Viruses: Structure, Physiology, Life Cycle, and Related Infectious Agents

Viruses

I. General Characteristics & General Morphology

Viruses are unique infectious agents that lack cellular structure and depend on host cells for replication and metabolism. Their morphology and genetic material vary, but they share several defining features.

• No cells: Viruses do not possess a cell membrane or cellular organelles.

• Chromosome, capsid, envelope: The viral chromosome (DNA or RNA) is enclosed in a protein coat called the capsid. Some viruses also have a lipid envelope derived from the host cell membrane, with embedded viral proteins.

• No ribosomes: Viruses lack ribosomes and cannot synthesize proteins independently.

• Metabolic dependence: Viruses rely on host cell machinery for energy, amino acids, nucleotides, and other metabolic needs.

• Assembly: Viral components are synthesized separately and then assembled into mature virions.

• Genetic material: Viruses contain either DNA or RNA, but never both. The genetic material is always enclosed within the capsid.

II. General Physiology

Virions are mature virus particles that utilize the host cell's metabolic machinery to replicate and produce new viral components. The process involves hijacking the host's systems for nucleic acid and protein synthesis.

• Replication enzymes and substrates: Viruses use host cell enzymes and nucleotides for replication.

• Transcription enzymes and substrates: Host RNA polymerases and nucleotides are used for transcription.

• Translation apparatus: Host ribosomes and amino acids are used for translation of viral proteins.

• Metabolic energy: Viruses depend on host ATP for energy.

Viral components (chromosome and capsid proteins) are synthesized separately and then assembled. Some viruses can infect the same cell and produce different types of virions.

III. Viral Life Cycle

The viral life cycle consists of several steps, including attachment, penetration, synthesis, assembly, and release. Each step is crucial for successful infection and propagation.

• Attachment: Viruses bind to specific receptors on the host cell surface. This specificity determines tissue and species tropism. Some exceptions exist (e.g., rabies, West Nile virus, Ebola).

• Penetration: Viruses enter the host cell by injection (bacteriophages), fusion (enveloped viruses), or endocytosis.

• Synthesis: Viral proteins and nucleic acids are synthesized using host cell machinery. The order of synthesis is tightly regulated.

• Assembly: Viral components are assembled into mature virions.

• Release: Virions are released from the host cell by lysis (non-enveloped viruses) or budding (enveloped viruses).

Synthesis in More Detail for Selected Viruses

• dsDNA viruses: The chromosome is a double-stranded DNA molecule.

  • Host RNA polymerase transcribes viral genes.

  • Host ribosomes translate early and late proteins.

  • DNA is replicated.

• +RNA viruses: The single-stranded RNA chromosome acts as mRNA.

  • Host ribosomes translate viral proteins directly.

  • RNA-dependent RNA polymerase synthesizes complementary RNA strands.

  • New RNA strands serve as templates for further replication and translation.

• -RNA viruses: The single-stranded RNA chromosome is anti-parallel to mRNA.

  • RNA-dependent RNA polymerase synthesizes mRNA from the viral RNA genome.

  • Host ribosomes translate mRNA into viral proteins.

• Retroviruses: These viruses use reverse transcriptase to synthesize DNA from their RNA genome.

  • Reverse transcriptase synthesizes a complementary DNA strand from viral RNA.

  • Integrase incorporates the viral DNA into the host genome.

  • Host cell machinery transcribes and translates viral genes.

IV. Viruses and Cancer

Some viruses are oncogenic, meaning they can cause cancer by integrating their genetic material into host cell DNA and disrupting normal cell regulation. Human papillomavirus (HPV) is a well-known example, causing cervical cancer.

• Oncogenes: Viral genes that can induce uncontrolled cell division.

• HPV: DNA virus associated with cervical and other cancers.

• Other oncogenic viruses: Hepatitis B and C viruses, Epstein-Barr virus.

V. Prions

Prions are infectious proteins that cause neurodegenerative diseases. They lack nucleic acids and are resistant to standard methods of inactivation.

• Structure: Misfolded normal host glycoprotein.

• Diseases: Creutzfeldt-Jacob disease, Bovine Spongiform Encephalopathy (mad cow disease).

• Transmission: Can occur through ingestion of contaminated tissue.

VI. Viroids

Viroids are small, circular RNA molecules that infect plants. They do not encode proteins and cause disease by interfering with host gene expression.

• Structure: RNA, 300-400 nucleotides.

• Pathogenicity: Cause disease in plants, often transmitted by insects or mechanical means.

VII. Coat Protein Mediated Resistance

Biotechnological approaches have introduced viral coat protein genes into plants to confer resistance against viral infection. This method is used in agriculture to protect crops from devastating viral diseases.

• Example: Grapevine fanleaf virus resistance in grape plants.

• Mechanism: Expression of viral coat protein in the plant prevents successful infection by the virus.

• Risks: Potential for unintended effects, such as production of coat protein for animal viruses.

Table: Comparison of Infectious Agents

Agent	Genetic Material	Protein Coat	Replication Method	Diseases Caused
Virus	DNA or RNA	Yes (capsid)	Host cell machinery	Influenza, HIV, HPV, etc.
Prion	None	No	Protein misfolding	Creutzfeldt-Jacob, BSE
Viroid	RNA	No	Host cell RNA polymerase	Plant diseases

Additional info: The notes have been expanded for clarity and completeness, with definitions, examples, and a comparison table added for academic context.