Viruses
🎯What you need to be able to do
- State the few structural features shared by all viruses.
- Describe the diversity of virus structure, using bacteriophage lambda, coronaviruses and HIV as examples.
- Describe the phases of the lytic cycle and the lysogenic cycle of bacteriophage lambda.
- Discuss the evidence that viruses have several origins, and why their shared features may be the result of convergent evolution.
- Explain why some viruses evolve very rapidly, using influenza and HIV, and the consequences for treating the diseases they cause.
📚The biology
What all viruses have in common
Viruses are extremely varied, so the list of features shared by all of them is short:
Typically 20–300 nm, far smaller than a bacterium. Unlike cells, they do not grow: a virus particle is assembled at its final size.
Their genetic material is either DNA or RNA — never both.
A coat made of protein subunits that encloses and protects the nucleic acid.
There is nothing inside the capsid in which metabolism could happen.
Some carry one or two enzymes needed to start infection (such as reverse transcriptase in HIV); none carry the enzymes of metabolism.
Diversity of virus structure
Beyond those shared features, viruses differ in almost every way:
- The genetic material may be DNA or RNA, and either can be single-stranded or double-stranded.
- Some are enveloped: as they leave a host cell they wrap themselves in a piece of the host’s plasma membrane, studded with viral proteins. Others are not enveloped and consist only of a capsid.
- Capsid shapes vary: many are icosahedral (twenty-sided), some are helical rods, and some have complex structures with tails.
Infects the bacterium E. coli. Double-stranded DNA packed in an icosahedral protein head, attached to a long protein tail with a tip that binds the host. Not enveloped.
(e.g. SARS-CoV-2.) Single-stranded RNA, one of the largest RNA genomes of any virus. Enveloped, with spike proteins projecting from the envelope that bind to receptors on host cells — the “crown” that gives them their name.
A retrovirus. Two copies of single-stranded RNA inside a cone-shaped capsid, with the enzyme reverse transcriptase. Enveloped, with glycoproteins that bind to receptors on helper T-cells.
Viruses depend on host cells
A virus has no metabolism of its own. To reproduce, it needs a host cell to supply energy (ATP), nutrients (nucleotides and amino acids), ribosomes for protein synthesis, and most of the enzymes. Each virus can only infect particular host cells, because its surface proteins must bind to specific receptor molecules on the host’s surface.
The lytic cycle of bacteriophage lambda
In the lytic cycle the virus reproduces straight away and destroys the host cell.
- Attachment. The tip of the phage tail binds to a specific receptor protein on the surface of an E. coli cell.
- Injection. The phage injects its DNA through the cell wall and membrane into the cytoplasm. The empty capsid stays outside.
- Synthesis. The phage DNA is replicated many times, and its genes are transcribed and translated by the host’s RNA polymerase and ribosomes, using the host’s nucleotides, amino acids and ATP, to make capsid and tail proteins.
- Assembly. New phage DNA is packed into newly made heads, and tails are attached, producing complete phage particles.
- Lysis and release. Phage-coded enzymes break down the bacterial cell wall from inside. The cell bursts (lyses), releasing around a hundred new phages, each able to infect another cell.
The lysogenic cycle of bacteriophage lambda
Lambda can also take a quieter route.
- Attachment and injection happen as in the lytic cycle.
- Integration. Instead of being copied immediately, the lambda DNA is inserted into the bacterial chromosome at a specific site. The integrated viral DNA is called a prophage.
- Dormancy. A repressor protein made from a lambda gene keeps the genes of the lytic cycle switched off. The host cell is not harmed.
- Replication with the host. Every time the bacterium divides, the prophage is copied along with the host chromosome, so all the descendants of the infected cell carry it.
- Induction. If the host cell is stressed — for example by DNA damage from ultraviolet light — the repressor is destroyed, the prophage is cut out of the chromosome, and the virus enters the lytic cycle, destroying the cell.
The two strategies suit different conditions. The lytic cycle produces many viruses quickly when hosts are plentiful. The lysogenic cycle lets the virus survive, copied for free, when hosts are scarce, and “abandon ship” when the host is about to die.
Where viruses came from
Viruses are so diverse — in their genetic material, structure and replication — that it is unlikely they all share a single origin. Several hypotheses are debated, and different groups of viruses may have arisen in different ways:
- The escape (progressive) hypothesis: pieces of genetic material, such as plasmids or transposons, escaped from cells, gained the ability to move between cells and acquired protein coats.
