies dormant |
| Fate of the host cell | Killed — burst open (lysis) to release virions | Survives; keeps living and dividing normally |
| New virus made now? | Yes — many virions released straight away | No — none made while latent |
| How it spreads | Horizontally — new virions infect nearby cells | Vertically — copied into every daughter cell when the host divides |
| Speed | Fast | Slow / latent until induced |
| Phage type | Virulent phage | Temperate phage |
Key Idea: Lytic = kill now. Copy the genome immediately, make many virions, burst the host open. Lysogenic = hide now, maybe kill later. Integrate as a prophage, stay latent, get copied into every daughter cell, and only go lytic on induction. A temperate phage can do both.
🧬 Retroviruses: HIV & reverse transcriptase (1.5.4)
A retrovirus is an enveloped RNA virus that breaks the usual rule of information flow. It carries the enzyme reverse transcriptase, which makes DNA from its RNA template — the reverse of normal transcription. That viral DNA then integrates into the host genome as a provirus, which is later transcribed to make new viruses. The classic example is HIV: its spikes bind the CD4 receptor on helper T-lymphocytes. By infecting and destroying these immune cells it causes AIDS. Reverse transcriptase has no proofreading, so HIV mutates extremely fast — hence drug resistance, immune escape and the absence of an effective vaccine. The enzyme's uniqueness also makes it a prime drug target.
HIV is the enveloped type on the right: an RNA genome plus the enzyme reverse transcriptase, inside a capsid, wrapped in a lipid envelope whose glycoprotein spikes bind the CD4 receptor on helper T-lymphocytes. The spikes decide which cells it can infect.
🔒 Interactive diagram
Explore the labelled diagram, charts and maps for this topic in study mode.
| Normal cell flow | Retrovirus (e.g. HIV) flow |
|---|---|
| DNA → RNA (transcription) | RNA → DNA (reverse transcription) — the reverse direction |
| Enzyme: RNA polymerase | Enzyme: reverse transcriptase, carried inside the virus |
| Genes stay in the cell's own DNA | Viral DNA integrates into the host genome as a provirus |
| — | Provirus is later transcribed to make new virus particles |
Retro = backwards. A retrovirus runs transcription backwards: RNA → DNA using reverse transcriptase. The DNA copy slots into your genome (a provirus) and is read out later. HIV attacks the very cells (CD4 helper T-cells) that coordinate the immune response — which is why it is so damaging.
🧬 Origin & rapid evolution of viruses (1.5.5)
Where did viruses come from? The honest answer is we are not sure, and they are probably polyphyletic — i.e. they arose several independent times. Three leading hypotheses are the escape, regressive and virus-first ideas. What is certain is that viruses evolve extremely rapidly, because of huge population sizes, very short generation times and high mutation rates — especially RNA viruses, whose polymerases lack proofreading. That fast evolution explains real-world problems: influenza's antigenic drift and shift, HIV's drug resistance, and the continual emergence of new viral diseases.
| Hypothesis | The idea |
|---|---|
| Escape (progressive) | Viruses began as host genes / mobile genetic elements that escaped and gained a protein capsid |
| Regressive (reduction) | Viruses are once free-living cellular parasites that lost everything except the genes to replicate |
| Virus-first (co-evolution) | Virus-like replicators arose alongside the earliest cells, before modern cells existed |
Three multipliers stack up: enormous numbers of virions, generation times of hours, and error-prone copying (RNA viruses worst of all). More copies + faster turnover + more mistakes = more variation for selection to act on — so vaccines and drugs are quickly outrun, and the flu vaccine must be updated every year.
✍️ Worked examples
IB-style question — why a virus is not a cell
A student claims a virus is the smallest type of living cell. Using the structure of a virus, give two reasons this claim is wrong. [2]
Model answer:
Reason 1 — no cell machinery. A virus is just a genome inside a protein capsid (sometimes an envelope); it has no cytoplasm, no ribosomes and no metabolism, so it cannot carry out the functions of life on its own.
Reason 2 — cannot replicate alone. A virus can only reproduce by getting inside a host cell and hijacking the host's machinery — it is an obligate intracellular parasite, not a self-sufficient cell. (1 mark per valid reason.)
A virus is non-cellular: it is only a nucleic-acid genome in a protein capsid, with no cytoplasm, ribosomes or metabolism, and it cannot reproduce by itself — it must hijack a host cell. So it is not a living cell.
IB-style question — lytic vs lysogenic
Distinguish between the lytic and lysogenic cycles of a bacteriophage. [3]
Model answer:
Lytic — what happens. The viral genome is copied immediately, new virions are assembled, and the host cell is lysed (burst open) to release them straight away, so the host is killed.
