1) Virion components: the “parts list” and what each part does
A virion is the complete infectious particle that exists outside a host cell. Viruses are not cells: they do not have ribosomes, do not make ATP, and do not grow by dividing. Instead, a virion is built to protect a genome, deliver it into a host cell, and start a takeover of the host’s molecular machinery.
Genome (DNA or RNA): the instruction set
The viral genome contains the information needed to make new virions and to manipulate the host. Viral genomes can be DNA or RNA, and can be single-stranded (ss) or double-stranded (ds). Some are segmented (split into multiple pieces), which can affect how viruses evolve and reassort.
- Functional implication: The genome type strongly influences how the virus makes mRNA and replicates its genome inside the cell (what enzymes it must bring vs borrow from the host).
- Practical example: Many RNA viruses mutate rapidly because their polymerases often lack proofreading, which can help them adapt to host defenses.
Capsid: the protective protein shell
The capsid is a protein coat that packages and protects the genome. Capsids are built from repeating protein subunits (capsomeres), allowing efficient assembly.
- Functional implication: Capsids provide physical stability in the environment and can participate in attachment and entry.
- Practical example: A sturdy capsid helps a virus survive on surfaces or in the gastrointestinal tract.
Envelope (when present): a host-derived membrane with viral proteins
Some viruses have an envelope, a lipid membrane typically acquired from the host cell during budding. The envelope contains viral proteins (often glycoproteins) that are essential for binding and entry.
- Functional implication: Enveloped viruses often enter cells by membrane fusion or endocytosis and are typically more sensitive to drying, heat, and detergents because lipids are easily disrupted.
- Practical example: Soap can inactivate many enveloped viruses by dissolving the lipid envelope, preventing entry.
Attachment proteins: the “key” that fits a host “lock”
Viruses must attach to specific molecules on a host cell surface. These viral molecules are often called attachment proteins (or spikes). In non-enveloped viruses, attachment proteins are part of the capsid; in enveloped viruses, they are embedded in the envelope.
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- Functional implication: Attachment proteins largely determine host range (which species can be infected) and tropism (which tissues/cell types are infected).
- Practical example: A virus that binds a receptor found only on respiratory epithelial cells will preferentially infect the airway.
Step-by-step: how virion structure maps to the early infection steps
- Attachment: Viral attachment proteins bind a specific receptor (and sometimes a co-receptor) on the host cell.
- Entry: Non-enveloped viruses often enter via endocytosis and then escape the endosome; enveloped viruses may fuse with the plasma membrane or fuse after endocytosis.
- Uncoating: The capsid disassembles (fully or partially), releasing the genome where replication can begin (cytoplasm or nucleus depending on the virus).
2) Viral diversity: genome types and shapes, and why they matter
Viral categories are not just labels; they predict how a virus behaves in the environment and inside cells.
Genome types: ss/ds, RNA/DNA, and functional meaning
| Genome category | What it means | Functional consequences (high-level) |
|---|---|---|
| dsDNA | Double-stranded DNA genome | Often uses host-like replication strategies; many rely on host nuclear enzymes or encode their own DNA polymerase. |
| ssDNA | Single-stranded DNA genome | Must be converted to dsDNA before transcription; often smaller genomes. |
| dsRNA | Double-stranded RNA genome | Host cells do not normally make dsRNA; viruses often carry enzymes to make mRNA and must manage strong innate immune detection. |
| ssRNA (+) | Positive-sense RNA can act like mRNA | Genome can be translated soon after entry; replication requires making a complementary negative strand. |
| ssRNA (−) | Negative-sense RNA is complementary to mRNA | Must bring or encode an RNA-dependent RNA polymerase to make mRNA first. |
| Retro-like (RNA → DNA) | RNA genome copied into DNA inside host | Requires reverse transcription; DNA form can integrate into host genome, enabling long-term persistence. |
Virion shapes: icosahedral, helical, complex
Virion shape reflects how capsid proteins assemble and how the particle balances stability with efficient genome packaging.
- Icosahedral: A roughly spherical capsid with 20 triangular faces. Functional meaning: very efficient use of repeating subunits; often stable in the environment.
- Helical: Capsid proteins wrap around the genome in a spiral, forming rod-like or filamentous particles. Functional meaning: length can scale with genome size; common in some plant viruses and many enveloped animal viruses.
- Complex: Structures that are not purely icosahedral or helical, such as many bacteriophages with a head-and-tail design. Functional meaning: specialized machinery can inject genomes through barriers like bacterial cell walls.
Step-by-step: predicting environmental stability from structure
- Check for an envelope: If present, predict higher sensitivity to detergents, drying, and solvents.
- Consider capsid robustness: Non-enveloped icosahedral capsids are often more resistant to environmental stressors.
- Consider transmission route: Viruses that spread via fecal–oral routes often need high stability; respiratory spread may tolerate lower stability if transmission is frequent.
3) Host range and tropism: why viruses infect specific hosts and tissues
Host range describes which species a virus can infect. Tropism describes which cell types or tissues within a host are infected. Both are determined by a chain of requirements; receptor binding is necessary but not sufficient.
Receptors and entry factors: the first gate
To infect a cell, a virus must bind a surface molecule (receptor). Some viruses also require a co-receptor or specific host proteases to activate fusion proteins.
- Why this matters: If a receptor is absent, the virus cannot enter, even if everything else would work.
- Practical example: A virus that binds a receptor expressed only on liver cells will show liver tropism.
Intracellular compatibility: the second gate
After entry, the virus must successfully replicate. This depends on whether the cell provides needed factors (nucleotides, enzymes, transcription machinery) and whether the virus can counteract cellular defenses.
