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

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Characterizing and Classifying Viruses, Viroids, and Prions

Characteristics of Viruses

Viruses are minuscule, acellular infectious agents that possess either DNA or RNA as their genetic material. They are responsible for numerous diseases in humans, animals, plants, and bacteria. Viruses lack the ability to carry out metabolic processes, grow, or respond to their environment independently. Instead, they rely on host cells to reproduce and increase their numbers. Viruses exist in two states: extracellular (virion) and intracellular.

  • Virion: The extracellular state, consisting of a protein coat (capsid) surrounding the nucleic acid. Some virions have a phospholipid envelope.

  • Intracellular state: The capsid is removed, and the virus exists as nucleic acid within the host cell.

  • No cytoplasmic membrane, cytosol, or organelles.

Virion structure showing capsid and nucleic acid

Genetic Material of Viruses

Viruses display greater diversity in their genomes compared to cells. Their genetic material can be DNA or RNA, but never both. The genome may be double-stranded (dsDNA, dsRNA) or single-stranded (ssDNA, ssRNA), linear and segmented, or single and circular. Viral genomes are much smaller than those of cells.

  • Classification: Based on nucleic acid type, genome structure, and replication strategy.

  • Examples: Influenzavirus (segmented RNA), Poliovirus (single RNA).

Relative sizes of viral genomes compared to cellular genomes

Hosts of Viruses

Viruses typically infect specific host cells due to the affinity between viral surface proteins and complementary proteins on the host cell surface. Some viruses are highly specific, infecting only certain cell types in particular hosts, while others (generalists) can infect many kinds of cells or hosts. All types of organisms are susceptible to some virus.

  • Specificity: Determined by viral surface proteins.

  • Examples: HIV (specific), West Nile virus (generalist).

Examples of plant, bacterial, and human hosts of viral infections

Capsid Morphology

The capsid provides protection for the viral nucleic acid and facilitates attachment to host cells. Capsids are composed of protein subunits called capsomeres, which may be made of one or several types of proteins.

Viral Shapes

Viruses are classified by their virion shape. The three basic types are:

  • Helical: Rod-shaped, with nucleic acid wound in a spiral.

  • Polyhedral: Many-sided, often icosahedral.

  • Complex: More intricate structures, such as bacteriophages.

Three basic types of viral shapes: helical, polyhedral, complex Complex shape of bacteriophage T4

The Viral Envelope

Some viruses acquire an envelope from the host cell during replication or release. The envelope consists of a phospholipid bilayer and proteins, including virally coded glycoproteins (spikes) that play a role in host recognition. Enveloped viruses are generally more fragile than naked viruses.

Enveloped virion structure

Classification of Viruses

Viruses are classified based on the type of nucleic acid, presence of an envelope, shape, and size. Viral genera are organized into families, but relationships among viruses are not fully understood.

Viral Replication: Lytic Cycle

Viral replication depends on host organelles and enzymes. The lytic cycle results in the death and lysis of the host cell and consists of five stages:

  1. Attachment: Virus attaches to host cell via tail fibers and specific receptors.

  2. Entry: Lysozyme weakens cell wall, tail sheath contracts, genome injected.

  3. Synthesis: Viral genome directs synthesis of viral components.

  4. Assembly: Capsid and other components assemble into mature virions.

  5. Release: Lysozyme and virion release cause cell lysis.

Lytic replication cycle in bacteriophages Pattern of virion abundance in lytic cycle

Viral Replication: Lysogenic Cycle

The lysogenic cycle is a modified replication cycle in which infected host cells grow and reproduce normally for generations before lysing. Temperate phages integrate their genome into the host chromosome, becoming a prophage. Lysogenic conversion occurs when phages carry genes that alter the phenotype of a bacterium.

  • Induction: Prophage excised from chromosome, reenters lytic phase.

  • Inductive agents: UV light, X-rays, carcinogenic chemicals.

Bacteriophage lambda structure Lysogenic replication cycle in bacteriophages

Replication of Animal Viruses

Animal viruses follow similar replication pathways as bacteriophages, with differences due to the presence of an envelope, eukaryotic cell structure, and lack of cell wall. Attachment occurs via glycoprotein spikes or other molecules. Entry and uncoating can occur by direct penetration, membrane fusion, or endocytosis.

  • Direct penetration: Naked viruses inject genome.

  • Membrane fusion: Viral envelope fuses with cell membrane.

  • Endocytosis: Host cell engulfs virus.

