IB BIOLOGY • UNITY AND DIVERSITY

Apply Viruses

Explore how viruses blur the line between living and non-living and shape biology, medicine, and biotechnology.

Historical Context & Motivation

Long before microscopes could reveal the tiniest agents of disease, farmers and physicians knew that certain illnesses spread in mysterious ways. The story of virology—the study of viruses—began with a simple agricultural puzzle: why were tobacco plants developing a mosaic pattern of discoloured leaves, and why could the disease pass through porcelain filters designed to trap all known bacteria? That question launched a century of discoveries that reshaped medicine, genetics, and our understanding of life itself.

1892
Ivanovsky's Filtration Experiment
Dmitri Ivanovsky demonstrated that the agent causing tobacco mosaic disease passed through a Chamberland filter, proving it was smaller than any known bacterium.
1898
Beijerinck Names the Agent
Martinus Beijerinck coined the term contagium vivum fluidum ("contagious living fluid") and proposed that the pathogen was a new category of infectious agent—a virus.
1935
TMV Crystallized
Wendell Stanley crystallized Tobacco Mosaic Virus (TMV), showing that viruses could behave like chemicals—a property no living cell exhibits. He later won a Nobel Prize.
1952
Hershey–Chase Experiment
Alfred Hershey and Martha Chase used bacteriophages to confirm that DNA, not protein, is the hereditary material—one of biology's most pivotal experiments.
2020
SARS-CoV-2 & mRNA Vaccines
The COVID-19 pandemic spurred the fastest vaccine development in history, using knowledge of viral structure and mRNA technology to combat SARS-CoV-2.

These milestones reveal a central question that IB Biology asks you to grapple with: Are viruses alive? To answer that, we need to understand what viruses are made of, how they replicate, and why they matter so much for human health and biotechnology.

Core Principles & Definitions

Before you can apply your knowledge of viruses, you need a solid grasp of their defining features. A virus is a non-cellular infectious agent consisting of nucleic acid enclosed in a protein coat. Viruses lack the machinery for independent metabolism, so they must hijack a host cell's resources to reproduce. The IB syllabus groups several core ideas together under the concept of viral biology.

1

Obligate Intracellular Parasites

Viruses can only replicate inside a living host cell. Outside a cell, a virus particle (virion) is metabolically inert—it cannot carry out respiration, synthesize proteins, or grow on its own.
2

Genetic Material: DNA or RNA

A virus contains either DNA or RNA as its genome—never both. The genome can be single-stranded or double-stranded, and it encodes the proteins the virus needs for replication and assembly.
3

Protein Capsid

The nucleic acid core is surrounded by a capsid—a protective protein shell made of repeating subunits called capsomeres. Capsid shape (icosahedral, helical, or complex) helps classify viruses.
4

Envelope (Some Viruses)

Some viruses, such as influenza and HIV, have a lipid bilayer envelope derived from the host cell membrane. Glycoprotein spikes on the envelope help the virus attach to host cells.
5

Host Specificity

Viruses infect specific hosts and cell types because their surface proteins must bind to matching receptors on the host cell. This lock-and-key interaction determines tropism—the range of cells a virus can infect.
KEY TAKEAWAY
Think of a virus like a USB drive with a corrupted file. The USB drive (virus) contains instructions (genetic material) but has no processor or power supply of its own—it needs to be plugged into a computer (host cell) to run its program. Once inside, the program hijacks the computer's hardware to make copies of itself, sometimes crashing the system in the process.

Virus Structure — Visual Explanation

Visualizing the architecture of a virus is essential for understanding how these tiny agents infect cells. The diagram below shows a generalised enveloped virus alongside a non-enveloped (naked) virus, highlighting the key structural components you need to know for the IB exam.

The left panel shows an enveloped virus with glycoprotein spikes (amber), a lipid envelope (violet dashed), and a capsid (pink) surrounding the nucleic acid (cyan). The right panel shows a non-enveloped virus with an icosahedral capsid (cyan) directly protecting the DNA (green). Enveloped viruses are generally more susceptible to disinfectants because their lipid coat is fragile.

Notice that both types share a nucleic acid core and a protein capsid—these are the universal features of all viruses. The presence or absence of an envelope has practical consequences: enveloped viruses like influenza are easily destroyed by soap because soap dissolves lipids, whereas non-enveloped viruses like norovirus are much harder to eliminate and can persist on surfaces for days.

Viral Replication Cycles

Since viruses cannot reproduce on their own, they follow a specific sequence of steps to commandeer a host cell. The IB syllabus requires you to understand two major replication pathways: the lytic cycle and the lysogenic cycle. Both begin the same way—with the virus attaching to a host cell—but they diverge dramatically after the viral genome enters the cell.

