Master IB Biology A2.3: Viruses with notes created by examiners and strictly aligned with the syllabus.
A2.3.1 Structural features common to viruses
A2.3.2 Diversity of structure in viruses
A2.3.3 Lytic cycle of a virus
A2.3.4 Lysogenic cycle of a virus
A virus is a non-cellular infectious agent that contains genetic material inside a protein coat and can reproduce only inside a host cell. So viruses are not cells. Nearly everything they do relies on the cell they infect.
Viruses share only a small set of features, which is one reason they don’t fit neatly beside living organisms in classification. All viruses have a small, fixed size, a nucleic acid genome, a protein capsid, no cytoplasm, and few or no enzymes.

A host cell is a cell that is entered and used by a virus for viral replication. This answers the guiding question, “How can viruses exist with so few genes?” They can carry very few genes because the host provides the cytoplasm, energy supply, raw materials, ribosomes, many enzymes and much of the machinery needed to make viral components.
Viruses are tiny compared with cells, often tens to hundreds of nanometres across. Their small size helps them enter host cells. It also reflects what they don’t have: no cytoplasm, ribosomes, mitochondria, chloroplasts, nuclei, or the general cell contents expected in a living cell.
Their size is fixed too. A bacterium or an animal cell grows before it divides; a virus doesn’t grow. Inside a host cell, new virus particles are assembled from separate components, and once assembly is complete, the particle has already reached its final size.
A nucleic acid is a polymer made of nucleotide monomers that stores or transmits genetic information. In viruses, the nucleic acid is either DNA or RNA. A genome is the complete set of genetic material in an organism or virus. Viral genomes include genes used to make viral components and, in some viruses, a small number of viral enzymes.
Viruses use the same basic genetic code as cells. That matters because the host’s protein-synthesis machinery has to read viral genes. If the code did not match, host ribosomes would not make the correct viral proteins.
A capsid is a protein coat that encloses the viral genome and protects it outside the host cell. Capsids are made from repeating protein subunits, so many viruses have regular, symmetrical shapes.
A cytoplasm is the cell material inside the plasma membrane, excluding the nucleus in eukaryotic cells, that contains the enzymes, ribosomes and dissolved substances needed for cell metabolism. Since viruses have no cytoplasm, they cannot carry out ordinary cellular metabolism.
An enzyme is a protein or RNA catalyst that increases the rate of a biochemical reaction without being used up. Viruses have few or no enzymes because the host does most of the biochemical work for them. The enzymes they carry or code for are usually linked to genome replication, entry into cells, integration into host DNA, or release from the host cell.
Viruses share a handful of basic features, but they differ a lot in shape, structure and genome type. Some are roughly spherical. Others are helical, have complex head-and-tail structures, or are wrapped in a membrane envelope taken from a host cell.

Viral genetic material may be DNA or RNA. Either may be single-stranded or double-stranded. The genome can also differ in length and arrangement, for example as one molecule or several separate molecules.
A single-stranded genome is a viral genome in which each nucleic acid molecule has one nucleotide strand rather than two paired strands. A double-stranded genome is a viral genome in which complementary nucleotide strands are paired by base bonding.
RNA viruses don’t all use their RNA in the same way. Some RNA can act directly as messenger RNA, some must first be copied into messenger RNA, and retroviruses convert RNA into DNA before making more viral products.
A retrovirus is an RNA virus that uses reverse transcription to make a DNA copy of its RNA genome after entering a host cell. HIV is the syllabus example to remember here.
An envelope is a membrane surrounding some virus particles that is derived from host cell membrane and contains viral proteins used in attachment or entry. Enveloped viruses often infect animal cells because budding from a host membrane is a common release route in those cells.
A non-enveloped virus is a virus particle that lacks a surrounding membrane and has its capsid as the outer protective layer. Bacteriophage lambda is non-enveloped. Many viruses that infect bacteria are in this group.
The three guide examples show the range well. Bacteriophage lambda is a DNA virus that infects Escherichia coli. Coronaviruses are enveloped RNA viruses that infect animal cells. HIV is an enveloped retrovirus that infects human immune cells.
Comparison of key structural features in three virus examples.
| Virus | Genome type | Strandedness | Envelope | Host cell type | Distinctive structural features |
|---|---|---|---|---|---|
| Bacteriophage lambda | DNA | Double-stranded | Absent | E. coli bacterial cells | Protein head containing DNA; tail for attachment and DNA injection |
| Coronavirus | RNA | Single-stranded | Present | Animal cells | Membrane envelope with surface spike proteins giving a crown-like outline |
| HIV | RNA retrovirus | Single-stranded | Present | Human immune cells | Envelope; RNA genome; reverse transcriptase enzyme for making DNA |
A bacteriophage is a virus that infects bacteria. Bacteriophage lambda has a head containing DNA and a tail structure used to attach to and inject DNA into E. coli. A coronavirus is an enveloped RNA virus with surface spike proteins that give the particle a crown-like outline. HIV has an envelope, RNA genome and reverse transcriptase enzyme.
Don’t try to memorize every structural detail of every virus. Focus on the variation: genome type, strandedness, envelope presence, host type and overall shape.
The lytic cycle is a viral replication cycle where a virus enters a host cell, makes new virus particles, and causes the host cell to burst. In bacteriophage lambda, the host is Escherichia coli, often shortened to E. coli.
This cycle makes viral dependence easy to see. Lambda brings genetic instructions and some virus-specific functions, but the bacterium provides energy, nutrients, ribosomes, nucleotides, amino acids and much of the enzymatic machinery. Viruses don’t arrive with a working cell; they take one over.