- The reduction (regressive) hypothesis: viruses descend from once free-living cells that became parasites and gradually lost the genes they no longer needed. Giant viruses, with genomes larger than some bacteria, are cited in support.
- The virus-first hypothesis: viruses arose before or alongside the first cells.
If viruses do have several origins, why do they look alike? All viruses share an extreme form of obligate parasitism. Any lineage that adopts that lifestyle will be selected for the same features: small size, a protective protein coat, and loss of metabolism. Their shared features can therefore be explained as convergent evolution, not as common ancestry. And viruses use the same genetic code as living organisms, which is consistent with their having come from cells, since they must be translated by their host’s ribosomes.
Rapid evolution in viruses
Some viruses evolve faster than any other biological entity. The reasons combine:
- High mutation rates. RNA viruses copy their genomes with RNA polymerases (or, in retroviruses, reverse transcriptase) that have no proofreading, so many mistakes are made at each copy.
- Very short generation times — hours rather than years.
- Enormous population sizes: an infected person can carry billions of virus particles, so even rare mutations occur many times.
- Strong selection by the host’s immune system and by drugs, which favours any variant that escapes them.
Mutations constantly change the surface proteins (haemagglutinin and neuraminidase) that antibodies recognize: this antigenic drift means immunity from last year’s infection or vaccine protects less well. Its genome is in separate segments, so when two strains infect the same cell — for example a bird strain and a human strain in a pig — segments can mix, producing a radically new strain (antigenic shift) that can cause a pandemic.
Reverse transcriptase makes frequent errors, so the virus population inside a single patient becomes genetically diverse within weeks. Variants that escape the immune response or resist a drug are selected, and the diversity makes it extremely hard to design a vaccine.
Consequences for treatment:
- Influenza vaccines must be updated every year, based on predictions of which strains will circulate, and they are only partly effective when the prediction is wrong.
- HIV is treated with a combination of several antiretroviral drugs at once, each acting on a different target. A virus would need several resistance mutations simultaneously to survive, which is very unlikely; a single drug on its own is quickly defeated by resistance.
- Antibiotics have no effect on any virus (C3.2).
✏️Worked example
(a) Calculate the number of phages present after 2 hours.
(b) Suggest why the actual number would be much lower.
(c) Explain why, if the culture were short of bacteria, a phage that entered the lysogenic cycle might leave more descendants than one that entered the lytic cycle.
(a) Two hours is 120 minutes, which is 120 ÷ 40 = 3 cycles. Each cycle multiplies the number of phages by 100:
So one phage becomes a million phages in two hours.
(b) The assumptions are unrealistic. Not every released phage will meet and infect a bacterium; several phages may infect the same cell; the supply of uninfected bacteria will run out as they are destroyed; and some phages will be damaged or inactivated.
(c) In the lytic cycle, each infection destroys the host. If there are few bacteria, most of the hundreds of phages released will find no host, and without a host a phage cannot reproduce. In the lysogenic cycle, the viral DNA is integrated as a prophage and copied every time the bacterium divides, without harming it. As the bacterial population grows, so does the number of copies of the phage genome. When conditions change — more hosts, or a stressed host — the prophage can be induced to enter the lytic cycle.
📝Practise
Work through these on paper, then reveal the answer. All are HL only.
1. List four structural features shared by all viruses.
2. Compare the structure of bacteriophage lambda and HIV.
3. Distinguish between the lytic and lysogenic cycles of bacteriophage lambda.
4. Explain why the shared features of viruses do not necessarily show that they share a common ancestor.
5. Explain why a new influenza vaccine is needed every year.
6. Suggest why HIV infection is treated with a combination of several antiretroviral drugs rather than a single drug.
🔗Go deeper — other people’s work
These are external resources, not mine. If one stops working, tell me and everything above it on this page still stands.
- ViralZone (SIB Swiss Institute of Bioinformatics) — one-page summaries with clear diagrams of every virus family, including lambda, coronaviruses and HIV.
- HHMI BioInteractive — animations of viral life cycles and of HIV evolution within a patient.
- World Health Organization — the twice-yearly influenza vaccine composition recommendations, which show antigenic drift in action.