The Lytic Cycle

In the lytic cycle, the virus takes over the host cell immediately. During attachment, specific proteins on the viral surface bind to complementary receptors on the host cell membrane—this is why viruses show host specificity. Next, during penetration, the viral nucleic acid is injected into (or engulfed by) the host cell. The host's own enzymes and ribosomes are redirected during biosynthesis to transcribe and translate the viral genome, producing new viral proteins and nucleic acid copies. These components are then brought together during assembly, forming complete new virions. Finally, during lysis, the host cell bursts open, releasing hundreds of new virus particles that can infect neighbouring cells.

The Lysogenic Cycle

Some viruses take a stealthier approach. In the lysogenic cycle, the viral DNA integrates into the host chromosome and becomes a provirus (or prophage in bacteriophages). Every time the host cell divides, it copies the viral DNA along with its own genome, unknowingly spreading the viral genes to its daughter cells. The virus can remain dormant for many generations. However, a trigger such as UV radiation, stress, or a weakened immune system can cause the provirus to excise from the chromosome and enter the lytic cycle, destroying the host cell.

💡 IB Exam Tip
The IB often asks you to distinguish between lytic and lysogenic cycles. Remember: lytic = lysis = cell destruction, while lysogenic = lying low = integration and dormancy. HIV is a classic example of a virus that can follow both pathways.

Lytic vs. Lysogenic — Visual Comparison

The upper panel (pink) traces the five stages of the lytic cycle ending in cell destruction. The lower panel (violet) shows the lysogenic cycle where viral DNA integrates into the host genome and replicates passively. The amber arrow shows the critical switch point—induction—where an environmental trigger pushes the dormant virus into the lytic pathway.

A key concept to remember is that the lysogenic cycle is not a dead end. Many temperate viruses, including bacteriophage lambda (λ) and HIV, can switch between the two pathways depending on conditions. HIV, for example, uses the enzyme reverse transcriptase to convert its RNA genome into DNA before integrating into the host chromosome as a provirus. This integration is why HIV is so difficult to cure: even when antiretroviral drugs suppress active replication, the proviral DNA hiding inside immune cells can reactivate at any time.

Worked Example — Tracing a Viral Infection

Let's apply what you've learned by walking through how SARS-CoV-2 infects a human respiratory cell. This is the type of structured reasoning the IB exam rewards.

How SARS-CoV-2 Infects a Human Cell
1
Step 1 — Identify the Virus TypeSARS-CoV-2 is an enveloped RNA virus with spike glycoproteins on its surface. Its genome is single-stranded positive-sense RNA, approximately 30,000 nucleotides long.
Enveloped, +ssRNA virus
2
Step 2 — AttachmentThe spike (S) protein on the viral envelope binds specifically to the ACE2 receptor on the surface of human respiratory epithelial cells. This receptor–ligand interaction determines the virus's tropism—it primarily infects cells in the lungs, nasal passages, and intestines where ACE2 is abundant.
S protein binds ACE2 receptor → host specificity
3
Step 3 — Penetration & UncoatingAfter binding, the host cell membrane fuses with the viral envelope (aided by host proteases like TMPRSS2), releasing the RNA genome into the cytoplasm. The capsid disassembles during this process.
Viral RNA released into host cytoplasm
4
Step 4 — BiosynthesisBecause the viral RNA is positive-sense, host ribosomes can translate it directly into viral proteins, including RNA-dependent RNA polymerase (RdRp). RdRp then replicates the viral RNA to make many copies of the genome. Other host ribosomes produce structural proteins (S, M, N, E) that will form new virions.
Host ribosomes make viral proteins; RdRp copies viral RNA
5
Step 5 — Assembly & ReleaseNew viral RNA molecules are packaged into nucleocapsids. Structural proteins are inserted into membranes of the endoplasmic reticulum and Golgi apparatus. Complete virions bud off from the host cell in vesicles and are released by exocytosis, gaining their lipid envelope in the process. The host cell may die or continue shedding virus.
New enveloped virions exit via exocytosis → lytic-like outcome
🎯 Why This Matters
Understanding each step of viral entry and replication reveals drug targets. For example, mRNA vaccines train the immune system to recognise the spike protein (Step 2), while the antiviral drug remdesivir inhibits RdRp (Step 4). Each intervention targets a specific stage of the cycle.

Viruses vs. Living Cells — A Critical Comparison

One of the most debated questions in biology is whether viruses are alive. The IB expects you to compare viruses with cells using the characteristics of life. The table below lays out the key differences.

Comparison of living cells and viruses across key biological characteristics
CharacteristicLiving CellsViruses
MetabolismCarry out enzymatic reactions, respiration, and biosynthesis independentlyNo metabolism outside a host cell; no ATP production
ReproductionBinary fission (prokaryotes) or mitosis/meiosis (eukaryotes)Cannot reproduce independently; require host cell machinery
Genetic MaterialAlways DNA (both single- and double-stranded forms common)Either DNA or RNA, never both; can be ss or ds
RibosomesPresent (70S in prokaryotes; 80S in eukaryotes)Absent—viruses cannot make their own proteins
Cell MembraneAlways present; phospholipid bilayerNo cell membrane; some have a stolen lipid envelope
EvolutionEvolve through mutation, recombination, and selectionEvolve rapidly via mutation (especially RNA viruses with no proofreading)
Response to EnvironmentHomeostasis; respond to stimuliNo homeostasis; no response to stimuli
KEY TAKEAWAY
Viruses occupy a grey zone between chemistry and biology. They share some features with living things—they have genetic material, they evolve, and they can reproduce (with help). But they lack metabolism, ribosomes, and homeostasis. Think of a virus as a set of IKEA furniture instructions without any tools: the instructions contain all the information needed to build something, but without borrowing someone else's tools (the host cell), nothing gets assembled.