- Why this matters: A virus may attach and enter but fail to replicate if the cell lacks a required factor.
Immune and anatomical barriers: the third gate
Even if cells are permissive, infection depends on whether the virus can reach them (anatomy) and whether it can withstand local immune defenses.
- Examples of barriers: mucus and cilia in airways, stomach acidity, skin, and local innate immune responses.
Why bacteriophages infect bacteria (and not animals), and vice versa
Bacteriophages (phages) are viruses that infect bacteria. Their host specificity is shaped by:
- Cell surface targets: Phages bind bacterial surface structures (e.g., specific outer membrane proteins, pili, teichoic acids, or polysaccharides) that animal cells do not have.
- Delivery mechanism: Many phages use a tail apparatus to inject nucleic acid through bacterial cell envelopes—an entry strategy not used for animal cells.
- Replication requirements: Phage gene expression and replication are tuned to bacterial transcription/translation timing and bacterial intracellular conditions.
Animal and plant viruses, in contrast, are adapted to eukaryotic cell entry pathways (endocytosis, membrane fusion) and to eukaryotic intracellular organization.
Plant virus specificity: an extra access problem
Plant cells have rigid cell walls. Many plant viruses rely on wounds or vectors (like insects) to bypass the wall and reach the plasma membrane. Tropism can also depend on the ability to move cell-to-cell through plasmodesmata.
4) Outcomes of infection at the cell level: what happens after replication begins
Once a virus successfully replicates, the infection can produce different cellular outcomes. These outcomes are conceptual categories; real infections can shift over time.
Cytolytic infection (cell death)
In a cytolytic outcome, the infected cell is damaged or killed as new virions are produced and released.
- Mechanisms: membrane disruption during release, shutdown of host protein synthesis, or triggering of programmed cell death pathways.
- Functional implication: often associated with acute symptoms due to tissue damage and inflammation.
Persistent infection (ongoing production without immediate cell death)
In a persistent infection, the cell survives while producing virus at low or moderate levels, or intermittently.
- Functional implication: can lead to long-term shedding and chronic disease processes.
- Conceptual clue: persistence often requires balancing replication with avoiding killing the host cell too quickly.
Latent infection (genome remains, little to no virion production)
In latency, the viral genome remains in the cell with minimal gene expression and no continuous production of virions. Reactivation can occur when conditions change (e.g., stress, immune suppression, cell differentiation state).
- Functional implication: allows the virus to “hide” from immune detection and persist for long periods.
Step-by-step: a conceptual decision tree for infection outcomes
- Does the virus rapidly produce high levels of progeny? If yes, cell stress and death are more likely (cytolytic).
- Can the cell tolerate viral replication? If yes, ongoing production may occur (persistent).
- Can the virus minimize gene expression and maintain its genome? If yes, latency is possible.
- What changes could reactivate replication? Consider immune status, cell signaling changes, or tissue damage.
5) Intro to immune recognition: how the body “notices” viruses (high level)
Immune recognition can be framed as two overlapping systems: innate (fast, pattern-based) and adaptive (slower, highly specific with memory). This section focuses on cues rather than detailed pathways.
Innate cues: patterns that suggest “viral infection”
- Unusual nucleic acids: dsRNA, RNA with certain chemical features, or DNA in unexpected cellular locations can act as danger signals.
- Cell stress signals: infected cells can display signs of distress that recruit immune responses.
- Interferon signaling (conceptual): cells can warn neighbors to enter an antiviral state, reducing viral replication efficiency.
Structure connection: viruses that produce dsRNA intermediates or expose nucleic acids during entry/uncoating may trigger stronger innate detection.
Adaptive cues: specific recognition of viral parts
- Antibodies: bind exposed viral structures (often attachment proteins) and can block entry (neutralization).
- T cells: detect viral peptides presented by infected cells, enabling targeted killing of infected cells and coordination of immune responses.
Structure connection: attachment proteins on the virion surface are common antibody targets; viruses may evolve changes in these proteins to escape recognition.
Simple matching exercises: structure feature → likely behavior
Match each structure feature (left) to the most likely behavior/outcome (right). Some behaviors may match more than one feature; choose the best match.
| Structure feature | Likely behavior/outcome |
|---|---|
| A. Envelope present | 1. Often disrupted by detergents and drying |
| B. Non-enveloped capsid | 2. Often more stable on surfaces and in the environment |
| C. Negative-sense ssRNA genome | 3. Must carry or rapidly produce an RNA-dependent RNA polymerase to make mRNA |
| D. Complex phage tail structure | 4. Specialized for binding bacterial surfaces and injecting genome through bacterial envelopes |
| E. Attachment protein binds a receptor found mainly on neurons | 5. Neurotropism (preference for nervous tissue) |
| F. Genome integrates into host DNA (in DNA form) | 6. Increased potential for long-term persistence/latency |
| G. Icosahedral capsid with repeating subunits | 7. Efficient assembly and often strong physical stability |
Answer key (hide this during self-testing)
- A → 1
- B → 2
- C → 3
- D → 4
- E → 5
- F → 6
- G → 7
Quick practice: apply the matching logic to real-life scenarios
- Scenario 1: A virus spreads well via contaminated hands and surfaces. Which structural feature is most consistent? (Hint: envelope vs non-envelope.)
- Scenario 2: A virus infects only a narrow range of bacterial strains. Which virion component most likely explains this specificity? (Hint: binding.)
- Scenario 3: A virus can remain silent for years and then reactivate. Which genome behavior supports this? (Hint: genome maintenance.)
