Viruses

Structural features common to ALL viruses:

• Small and a fixed size — typically ~20–300 nm, far smaller than cells; each virus type has a characteristic size and shape.
• A nucleic acid genome — either DNA or RNA (never both), which may be single- or double-stranded.
• A protein coat (capsid) built from repeating protein subunits (capsomeres) that encloses and protects the genome.
• No cytoplasm, no organelles, no ribosomes — viruses carry out no metabolism of their own. They cannot make proteins or ATP and rely entirely on the host cell's machinery.

Diversity of viruses. Despite a shared basic plan, viruses are remarkably varied:

• Genome type — viruses are classified by their nucleic acid: ssDNA, dsDNA, ssRNA and dsRNA. This range is wider than in cellular life, whose genomes are always dsDNA.
• Envelope — some viruses are surrounded by a lipid envelope taken from a host membrane during release, studded with viral glycoprotein spikes (e.g. coronavirus / SARS-CoV-2, HIV, influenza). Non-enveloped (naked) viruses have only the capsid (e.g. adenovirus, many bacteriophages) and tend to be hardier in the environment.
• Capsid shape — helical, polyhedral/icosahedral, or complex (as in many bacteriophages).
• Host range — viruses infect animals, plants, fungi and bacteria.

Bacteriophage example. A bacteriophage ("phage") infects bacteria and is a classic IB example. It has an icosahedral head containing the DNA genome, a tail sheath, and tail fibres that attach to specific receptors on the host's cell wall. It injects its DNA into the bacterium, leaving the empty capsid (the "ghost") outside.

Because viruses have no metabolism, they must hijack a host cell to reproduce. Two replication pathways are studied, classically using bacteriophages.

The lytic cycle (rapid, destroys the host):

1. Attachment — the virus binds to specific receptors on the host surface (tail fibres of a phage recognise the bacterial cell wall).
2. Entry — the genome enters the host (a phage injects its DNA; enveloped animal viruses fuse with or are taken into the membrane).
3. Replication — host enzymes and ribosomes are redirected to copy the viral genome and make viral proteins.
4. Assembly — new genomes and capsids self-assemble into complete virus particles (virions).
5. Release (lysis) — the host cell bursts (lyses), releasing many new viruses to infect other cells.

The lysogenic cycle (latent, the host survives — for now):

1. Attachment and entry as above.
2. Integration — the viral DNA inserts into the host chromosome, becoming a prophage (in bacteria) / provirus (in animal cells).
3. Latency — the integrated DNA is replicated passively every time the host cell divides, so all daughter cells inherit it, with no new viruses made and no symptoms.
4. Induction — a trigger (e.g. UV light, stress, chemicals) causes the prophage to excise and switch into the lytic cycle, producing and releasing new viruses.

So the lysogenic route lets a virus persist quietly and spread vertically through cell division, before later switching to the destructive lytic route. Viruses such as HIV and herpes integrate as proviruses, which is why these infections can be lifelong with flare-ups.

Are viruses living organisms? This is a genuine scientific debate, and the IB expects you to argue both sides.

Reasons viruses are considered NON-living:

• They are acellular — not made of cells, so they break cell theory.
• They have no metabolism of their own and cannot make ATP or proteins.
• They cannot reproduce independently — they are obligate intracellular parasites that need a host cell's machinery.
• Outside a host they are inert particles that can even be crystallised.

Reasons some argue viruses ARE living (or borderline):

• They contain genetic material (DNA or RNA) and can pass it to offspring.
• They can reproduce (inside a host) and evolve by natural selection.
• They show adaptation and have a clear evolutionary history.

Most biologists place viruses at the boundary of living and non-living — they behave as inert chemicals outside a cell but as replicating, evolving entities inside one.

Rapid evolution of viruses. Viruses evolve extremely fast for several linked reasons:

• High mutation rate — viral genome-copying enzymes often lack proofreading, so errors accumulate. This is especially true of RNA viruses (influenza, SARS-CoV-2, HIV), whose RNA polymerases are very error-prone.
• Short generation time + huge numbers — billions of virions can be produced from one host, giving abundant variation for selection to act on.
• Strong selection pressure — host immunity, antiviral drugs and vaccines select for variants that escape them.
• Genome reassortment/recombination — when two strains infect one cell, segments can be swapped (e.g. influenza), producing major new variants suddenly.

Antigenic variation. Mutations change the surface proteins (antigens) the immune system recognises, so previously-made antibodies no longer bind well. This is why new influenza vaccines are needed each year and why SARS-CoV-2 variants continued to emerge.

Emergence of new diseases. Rapid evolution, plus the ability to jump between host species (zoonosis), means new viral diseases keep emerging — e.g. pandemic influenza strains and SARS-CoV-2.