Viruses, Viroids, and Prions: Structure, Classification, and Life Cycles

Chapter 13: Viruses, Viroids, and Prions

Learning Objectives

• Differentiate a virus from a bacterium.

• Describe the structure of both enveloped and non-enveloped viruses.

• Provide examples of viral family, genus, and common names.

• Explain how bacteriophages and animal viruses are cultured.

• List techniques used to identify viruses.

• Describe the lytic and lysogenic cycles of bacteriophages.

• Define proto-oncogene, oncogene, and transformed cell.

• Differentiate between latent and persistent viral infections.

• Contrast viruses, viroids, and virusoids.

• Discuss how proteins (prions) can be infectious.

Distinctive Features of Viruses

Obligatory Intracellular Parasites

Viruses are unique infectious agents that require living host cells to multiply. Unlike bacteria, they cannot reproduce or carry out metabolic processes independently.

• Require living host cells for replication.

• Utilize host cell's synthesizing machinery for multiplication.

• Contain DNA or RNA as genetic material, never both.

• Genetic material is surrounded by a protein coat (capsid).

• Lack ribosomes and ATP-generating mechanisms.

Types of Viruses

• Bacteriophages: Infect bacteria; receptor sites may be on cell wall, fimbriae, or flagella.

• Animal viruses: Infect animal cells; receptor sites are typically on the plasma membrane.

• Plant, insect, fungal, algal viruses: Infect respective hosts.

• Giant viruses: Large enough to be seen under a light microscope; involved in microbial food webs.

• Virophages: Viruses that infect other viruses.

Viral Structure

Virion: The Complete Viral Particle

A virion is a fully developed, infectious viral particle capable of transmission and infection.

• Viral genome: DNA or RNA, single- or double-stranded, linear or circular.

• Capsid: Protein coat made of subunits called capsomeres.

• Envelope (in some viruses): External to the capsid, composed of lipid, protein, and carbohydrate; derived from host cell membrane during viral exit (budding).

• Spikes/Peplomers: Glycoprotein projections from the capsid or envelope; mediate host cell recognition and attachment (host cell tropism).

General Morphology of Viruses

Major Viral Shapes

Viruses exhibit diverse morphologies, which are important for classification and identification.

• Helical viruses: Hollow, cylindrical capsid; e.g., Rabies virus, Ebola virus.

• Polyhedral viruses: Many-sided, most commonly icosahedral (20 triangular facets, 12 corners); e.g., Adenoviruses, Poliovirus.

• Enveloped viruses: Spherical or pleomorphic; envelope surrounds the capsid; e.g., Influenza virus.

• Complex viruses: Possess additional structures such as tail fibers and secondary envelopes; e.g., Bacteriophage.

Taxonomy of Viruses

Classification System

Viruses are classified based on their genetic material and replication strategy.

• Family names end in -viridae (e.g., Herpesviridae).

• Genus names end in -virus (e.g., Herpes Simplex Virus).

• Species: Group of viruses sharing genetic information and ecological niche (host).

• Common names are used for species; subspecies are designated by numbers.

Host Range and Viral Transmission

Host Range

Viruses can infect a wide variety of hosts, but each virus typically has a specific host range determined by compatibility with host cell receptors.

• Hosts include animals, humans, plants, fungi, protozoa, insects, bacteria, and archaea.

Viral Transmission

• Direct contact

• Vector transmission: Vectors may be mechanical (carrying virus on body) or biological (virus replicates within vector).

Multiplication of Bacteriophages

Lytic Cycle

The lytic cycle results in the destruction of the host cell and release of new phage particles.

1. Attachment: Phage attaches to host cell via tail fibers.

2. Penetration: Phage injects DNA into host cell; lysozyme opens cell wall.

3. Biosynthesis: Phage DNA and proteins are synthesized; host cell protein synthesis is halted.

4. Maturation: Assembly of phage particles.

5. Release: Host cell lyses, releasing new phages.

Lysogenic Cycle

In the lysogenic cycle, phage DNA integrates into the host genome and replicates with it, without killing the host cell immediately.

• Prophage: Phage DNA incorporated into host DNA.

• Phage conversion: Host cell exhibits new properties (e.g., toxin production).

• Specialized transduction: Specific bacterial genes transferred to another bacterium via a phage.

Multiplication of Animal Viruses

General Steps

Animal viruses follow a multi-step process to infect host cells.

1. Attachment: Virus binds to host cell membrane receptors.

2. Entry: By receptor-mediated endocytosis or membrane fusion.

3. Uncoating: Viral nucleic acid is separated from its capsid by viral or host enzymes.

4. Biosynthesis: Production of viral nucleic acids and proteins.

5. Maturation: Assembly of viral components.

6. Release: By budding (enveloped viruses) or rupture (non-enveloped viruses).

Mechanisms of Entry and Uncoating

• Direct penetration: Capsid remains outside; genome enters cell.

