BackCharacterizing and Classifying Viruses, Viroids, and Prions
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Characterizing and Classifying Viruses, Viroids, and Prions
Characteristics of Viruses
Viruses are acellular, infectious agents that lack cell structure and metabolic capabilities. They require host cells to reproduce and are responsible for numerous diseases in plants, animals, and other organisms.
Definition: A virus is a minuscule, acellular agent composed of nucleic acid (DNA or RNA) surrounded by a protein coat (capsid).
Virion: The extracellular form of a virus, consisting of nucleic acid and capsid; may have an envelope.
Nucleocapsid: The combination of nucleic acid and capsid.
Envelope: Some viruses possess a phospholipid membrane acquired from the host cell, making them enveloped virions.
Intracellular State: Once inside a host cell, the capsid is removed, and the virus exists as nucleic acid.
Example: The Tobacco Mosaic Virus (TMV) was the first virus isolated and visualized using electron microscopy.
Genetic Material of Viruses
Viral genomes vary in type and structure, which is a key factor in their classification.
Types: DNA or RNA, which may be double-stranded (ds) or single-stranded (ss).
Forms: Linear or circular, single or multiple molecules.
Size: Viral genomes are much smaller than cellular genomes (e.g., bacteriophage MS2 has only three genes).
Example: Viral genomes are described as dsDNA, ssDNA, dsRNA, or ssRNA.
Hosts of Viruses
Viruses exhibit host specificity, infecting particular cell types due to molecular affinity between viral and host surface proteins.
Range: Viruses infect archaea, bacteria (bacteriophages), plants, protozoa, fungi, and animals.
Fungal Viruses: Often lack an extracellular stage; spread by cell fusion.
Example: Bacteriophages infect bacteria; animal viruses infect specific animal cells.
Sizes of Viruses
Viruses are extremely small, often requiring electron microscopy for visualization.
Smallest: 17 nm diameter
Largest: ~500 nm, comparable to the smallest bacterial cells
Capsid Morphology
The capsid is a protein shell composed of subunits called capsomeres, which protect the viral genome and aid in host attachment.
Capsomeres: May be made of one or several types of proteins.
Viral Shapes
Viruses are classified by their shape, which is determined by capsid structure.
Helical: Capsomeres form a tube-like structure around the nucleic acid.
Polyhedral: Spherical, often icosahedral (20 faces).
Complex: Capsids with multiple shapes and structures.
The Viral Envelope
Some viruses have an envelope derived from the host cell membrane, containing viral proteins for host recognition.
Enveloped Virion: Has a membrane surrounding the capsid.
Naked Virion: Lacks an envelope; more resistant to environmental conditions but more easily recognized by the immune system.
Envelope Acquisition: Occurs during viral replication or release.
Classification of Viruses
Viruses are classified based on nucleic acid type, envelope presence, shape, and size.
Family and Genus: Viral families and genera are named based on characteristics or important members.
Species: Common English names in italics (e.g., rabies virus).
Viral Replication
Viruses depend on host cells for replication, lacking necessary enzymes and ribosomes. Replication cycles vary, with lytic and lysogenic pathways being prominent.
Lytic Replication: Results in cell lysis and release of new virions.
Lysogenic Replication: Viral genome integrates into host DNA, remaining dormant until induction.
Lytic Replication of Bacteriophages
Bacteriophage T4 is a model for lytic replication, involving five stages:
Attachment: Virion attaches to host cell via tail fibers.
Entry: Lysozyme weakens cell wall; DNA is injected.
Synthesis: Host DNA degraded; viral proteins and genome synthesized.
Assembly: Capsomeres assemble spontaneously; genome is packaged.
Release: Lysozyme causes cell lysis, releasing virions.
Lysogenic Replication of Bacteriophages
Temperate phages (e.g., lambda phage) integrate their genome into the host chromosome as a prophage, which is replicated with the host DNA.
Lysogenic Conversion: Prophage genes can alter host phenotype (e.g., toxin production).
Induction: Prophage excised, resumes lytic cycle.
Replication of Animal Viruses
Animal viruses replicate similarly to bacteriophages but differ in entry and uncoating mechanisms due to the absence of cell walls and presence of envelopes.
