Characterizing and Classifying Viruses, Viroids, and Prions: Study Notes

Characterizing and Classifying Viruses, Viroids, and Prions

Viral Replication in Animal Cells

Animal viruses replicate using pathways similar to bacteriophages, but with distinct differences due to the presence of envelopes, the eukaryotic nature of animal cells, and the absence of cell walls. The replication process involves several stages: attachment, entry, uncoating, synthesis, assembly, and release.

Attachment

• Chemical attraction occurs between viral proteins and cell receptors.

• Animal viruses lack tails or tail fibers; instead, they use glycoprotein spikes or other attachment molecules.

Entry and Uncoating

• Viruses enter host cells by three main mechanisms:

  • Direct penetration: Viral genome enters the cell, leaving the capsid outside.

  • Membrane fusion: Viral envelope fuses with the host membrane, releasing the genome.

  • Endocytosis: Host cell engulfs the virus, which is then uncoated inside the cell.

Synthesis

• DNA viruses often enter the nucleus for replication.

• RNA viruses typically replicate in the cytoplasm.

• Retroviruses use a DNA intermediary transcribed by viral reverse transcriptase.

Assembly and Release

• Most DNA viruses assemble in the nucleus; most RNA viruses assemble in the cytoplasm.

• Enveloped viruses acquire host membrane during release (budding).

• Naked viruses are released by exocytosis or lysis.

Latency

• Some animal viruses remain dormant as latent viruses or proviruses.

• Latency may last years; provirus incorporation into host DNA is permanent.

Comparison of Bacteriophage and Animal Virus Replication

This table summarizes the key differences between bacteriophage and animal virus replication.

Step	Bacteriophage	Animal Virus
Attachment	Proteins on tail attach to proteins on cell wall	Spikes, capsid, or envelope proteins attach to proteins or glycoproteins on cell membrane
Penetration	Genome is injected into cell or diffuses into cell	Capsid enters cell by direct penetration, fusion, or endocytosis
Uncoating	None	Removed by cellular enzymes
Site of Synthesis	In cytoplasm	RNA viruses in cytoplasm; most DNA viruses in nucleus
Site of Assembly	In cytoplasm	RNA viruses in cytoplasm; most DNA viruses in nucleus
Mechanism of Release	Lysis	Budding (enveloped viruses) or exocytosis/lysis (naked viruses)
Nature of Chronic Infection	Lysogeny; always incorporated into host chromosome, may leave host chromosome	Latency, with or without incorporation into host DNA; incorporation is permanent

The Role of Viruses in Cancer

Viruses can contribute to cancer by affecting protooncogenes and oncogenes, which regulate cell growth and division. Environmental factors and viral infections can activate oncogenes, leading to uncontrolled cell division.

• Viruses may carry oncogenes or promote activation of host oncogenes.

• Some viruses interfere with tumor repression.

• Examples of virus-induced cancers: Burkitt’s lymphoma, Hodgkin’s disease, Kaposi’s sarcoma, cervical cancer.

Culturing Viruses in the Laboratory

Viruses require host cells for growth and cannot be cultured in standard microbiological media. Three main methods are used: mature organisms, embryonated eggs, and cell cultures.

Culturing in Mature Organisms

• Bacteriophages are grown in bacteria using liquid cultures or agar plates.

• Lysis of bacteria produces plaques, which allow estimation of phage numbers by plaque assay.

Culturing in Plants and Animals

• Viruses can be cultured in various plants and animals, though laboratory animals are costly and raise ethical concerns.

Culturing in Embryonated Chicken Eggs

• Chicken eggs are inexpensive, large, free of contaminants, and contain nourishing yolk.

• Embryonic tissues provide ideal sites for viral growth; some vaccines are prepared in chicken cultures.

Other Parasitic Particles: Viroids and Prions

Viroids

Viroids are extremely small, circular pieces of single-stranded RNA (ssRNA) that are infectious and pathogenic in plants. They lack a capsid and do not code for proteins.

• Viroid RNA adheres to complementary plant RNA, leading to degradation by plant enzymes and disease.

Prions

Prions are proteinaceous infectious agents. They exist in two forms:

• Cellular PrP: Normal, functional structure with α-helices.

• Prion PrP: Disease-causing form with β-pleated sheets.

• Prion PrP induces cellular PrP to refold into the prion form, leading to disease.

Prion Diseases

• Prion diseases include spongiform encephalopathies (e.g., BSE, scrapie, kuru, CWD, vCJD).

• Characterized by large vacuoles in brain tissue, giving a spongy appearance.

• Transmitted by ingestion, transplantation, or contact with infected tissues.

• No standard treatment; prions are resistant to normal sterilization, destroyed by incineration or autoclaving in concentrated sodium hydroxide.

Comparison of Viruses, Viroids, Prions, and Bacterial Cells

This table compares the main properties of bacteria, viruses, viroids, and prions.

Property	Bacteria	Viruses	Viroids	Prions
Width	200–2000 nm	10–400 nm	2–10 nm	5 nm
Length	200–550,000 nm	10–400 nm	2–10 nm	5 nm
Nucleic Acid	Both DNA and RNA	Either DNA or RNA, never both	RNA only	None
Protein	Present	Present	Absent	Present
Cellular	Yes	No	No	No
Cytoplasmic Membrane	Present	Absent (some viruses have a membranous envelope)	Absent	Absent
Functional Ribosomes	Present	Absent	Absent	Absent
Growth	Yes	No	No	No
Self-Replicating	Yes	No	No	No, transforms PrP protein present in cell
Responsiveness	Present	Some bacteriophages respond to a host cell by injecting their genome	Absent	Absent
Metabolism	Present	Absent	Absent	Absent

Additional info: The notes above expand on brief points with academic context, definitions, and examples to ensure completeness and clarity for microbiology students.