Applications of Virology — Medicine & Biotechnology

Understanding viruses isn't just about preventing disease—it's also about harnessing their capabilities. The same properties that make viruses dangerous (host specificity, efficient gene delivery) make them incredibly useful tools in biotechnology and medicine.

Key applications of viruses in medicine and biotechnology
ApplicationHow Viruses Are UsedExample
VaccinesWeakened (attenuated) or inactivated viruses train the immune system to recognise viral antigens without causing diseaseMMR vaccine (attenuated); polio (inactivated or attenuated); COVID-19 mRNA vaccines use spike protein sequence
Gene TherapyModified viruses (viral vectors) deliver functional genes into patient cells to treat genetic disordersAdeno-associated virus (AAV) vectors used to treat spinal muscular atrophy (Zolgensma)
Phage TherapyBacteriophages that specifically infect and lyse pathogenic bacteria are used as alternatives to antibioticsTreatment of antibiotic-resistant Pseudomonas infections in cystic fibrosis patients
Oncolytic VirotherapyEngineered viruses selectively infect and destroy cancer cells while leaving healthy tissue unharmedT-VEC (talimogene laherparepvec), a modified herpes virus approved for melanoma
Molecular Biology ResearchBacteriophages were instrumental in discovering that DNA is the genetic material and remain key tools in genetic engineeringHershey–Chase experiment (1952); CRISPR systems derived from bacterial antiviral defences

The IB syllabus connects virology to broader themes of unity and diversity: all viruses share the core strategy of parasitising host cells, yet their diversity in structure, genome type, and replication mechanism is staggering. This diversity drives the continuous evolution of both viruses and their hosts, fuelling an evolutionary arms race that shapes immune systems, antibiotic resistance, and even the human genome—approximately 8% of human DNA is composed of ancient retroviral sequences.

🔭 Looking Ahead
At university level, you may study viral ecology (how viruses influence ocean nutrient cycles), virome research (the community of viruses living on and in us), or synthetic virology (designing viruses from scratch for biotechnology). These advanced fields all build on the foundational concepts covered here.

Practice Problems

PROBLEM 1CONCEPTUAL
Explain why viruses are described as 'obligate intracellular parasites.' In your answer, identify at least two cellular components that viruses lack but need in order to reproduce.
PROBLEM 2BASIC CALCULATION
A single bacteriophage infects a bacterial cell and produces 200 new phage particles in one lytic cycle that takes 30 minutes. If all released phages immediately infect new cells and each produces 200 new phages, how many phage particles exist after two complete lytic cycles (60 minutes total)? Assume unlimited host cells.
PROBLEM 3INTERMEDIATE
Compare and contrast the lytic and lysogenic cycles. Under what conditions might a temperate phage switch from the lysogenic cycle to the lytic cycle? Explain the biological significance of this switch.
PROBLEM 4APPLIED
A hospital is dealing with an antibiotic-resistant bacterial infection. A researcher proposes using bacteriophage therapy instead of traditional antibiotics. Explain how phage therapy works, and discuss one advantage and one potential limitation compared to antibiotic treatment.
PROBLEM 5CRITICAL THINKING
Approximately 8% of the human genome consists of sequences derived from ancient retroviruses (endogenous retroviruses, or ERVs). Using your knowledge of the lysogenic cycle and retroviral replication, explain how retroviral DNA could become a permanent part of the human genome. Then evaluate whether the presence of ERVs supports or challenges the classification of viruses as non-living.

Lesson Summary

Viruses are non-cellular obligate intracellular parasites consisting of a nucleic acid genome (DNA or RNA, never both) enclosed in a protein capsid, and sometimes an additional lipid envelope studded with glycoprotein spikes. They lack ribosomes, metabolic enzymes, and the ability to produce ATP, which is why they cannot reproduce outside a host cell. Their host specificity depends on a lock-and-key interaction between viral surface proteins and host cell receptors.

Viruses replicate through the lytic cycle (attachment → penetration → biosynthesis → assembly → lysis, destroying the host cell) or the lysogenic cycle (viral DNA integrates as a provirus/prophage and replicates silently with the host genome until induction triggers the lytic pathway). Applications of virology include vaccines, gene therapy, phage therapy, and oncolytic virotherapy—all of which exploit the same viral mechanisms that cause disease, turning biology's smallest parasites into powerful tools for human health.

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