Revise Viruses for IB Biology (A2.3)

Strip a virus down to its essentials and you find the same minimal plan every time: a genome of nucleic acid enclosed in a protein coat called the capsid. Two features are worth stating precisely. First, the genome is a single type of nucleic acid — either DNA or RNA, never both — and it may be single- or double-stranded. Second, the capsid is made of PROTEIN subunits (capsomeres) that self-assemble around the genome, most often into a helical rod or an icosahedral shell. Some viruses, particularly those that infect animal cells, add one more layer: a lipid envelope taken from a host cell membrane as the virus buds out, studded with viral glycoproteins that let the virus recognise and enter its next host. Viruses are also extremely small — typically 20 to 300 nm across, far smaller than a bacterium and below the resolution of a light microscope.

That common plan supports remarkable diversity. Viral genomes come in four flavours — single- or double-stranded DNA, and single- or double-stranded RNA — which is a far wider range than cellular life, whose genome is always double-stranded DNA. Capsids differ in shape and symmetry; some viruses are enveloped and some are naked; sizes span more than an order of magnitude; and host ranges vary from a single bacterial species to broad groups of animals or plants. The bacteriophage, with its distinctive head-and-tail structure, looks nothing like the roughly spherical enveloped influenza virus, yet both fit the same definition. The lesson to carry into the exam is that the shared essentials — nucleic acid inside a protein capsid, small, non-cellular — are what unite viruses, while genome type, capsid shape, envelope and host range are the axes along which they diverge.

A virus is not a cell. It has no cytoplasm, no cell membrane of its own making, no organelles and — critically — no ribosomes. Because it has no ribosomes it cannot synthesise proteins, and because it has no metabolic machinery it cannot capture energy or carry out reactions. Outside a host cell, therefore, a virus is chemically inert: it does not grow, respond, use energy or replicate. It can only replicate by entering a living cell and commandeering that cell's ribosomes, enzymes, nucleotides and energy to build new viral components. This is why viruses are described as obligate intracellular parasites that are non-cellular and non-living outside a host. When IB asks whether viruses are alive, the strongest answer weighs both sides: they resemble living things in carrying genetic material and evolving by natural selection, but they fail the core criteria — no cellular structure, no metabolism, no independent reproduction — so they are best classed as non-living outside a host.

Bacteriophages give the clearest picture of viral replication because their two pathways are so distinct. The lytic cycle is the fast, destructive route. The phage attaches to the surface of a bacterium and injects its genome into the cell. That genome immediately takes over: the host's ribosomes and enzymes are redirected to transcribe and translate viral genes, so the cell stops making its own molecules and instead mass-produces viral genomes and capsid proteins. These self-assemble into hundreds of new phage particles. Finally the phage directs production of an enzyme that breaks down the bacterial cell wall, and the cell bursts — lyses — releasing the new virions to infect neighbouring cells. The defining feature of the lytic cycle is that the virus replicates immediately and kills (lyses) the host.

The lysogenic cycle is the patient alternative. Instead of taking over at once, the injected viral genome integrates into the bacterial chromosome, where it is called a prophage. In this integrated state the virus does not replicate independently or kill the host; instead, every time the bacterium copies its own DNA and divides, the prophage is copied along with it and passed silently to both daughter cells. A whole population of infected bacteria can therefore carry the dormant viral genome. This is not permanent: a trigger such as cellular stress or DNA damage (for example UV radiation) can cause the prophage to excise itself from the host chromosome and switch into the lytic cycle, at which point it replicates rapidly and lyses the host. So the two cycles are linked — lysogeny is a dormant reservoir that can flip to lytic destruction.

Most viruses run genetic information in the usual direction, DNA → RNA → protein, or use their RNA directly. Retroviruses break that pattern. A retrovirus, such as the Human Immunodeficiency Virus (HIV), has an RNA genome but carries the enzyme reverse transcriptase inside its capsid. Once inside a host cell, reverse transcriptase uses the viral RNA as a template to synthesise a complementary DNA strand, and then a double-stranded DNA copy of the whole genome. This viral DNA is inserted into the host cell's own genome, where it becomes a provirus. The integrated provirus can stay latent for years or be transcribed by the host's own RNA polymerase to make new viral RNA genomes and the mRNA for new viral proteins. In HIV the host cells are helper T-lymphocytes, and their progressive destruction cripples the immune system, eventually causing AIDS. Two exam-critical points: the enzyme is reverse transcriptase, and the information flow it drives is RNA → DNA, the reverse of transcription — which is where the name 'retro' comes from.

Viruses evolve faster than almost anything else alive, and the reason is built into how they copy their genomes. Viral polymerases — and reverse transcriptase in retroviruses — generally lack effective proofreading, so replication introduces mutations at a high rate. Combined with enormous population sizes and very short generation times, this means new variants arise constantly, and natural selection quickly favours any variant that escapes the host's immune response. The visible result is antigenic variation: the surface antigens the immune system recognises keep changing. In influenza this happens two ways. Antigenic drift is the gradual accumulation of point mutations in the genes for surface proteins, so immunity slowly stops matching the circulating virus — this is why flu vaccines are reformulated each year. Antigenic shift is an abrupt, major change that happens when two different influenza strains infect the same cell and reassort their segmented genomes, producing a virus with a new combination of surface proteins that almost nobody is immune to — the kind of event that can spark a pandemic.

The same features that define viruses make them difficult to fight. Because they replicate inside host cells using host machinery, most viral processes are hard to target with drugs without harming the host, so there are far fewer antivirals than antibacterials. Because they evolve so rapidly, immunity and vaccines are constantly outrun — antigenic variation forces vaccines to be updated and lets some viruses (like HIV) escape the immune response for years. Their ability to lie dormant, as an integrated provirus in the lysogenic state or a latent HIV provirus, means an infection can persist undetected and reactivate later. And their diversity and capacity to jump between host species means new viruses keep emerging. Taken together — intracellular replication, rapid evolution, latency, and emergence — these are the reasons viral diseases remain such a persistent public-health challenge.

A2.3 is dominated by extended explanation, and those marks are awarded analytically — each distinct valid biological point is worth one mark, and 'A' credits a correct detail. The engine does not reward length or repetition; it rewards separate, creditable ideas. Study how each mark below is tied to a specific named point rather than to loose phrasing, and note that stating the same idea twice scores only once.