A virulent virus is a virus that damages or kills its host cell during replication. Lambda is virulent when it follows the lytic cycle.
The phases can be traced in order:
A receptor is a molecule on a cell surface that binds a specific ligand, such as a viral attachment protein. A ligand is a molecule that binds specifically to another molecule, usually changing its activity or location.
Lysis works well for rapid spread, but the virus pays a price: killing the host cell removes the factory needed to make more virus. If all available host cells are destroyed, the virus population also runs out of places to replicate.
The lysogenic cycle is a viral life cycle where viral DNA integrates into the host genome and is copied with it, without new virus particles being made straight away. Bacteriophage lambda is again the example to use.

The opening steps look much like the lytic cycle. Lambda attaches to E. coli and injects its DNA. Then the important difference appears: the viral DNA does not immediately direct the cell to make many new phages. Instead, it inserts into the bacterial chromosome.
A prophage is viral DNA that has been integrated into a bacterial chromosome and is replicated with the host DNA. A temperate virus is a virus that can enter a lysogenic cycle instead of immediately causing lysis.
The phases are:
During lysogeny, the virus does not make complete virus particles. It gets copied passively as part of the host chromosome. This is why lysogeny can allow viral genetic material to persist when immediate lysis would be risky, for example when host cells are scarce.
The prophage does not have to stay there forever. If conditions change, viral genes can be activated and lambda can switch into the lytic cycle. Many textbooks call this switch induction, but for the syllabus the main point is enough: lysogenic viral DNA can later become active and cause lysis.
An obligate parasite is an organism or virus that can complete its reproductive cycle only by using a host. Viruses take this to an extreme. They don’t just draw nutrients from the host; they rely on host cells for energy supply, protein synthesis and most life functions.
The huge diversity of viruses points to several possible origins, not one tidy origin story. No set of genes is shared by all viruses, and viral structures vary too much for the simple idea that “all viruses descended from one ancestral virus” to be very convincing.

The genetic code is the set of rules by which nucleotide triplets in messenger RNA specify amino acids during protein synthesis. Viruses and living organisms use essentially the same genetic code. That links viruses strongly to cellular life, since host ribosomes must translate viral genes correctly.
This still doesn’t prove a single viral origin. It supports the idea that viruses arose after cells, or at least in close evolutionary connection with cells, because viruses depend on cellular translation.
A progressive origin hypothesis is an explanation for viral origin in which mobile genetic elements from cells gained genes for transmission between cells. In plain language: pieces of genetic material became better at moving around and eventually acquired capsids or envelopes.
A regressive origin hypothesis is an explanation for viral origin in which cellular organisms became increasingly dependent on hosts and lost genes and structures over time. In plain language: a parasitic cell lineage may have simplified until little remained beyond genetic material and transmission machinery.
Both hypotheses could be true for different viral groups. That’s the neat part: multiple origins help explain why viruses are so diverse while still sharing a parasitic way of life.
Convergent evolution is the independent evolution of similar features in different lineages because similar selection pressures favour similar solutions. Shared viral features may have evolved this way. Small size, a protective capsid and dependence on host cells are useful solutions for intracellular parasitism, even if different viruses reached them by different evolutionary routes.
Convergence can be driven by similar selection pressures, similar physical constraints and similar ecological roles. For viruses, the repeated problem is: how do you protect genetic material outside a cell, enter a host cell and get copied using host machinery?
This also links to the question of whether life’s history mainly shows increasing complexity or increasing simplicity. Viruses are a good reminder that evolution has no built-in direction toward complexity. Some lineages become more complex when complexity improves reproduction; others become simpler when dependence on a host makes genes and structures dispensable.
Evolution is a change in heritable characteristics of a population across generations. In viruses, that change can happen even during a single infection, because viral generations can be very short and viral populations can be enormous.
Some viruses evolve very rapidly for three main reasons:
A mutation is a heritable change in the nucleotide sequence of genetic material. A selection pressure is an environmental factor that affects which variants survive and reproduce. An antigen is a molecule recognized by immune receptors or antibodies, often a protein on the surface of a pathogen.

Influenza viruses are RNA viruses with segmented genomes. A segmented genome is a genome divided into separate nucleic acid molecules rather than one continuous molecule. That detail matters: if two influenza strains infect the same host cell, genome segments can be mixed into new combinations.
A strain is a genetic variant of a virus with distinct inherited features. New influenza strains arise by mutation and by reassortment of genome segments. Surface proteins such as haemagglutinin and neuraminidase act as antigens, so changes in these proteins can reduce recognition by existing immunity.
The result is familiar. People can catch influenza more than once, and influenza vaccines may need updating. A vaccine is a preparation containing antigens or genetic instructions for antigens that stimulates immune memory without causing the full disease.

HIV evolves rapidly, but the reason is slightly different. It is a retrovirus, so it copies its RNA genome into DNA using reverse transcriptase. Reverse transcriptase is an enzyme that synthesizes DNA using RNA as a template. This enzyme makes frequent copying errors, producing many HIV variants within one person.
HIV also comes under intense selection from the immune system and from antiretroviral drugs. Variants with changes in surface proteins may escape immune recognition. Variants with mutations that reduce drug effectiveness may survive treatment and become more common.

Rapid viral evolution makes treatment harder. A drug may work well at first, but resistant variants can be selected if they already exist or arise during replication. That is why HIV treatment usually uses combinations of antiretroviral drugs: it is much less likely that one viral genome will carry resistance to several drugs at once.
Rapid evolution also complicates prevention. For influenza, changing antigens mean vaccines must be reviewed and updated. For HIV, extreme variation is one reason a curative immune response and an effective universal vaccine have been so difficult to achieve.
The exam point is simple: fast viral evolution is not mysterious. Short generations create many opportunities, high mutation creates variation, and strong selection sorts that variation quickly.