A2.3 Viruses

Viruses sit at the strange boundary of biology: they carry genetic information and evolve, yet they cannot reproduce on their own and lack the machinery of a cell. A2.3 asks you to confront a fundamental question — are viruses alive? — and to understand how such minimal entities can hijack cells, cause disease and evolve at astonishing speed. Because they are so simple and so variable, viruses also illustrate the themes of unity and diversity vividly: a tiny set of components arranged in a huge variety of ways. Focus on why a virus must use a host cell, and the rest of the topic falls into place.

What a virus is — and whether it is alive

A virus is a tiny, non-cellular infectious particle. All viruses share a small number of common features: a nucleic acid genome (DNA or RNA) carrying their genes, and a protein coat (capsid) that protects it. Some, such as influenza and coronaviruses, additionally have a lipid envelope derived from the host cell membrane. Crucially, viruses have no cytoplasm, ribosomes or metabolism of their own.

This is why their status is debated. Viruses are obligate intracellular parasites: they cannot carry out the functions of life independently and can only replicate by taking over a living host cell. Outside a host they are inert. For the exam, present both sides: they have genes and evolve (life-like), but they lack cells, metabolism and independent reproduction (not life-like). The syllabus does not require a single verdict — it requires the reasoning.

Diversity of viral structure and genomes

Despite sharing a genome and a capsid, viruses are remarkably diverse, which the syllabus illustrates with two contrasting examples. Bacteriophages (which infect bacteria) have a double-stranded DNA genome and a complex structure with a head and tail. The SARS-CoV-2 coronavirus, by contrast, has a single-stranded RNA genome and a lipid envelope studded with spike proteins.

The key point is that viral genomes vary in ways cellular life does not: a virus may use DNA or RNA, and that nucleic acid may be single- or double-stranded. This variety in genome type is a defining feature of viral diversity and influences how each virus replicates and how it evolves.

The lytic and lysogenic cycles

Because they cannot reproduce alone, viruses replicate by directing a host cell to make new virus particles. Two strategies are studied, classically in bacteriophages:

• Lytic cycle: the virus injects its genome, immediately hijacks the host’s machinery to make many new viruses, and then lyses (bursts) the cell to release them. This is rapid and destroys the host cell.
• Lysogenic cycle: the viral genome integrates into the host’s DNA and is replicated harmlessly alongside it each time the host divides, remaining dormant as a provirus. Later, a trigger can switch it into the lytic cycle.

The distinction examiners look for is timing and host fate: lytic means immediate replication and host death; lysogenic means integration, dormancy and survival of the host until activation.

Rapid evolution and the origin of viruses

Viruses evolve exceptionally fast. They have short generation times and produce enormous numbers of offspring, and RNA viruses in particular copy their genomes with high mutation rates because they lack proofreading. This generates abundant variation on which natural selection acts quickly. The syllabus uses influenza as the example: its rapid antigenic change is why a new vaccine is needed each year and why drug resistance can emerge swiftly.

The origin of viruses is uncertain, and the syllabus frames it as competing hypotheses — for example that viruses arose from fragments of host genetic material that became mobile, or from once-cellular ancestors that lost most of their structure. Because viruses are so diverse, they may not all share a single origin. As with the origin of cells, the expected response is to discuss the hypotheses and acknowledge the uncertainty.