Lysogenic — what happens. The viral DNA integrates into the host chromosome as a prophage and stays dormant; it is copied passively when the host divides, so the host survives and no new virus is made (until induction).
The contrast. Lytic = fast, destructive, makes virions now; lysogenic = latent, integrated, harmless for now and only turns lytic on induction. A temperate phage can do both. (1 mark: lytic kills/makes virions now; 1 mark: lysogenic integrates as prophage/host survives; 1 mark: lysogenic can be induced to go lytic.)
Lytic: the genome is copied at once, virions assemble, and the cell is lysed and killed to release them. Lysogenic: the DNA integrates as a dormant prophage, copied with the host so the cell survives and no virus is made — until induction switches it to the lytic cycle.
IB-style question — HIV and reverse transcriptase
Explain how reverse transcriptase allows HIV to replicate, and why HIV evolves so rapidly. [4]
Model answer:
Reverse transcription. HIV is a retrovirus with an RNA genome; reverse transcriptase makes a DNA copy from that RNA — the reverse of normal transcription.
Integration. The DNA copy integrates into the host genome as a provirus, which is later transcribed to make new viral RNA and proteins for new virus particles.
No proofreading. Reverse transcriptase lacks proofreading, so it makes many copying errors (mutations) each cycle.
Rapid evolution. Combined with huge numbers of virions and short generation times, those mutations give lots of variation, so HIV evolves fast — leading to drug resistance, immune escape and no effective vaccine. (1 mark each: RNA→DNA by reverse transcriptase / integrates as provirus / enzyme lacks proofreading → mutations / fast evolution → resistance.)
Reverse transcriptase copies HIV's RNA genome into DNA, which integrates into the host genome as a provirus and is later transcribed to make new virus. The enzyme has no proofreading, so many mutations occur; with huge populations and short generations this drives rapid evolution, causing drug resistance and immune escape.
✅ Quick self-check
Tap each card to check yourself.
What is the minimum structure of any virus, and why is it non-cellular? A nucleic-acid genome (DNA or RNA) inside a protein capsid made of capsomeres; some add a lipid envelope with glycoprotein spikes. It has no cytoplasm, ribosomes or metabolism, so it is non-cellular and must replicate inside a host.
List the five steps of the lytic cycle in order. Attachment (bind a specific receptor) → entry (genome enters) → replication & synthesis (hijack host machinery to copy the genome and make capsids) → assembly → lysis & release (cell bursts, freeing new virions).
How does the lysogenic cycle differ from the lytic cycle? The viral DNA integrates into the host chromosome as a dormant prophage, copied passively with the host so the cell survives and no new virus is made — until induction (UV/stress) switches it to the lytic cycle. Lytic kills the host immediately.
What does reverse transcriptase do, and why does it matter for HIV? It makes DNA from the viral RNA template (the reverse of transcription); that DNA integrates as a provirus. The enzyme lacks proofreading, so HIV mutates fast — causing drug resistance, immune escape and no effective vaccine. HIV infects CD4 helper T-cells, causing AIDS.
Why do viruses, especially RNA viruses, evolve so rapidly? Huge population sizes, very short generation times and high mutation rates (RNA polymerases lack proofreading) together produce enormous variation, so selection acts fast — seen in influenza antigenic drift/shift and continual emergence of new viruses.
Why is the origin of viruses described as polyphyletic? Viruses probably arose several independent times, via different routes — the escape (host genes that gained a capsid), regressive (reduced free-living parasites) and virus-first (co-evolution with early cells) hypotheses.
Exam Tips
- Define a virus as a NON-CELLULAR infectious particle: a nucleic-acid genome in a protein capsid, sometimes with an envelope and spikes. No cytoplasm, ribosomes or metabolism — so it must be an obligate intracellular parasite.
- Learn the five lytic steps in order: attachment, entry, replication/synthesis, assembly, lysis & release. Stress that the host's machinery is hijacked.
- Attachment is specific (spikes/tail fibres fit a particular receptor) — this sets the virus's host range and explains host-jumping.
- Lytic vs lysogenic: lytic copies and lyses immediately (host killed); lysogenic integrates as a dormant prophage (host survives, copied with it) until induction turns it lytic. A temperate phage can do both.
- Retrovirus = backwards: reverse transcriptase makes DNA from RNA, which integrates as a provirus. HIV infects CD4 helper T-cells, causing AIDS; the enzyme is a key drug target.
- HIV evolves fast because reverse transcriptase lacks proofreading — high mutation rate plus huge numbers and short generations. That explains drug resistance and the lack of a vaccine.
- Viral origins are uncertain and probably polyphyletic: the escape, regressive and virus-first hypotheses. Don't state one as fact — name them as competing ideas.
- Rapid evolution (drift/shift in flu, emerging diseases) comes from large population size + short generation time + high mutation rate — name all three multipliers for full marks.