• Membrane fusion: Viral envelope fuses with host membrane; capsid enters cytoplasm.

• Endocytosis: Virus is engulfed; endolysosome forms; protease activation releases genome.

Replication of Viral Genomes

DNA Viruses

• Replication is similar to cellular DNA replication.

• Most DNA viruses replicate in the nucleus; viral proteins are made in the cytoplasm.

• Exceptions: Hepatitis B virus (DNA from RNA intermediary), Parvoviruses (ssDNA genomes).

RNA Viruses

• Replicate in the cytoplasm using RNA-dependent RNA polymerase.

• Types: Positive-sense ssRNA, Negative-sense ssRNA, dsRNA, Retroviruses.

• Retroviruses use reverse transcriptase to produce DNA from RNA template.

Outcomes of Eukaryotic Viral Infections

Cell Death and Persistence

• Lytic infection: Naked viruses may lyse cells.

• Budding: Enveloped viruses exit by budding, often without immediate cell death.

• Latent infection: Virus remains dormant; may reactivate (e.g., Herpes Simplex Virus).

• Persistent infection: Slow, chronic infection (e.g., Hepatitis C Virus).

Viruses and Cancer

Oncogenesis

Some viruses can induce cancer by disrupting normal cell regulation.

• Neoplasia: Uncontrolled cell division; mass of cells forms a tumor.

• Benign vs. malignant tumors: Malignant tumors invade and spread (metastasis).

• Proto-oncogenes: Promote cell growth and division; can become oncogenes if mutated or dysregulated.

• Oncogenes: Genes that can cause cancer when activated.

• Environmental factors: UV light, radiation, carcinogens, viruses.

HPV and Oncogenesis

• High-risk HPV strains produce E6 and E7 proteins.

• E7 inactivates RB tumor suppressor gene; E6 inactivates p53, preventing cell cycle arrest and apoptosis.

Viral Variation: Influenza Virus Example

Antigenic Drift and Shift

• Antigenic drift: Gradual mutations in viral genes (e.g., hemagglutinin, neuraminidase).

• Antigenic shift: Reassortment of segmented RNA genomes, producing new viral strains.

• Both processes contribute to vaccine resistance and emergence of new influenza strains.

Growing Viruses in the Laboratory

Bacteriophage Cultivation

• Grown in bacteria; form plaques (clearings) on bacterial lawns.

• Plaque-forming units (PFU) quantify viral particles.

Animal Virus Cultivation

• Grown in living animals (e.g., mice, rabbits, guinea pigs).

• Some viruses grown in embryonated eggs (used for vaccine production).

• Cell cultures: Diploid (limited generations) and continuous (cancer cells, e.g., HeLa cells).

Viral Identification Techniques

• Serological tests: Detect virus by reaction with antibodies.

• Nucleic acid tests: PCR and other molecular methods.

• Cytopathic effects (CPE): Morphological changes in infected cells observed in culture.

Plant Viruses, Viroids, and Virusoids

Plant Viruses

• Enter through wounds or via insect vectors.

• Cause diseases in economically important plants.

Viroids

• Short pieces of naked RNA; no protein coat.

• Cause diseases such as potato spindle tuber disease.

Virusoids

• Viroids enclosed in a protein coat; require co-infection with a virus for replication.

• Example: Hepatitis D virus (HDV) requires Hepatitis B virus for replication.

Prions: Proteinaceous Infectious Particles

Nature and Diseases

• Prions are misfolded proteins that can induce abnormal folding of normal proteins.

• Transmissible by ingestion, transplant, or surgical instruments.

• Cause spongiform encephalopathies: "Mad cow disease," Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome, sheep scrapie.

• Normal prion protein (PrPC) is converted to infectious form (PrPSc), which accumulates in brain cells.

Summary Table: Comparison of Viruses, Viroids, Virusoids, and Prions

Agent	Genetic Material	Protein Coat	Host	Example Disease
Virus	DNA or RNA	Present	Animals, plants, bacteria, fungi	Influenza, HIV, Rabies
Viroid	RNA (short, circular)	Absent	Plants	Potato spindle tuber disease
Virusoid	RNA (circular)	Present (requires helper virus)	Plants, animals (with co-infection)	Hepatitis D (with Hepatitis B)
Prion	None (protein only)	Absent	Animals (especially mammals)	Mad cow disease, CJD

Key Equations and Concepts

• Viral replication rate (generalized): $\text{Rate} = k[\text{Virus}][\text{Host Cell}]$

• Reverse transcription (retroviruses): $\text{RNA} \xrightarrow{\text{Reverse Transcriptase}} \text{DNA}$

Additional info: Academic context and examples have been expanded for clarity and completeness. The summary table is inferred from standard microbiology comparisons.