Attachment: Via glycoprotein spikes or capsid/envelope molecules.
Entry: Direct penetration, membrane fusion, or endocytosis.
Uncoating: Capsid removal to release genome.
Synthesis of Animal Viruses
Replication strategies depend on nucleic acid type:
dsDNA: Replication similar to cellular DNA; usually in nucleus.
ssDNA: Host enzymes synthesize complementary DNA; self-priming via hairpin loop.
+ssRNA: Direct translation; complementary -ssRNA synthesized as template.
Retroviruses: +ssRNA transcribed to DNA by reverse transcriptase; DNA integrated into host genome.
-ssRNA: RNA-dependent RNA transcriptase synthesizes mRNA.
dsRNA: +RNA strand translated; both strands serve as templates for replication.
Assembly and Release of Animal Viruses
Most DNA viruses assemble in the nucleus; RNA viruses in the cytoplasm. Enveloped viruses are released by budding, acquiring their envelope from host membranes. Naked viruses may cause cell lysis.
Budding: Allows persistent infection; cell remains alive for some time.
Latency of Animal Viruses
Some animal viruses (e.g., HIV, herpesviruses) can remain dormant in host cells as proviruses, integrated into the host genome. Latency may last years, and proviruses are not excised like prophages.
The Role of Viruses in Cancer
Viruses contribute to neoplasia (uncontrolled cell growth), which can result in benign or malignant tumors (cancer). Viral genes may activate protooncogenes or inhibit oncogene repressors, leading to cancer.
Examples: Hodgkin’s disease, Kaposi’s sarcoma, cervical cancer.
Both DNA and RNA viruses: Can induce cancer.
Culturing Viruses in the Laboratory
Viruses require host cells for growth and cannot be cultured in standard media. Several methods are used:
Mature Organisms: Bacteriophages grown in bacteria; plaques indicate lysis.
Embryonated Chicken Eggs: Used for culturing animal viruses and vaccine production.
Cell (Tissue) Culture: Diploid cell cultures (limited lifespan) and continuous cell cultures (derived from tumor cells, longer lasting).
Are Viruses Alive?
Viruses lack growth, self-reproduction, responsiveness, and metabolism outside host cells. However, they invade cells, control host machinery, possess genomes, and evolve, placing them on the threshold of life.
Other Parasitic Particles: Viroids and Prions
Viroids and prions are acellular infectious agents distinct from viruses.
Characteristics of Viroids
Structure: Small, circular RNA molecules without capsids.
Hosts: Infect plants, causing disease by binding to mRNA and triggering degradation.
Viroidlike Agents: Affect fungi; no known animal diseases.
Characteristics of Prions
Structure: Infectious protein particles lacking nucleic acids.
Replication: Convert normal cellular PrP (c-PrP) into disease-causing prion PrP (p-PrP) via templating.
Pathology: Prion PrP accumulates in the brain, causing neuronal death and spongiform changes.
Diseases: Bovine spongiform encephalitis (BSE), scrapie, variant Creutzfeldt-Jakob disease.
Resistance: Not destroyed by normal cooking or sterilization; destroyed by incineration and specific enzymes.
Prevention: Avoid animal-derived protein in feed.
Summary Table: Virus, Viroid, and Prion Comparison
Agent | Genetic Material | Structure | Host Range | Replication Method | Diseases |
|---|---|---|---|---|---|
Virus | DNA or RNA (ds or ss) | Capsid (may have envelope) | Bacteria, plants, animals, fungi, protozoa | Requires host cell machinery | Influenza, HIV, herpes, etc. |
Viroid | RNA (circular, ss) | No capsid | Plants | Host cell enzymes | Plant diseases (e.g., potato spindle tuber) |
Prion | None | Protein (PrP) | Animals (especially mammals) | Templating of normal proteins | BSE, scrapie, Creutzfeldt-Jakob disease |
Additional info: Prion diseases are unique in that they are caused by protein misfolding rather than nucleic acid mutations. Viroids are the smallest known infectious agents, and their mechanism of pathogenesis is still under study.