IB Biology · Theme A · A2.3 · HL only

Borrowed life.
Stolen machinery.

Not quite alive — but undeniably consequential. Tiny protein-coated genomes that outsource everything to a host.

6Sub-topics
18Key terms
HL onlyLevel
CellsLevel of organisation
RNA
Why this topic

What this topic answers.

Every sub-topic below feeds at least one of these questions.

Guiding question 1

How can viruses exist with so few genes?

Guiding question 2

In what ways do viruses vary?

HL extension

Higher Level only.

An extra 6 sub-topics for HL — same syllabus, deeper mechanism.

HL only

Structural features common to viruses

Structural features common to viruses

HL only

Diversity of structure in viruses

Diversity of structure in viruses

HL only

Lytic cycle of a virus

Lytic cycle of a virus

HL only

Lysogenic cycle of a virus

Lysogenic cycle of a virus

HL only

Evidence for several origins of viruses from other organisms

Evidence for several origins of viruses from other organisms

HL only

Rapid evolution in viruses

Consider the consequences for treating diseases caused by rapidly evolving viruses.

A2.3.1 · Common features

What every virus has.

Viruses are wildly diverse — but five features are shared across all of them. None of those features is enough to be alive.

Typical size
20–200 nm

Bacteria are 10–100× larger (~2,000–3,000 nm).

Genetic material
DNA or RNA

Single- or double-stranded.

Protein coat
capsid

Repeating protein subunits forming a defined shape.

Cytoplasm
none

And few or no enzymes either.

⚠️

Why this matters

No cytoplasm, no enzymes, no metabolism. A virus is an instruction set in a box. It can do nothing on its own; everything happens through hijacked host machinery.

A2.3.2 · Diversity of structure

Same idea, a thousand variations.

Within the basic plan (genetic material + capsid), viruses vary in almost every parameter. The IB names three exemplars: bacteriophage lambda, coronaviruses, HIV.

Shape

Three main types

Icosahedral — a 20-faced polyhedron (common). Helical — a rod or spiral. Complex — bacteriophages have an icosahedral head plus a helical tail plus fibre legs.

Genetic material

Four combinations

Single-stranded DNA · double-stranded DNA · single-stranded RNA · double-stranded RNA. Lambda is dsDNA; HIV is ssRNA; SARS-CoV-2 is ssRNA.

Envelope

Yes or no

Some viruses (HIV, coronaviruses, influenza) acquire an outer envelope of host-cell membrane during release. Others (like lambda) are non-enveloped.

A2.3.3 · The lytic cycle

Hijack, replicate, burst.

Lambda's fast option: enter the cell, take it over, make hundreds of copies, blow it up. Five clear stages.

  1. Attachment. The bacteriophage binds receptors on the E. coli surface. The capsid stays outside.
  2. Penetration. The phage injects its DNA into the cell, leaving the empty capsid attached to the wall.
  3. Replication of phage DNA. Viral endonucleases degrade the host chromosome. Host machinery is hijacked to synthesise many copies of the phage DNA and many capsid proteins.
  4. Assembly. Phage DNA and capsid proteins are assembled into hundreds of new phage particles inside the cell.
  5. Lysis. Phage-coded enzymes weaken the cell wall. The cell bursts, releasing the new phages to find more hosts.

Note: in the lytic cycle, phage DNA stays separate from the host chromosome the entire time. It hijacks; it does not integrate.

A2.3.4 · The lysogenic cycle

Integrate. Wait. Strike later.

Lambda's slow option: integrate into the bacterial chromosome and ride along through host generations, then break out when conditions are right.

  1. Attachment + penetration. Same as the lytic cycle — phage binds and injects its DNA.
  2. Prophage formation. Phage DNA is integrated into the E. coli chromosome. The phage DNA is now a prophage; the infected cell is a lysogen.
  3. Host reproduction. The lysogen divides normally. Each daughter cell carries a copy of the prophage. This can continue for many generations.
  4. Induction. A trigger (often stress — UV, chemicals) causes the prophage to excise itself from the chromosome.
  5. Switch to lytic. The free phage DNA replicates, assembly happens, lysis follows. New phages are released.
A2.3.5 · Several possible origins

Where did viruses come from?

No single hypothesis explains all viruses. The diversity may reflect multiple independent origins — and the structural similarities may be convergent evolution from being obligate parasites.

Hypothesis 1

Virus-first

Claim: viruses are older than cells — pre-cellular self-replicators that predated the first cell.

For: some viral genes have no cellular equivalent. Against: modern viruses require cells to replicate, so they can't have existed before cells.

Hypothesis 2

Escape

Claim: viruses are bits of DNA or RNA that escaped from cells and became independent infectious agents.

For: bacterial cells exchange genetic material — a known escape mechanism. Multiple escapes would explain diversity. Against: most viral genes aren't found in cells.

Hypothesis 3

Regressive

Claim: viruses were once cellular parasites that lost everything but the bare essentials of parasitism.

For: giant viruses have genomes resembling those of parasitic bacteria. Against: the smallest known cellular parasites don't look like viruses.

Common features across virus families (capsid, small genome, obligate parasitism) may be convergent evolution — the same lifestyle selects for the same general design, even from different origins.

A2.3.6 · Rapid evolution

Why viruses outrun our defences.

Viruses (especially RNA viruses) evolve at extraordinary rates. Three drivers — and two named examples.

Why so fast?

  • Very high replication rate — millions of virions per cell, each a chance for mutation.
  • No proofreading — RNA viruses (HIV, influenza, SARS-CoV-2) lack a DNA-polymerase-style proofreader, so error rates are orders of magnitude higher than in cells.
  • Strong selection by the immune system — mutated viruses that aren't recognised by existing antibodies survive and spread; the rest are eliminated.

Influenza — two routes

Antigenic drift

Slow, continuous

Gradual accumulation of point mutations in HA and NA surface proteins (antigens). New strains emerge each season — slight enough that previous immunity is partly lost. This is why the flu vaccine is updated every year.

Antigenic shift

Abrupt, dramatic

Two influenza strains co-infect a single host (e.g. a pig). When new virions assemble, gene segments from the two strains recombine. The result: a virus with HA + NA antigens nobody has seen before. Can cause pandemics.

HIV — extreme mutation rate

HIV is a retrovirus — its RNA is reverse-transcribed into DNA before integrating into the host genome. Reverse transcriptase is exceptionally error-prone. The result: within a single patient, HIV evolves into a swarm of related strains, and drug resistance can develop in months.

Consequences for medicine

  • Drugs need continual update to stay ahead of resistance.
  • Vaccines may lose effectiveness as antigens drift or shift.
  • Uncontained rapid evolution can drive epidemics and pandemics — exactly what happened with SARS-CoV-2 variants.

HL-only key terms

VirusCapsidBacteriophageLytic CycleLysisMetabolismLysogenic CycleProphageLysogenParasiteObligate ParasiteConvergent EvolutionAntibodiesAntigensImmunityMutationAntigenic driftAntigenic shift
Vocabulary

0 terms to own.

If you can't define one of these in a sentence, that's where to revise next.

IB Linking Questions

“What mechanisms contribute to convergent evolution?”

“To what extent is the natural history of life characterized by increasing complexity or simplicity?”