Three mechanisms of entry of animal viruses Uncoating of animal viruses

Synthesis of Animal Viruses

DNA viruses often enter the nucleus, while RNA viruses replicate in the cytoplasm. The strategy depends on the type of nucleic acid:

  • dsDNA viruses: Replication similar to cellular DNA.

  • ssDNA viruses: ssDNA folds to form dsDNA, replicated by cellular DNA polymerase.

  • +ssRNA viruses: Acts as mRNA, translated directly.

  • -ssRNA viruses: Requires RNA-dependent RNA transcriptase to make +ssRNA.

  • dsRNA viruses: Positive strand serves as mRNA; both strands act as templates.

  • Retroviruses: Use DNA intermediary transcribed by reverse transcriptase.

Synthesis of proteins and genomes in animal RNA viruses

Assembly and Release of Animal Viruses

Most DNA viruses assemble in the nucleus, while most RNA viruses assemble in the cytoplasm. Enveloped viruses are released via budding, which can result in persistent infections. Naked viruses are released by exocytosis or lysis.

Budding process in enveloped viruses

Latency of Animal Viruses

Some animal viruses remain dormant in host cells as latent viruses or proviruses. Latency may last for years, and incorporation of provirus into host DNA is permanent.

The Role of Viruses in Cancer

Cell division is tightly regulated by genes. Neoplasia is uncontrolled cell division, resulting in tumors. Malignant tumors are cancers, which can metastasize. Proto-oncogenes promote cell growth; their uncontrolled activation (oncogenes) can lead to cancer. Environmental factors and viruses can activate oncogenes.

  • Oncogene Theory: Multiple mutations (“hits”) are required to induce cancer.

  • Viruses: May cause 20–25% of human cancers, carry oncogenes, promote host oncogenes, or interfere with tumor repression.

  • Examples: Burkitt’s lymphoma, Hodgkin’s disease, Kaposi’s sarcoma, cervical cancer.

Oncogene theory of cancer induction

Culturing Viruses in the Laboratory

Viruses cannot grow in standard media and must be cultured inside host cells. Three types of media are used:

  • Mature organisms: Bacteria, plants, animals.

  • Embryonated eggs: Fertilized chicken eggs provide ideal sites for viral growth.

  • Cell cultures: Cells isolated and grown in medium or broth; includes diploid and continuous cell cultures.

Viral plaques in a lawn of bacterial growth Inoculation sites for culture of viruses in embryonated chicken eggs Example of cell culture

Are Viruses Alive?

There is debate about whether viruses are alive. Some consider them complex pathogenic chemicals, while others view them as the least complex living entities. Viruses invade cells, replicate, and evolve.

Other Parasitic Particles: Viroids and Prions

Viroids

Viroids are extremely small, circular pieces of ssRNA that are infectious and pathogenic in plants. They lack a capsid and do not code for proteins. Viroid RNA binds to complementary plant mRNA, forming dsRNA, which is degraded by plant enzymes, resulting in disease.

RNA strand of potato viroid Effect of viroids on plants

Prions

Prions are infectious agents composed entirely of protein. Cellular PrP (c-PrP) is made by mammals and has α-helices. Prion PrP (p-PrP) has β-pleated sheets and causes c-PrP to refold into p-PrP, leading to clumps that disrupt neuron function and cause spongiform encephalopathies.

  • Prion diseases: BSE, scrapie, kuru, CWD, vCJD.

  • Transmission: Ingestion, transplantation, contact with infected tissues.

  • Deactivation: Prions are resistant to standard sterilization; destroyed by incineration or autoclaving in concentrated sodium hydroxide.

Two stable forms of prion protein Templating action of prions Normal and spongiform encephalopathy brain tissue

Micro Matters: Pneumonia

Pneumonia is an infection of the lungs and can be caused by bacteria, fungi, or viruses. Bacterial pneumonia is often treatable with antibiotics, while fungal and viral pneumonia have fewer specific treatment options.

Summary Table: Comparison of Viruses, Viroids, Prions, and Bacterial Cells

Property

Viruses

Viroids

Prions

Bacterial Cells

Genetic Material

DNA or RNA

ssRNA

None

DNA

Protein Coat

Capsid

None

None

Cell wall/membrane

Replication

Host cell machinery

Host cell machinery

Templating

Binary fission

Pathogenicity

Humans, animals, plants, bacteria

Plants

Animals (esp. CNS)

Humans, animals, plants

Treatment

Antivirals, vaccines

None

None

Antibiotics

Additional info: Table entries inferred for completeness and clarity.

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