chapter 26

CHAPTER 26: Viruses

26.0 Introduction

  • Viruses lack many characteristics of life but are integral to the study of biology due to their ubiquity and impact on all living organisms.
  • All viruses contain genetic material in a protein shell (capsid).
  • Disease implications: viruses are responsible for diseases such as AIDS, the common cold, and cancers.
  • The global death toll from the 1918 influenza pandemic was between 50 to 100 million.

26.1 The Nature of Viruses

Learning Outcomes
  1. Describe the structures of viruses and their genomes.
  2. Explain why viruses are obligate cellular parasites.
Structure of Viruses
  • Basic structure: genome (DNA or RNA) enclosed in a protein capsid. If tightly associated, it is termed a nucleocapsid.
  • Capsids consist of one or more protein types forming structures such as icosahedrons or helical filaments.
  • Some viruses possess an envelope derived from host cell membranes.
  • Viral particles (virions) differ from cells: they lack metabolic activity, cytoplasm, and cannot replicate independently.
  • Viral genomes can be linear or circular, single-stranded or double-stranded.
  • Classification often based on the structure and type of the viral genome.
Viral Morphology
  • Viral capsids manifest in various shapes:
    • Helical: e.g., Tobacco Mosaic Virus (TMV)
    • Icosahedral: e.g., adenovirus (20 triangular facets)
    • Complex forms: Bacteriophages (binal symmetry - icosahedral head + helical tail).
  • Enveloped viruses exhibit greater diversity in morphology than naked viruses, which tend to be filamentous or icosahedral.
Obligate Cellular Parasites
  • Viruses require a host for replication and cannot survive or reproduce outside host cells.
  • Infected cells become factories for new virions, often using their cellular machinery:
    • Viral replication: requires taking over the host's cellular processes. Early genes take over machinery; late genes form capsid proteins for virion assembly.
    • The viral genome determines production and assembly.
Viral Genomes
  • Viral genomes inform their classification:
    • 70% of viruses are RNA-based (e.g., influenza, measles, COVID-19).
    • Unique replication mechanisms lead to higher mutation rates in RNA viruses, complicating vaccine and antiviral drug development.
    • Influenza viruses have segmented genomes, producing diversity during virion assembly.

26.2 Viral Diversity

Learning Outcomes
  1. Compare different classification systems for viruses.
  2. Describe the role played by metagenomics in describing viral diversity.
Classification Systems
  • Classifications based on:
    • Taxonomy
    • Disease types
    • Host range and tissue tropism
    • Genome type and expression.
  • Metagenomics is allowing for identifying novel viruses, emphasizing the necessity for consistent classification systems.
  • Baltimore Classification: organizes viruses based on expression and replication of their genomes into seven groups.
Taxonomic Classification
  • The ICTV has established a 15-rank system for viral taxonomy (including realms and species).
  • It bridges traditional systems with unique viral characteristics, aiming to keep pace with genomic discoveries.
Viral Ecology
  • Viral population dynamics remain understudied due to difficulties in culturing hosts and their viruses in the lab. Metagenomics aids this by revealing ecological roles.

26.3 Bacterial and Archaeal Viruses

Learning Outcomes
  1. Distinguish between lytic and lysogenic cycles in bacteriophage.
  2. Describe how viruses can contribute DNA other than their host.
  3. Explain the unusual features of archaeal viruses.
Bacteriophage
  • They are unique, affecting only bacteria, with diverse replication strategies:
    • Lytic Cycle: Results in cell death and virion release (steps: attachment, penetration, synthesis, assembly, release).
    • Lysogenic Cycle: Viral DNA integrates into the host chromosome, called a prophage, and can be passed on during cell division. It can enter the lytic cycle under stress conditions.
Phage Conversion
  • Expression of prophage genes can alter the phenotype of the host, providing advantageous traits, such as resistance to further infections.
  • Example: CTX phi virus increases pathogenicity in Vibrio cholerae, which then causes cholera.
Archaeal Viruses
  • Unique diverse morphologies, with some resembling known bacterial or eukaryotic viruses. Most possess linear or circular DNA and demonstrate sophisticated complexities in infection mechanisms.

26.4 Viral Diseases of Humans

Learning Outcomes
  1. Describe the differences between acute and persistent infections.
  2. Relate antigenic drift and antigenic shift to seasonal flu outbreaks and pandemics.
  3. Give examples of chronic and latent viral infections.
Viral Infections and Disease Progression
  • Infection routes: most commonly through respiratory epithelia.
  • Acute Infections: Rapid onset of high viral load, e.g., influenza viruses.
  • Persistent Infections: These can be chronic, latent, or slowly progressing. Each has varying degrees of viral load and symptomatic expressions.
Examples of Viral Infections
  1. Influenza Virus: Spreads rapidly via respiratory droplets, main concern is antigenic drift and shift.
    • Antigenic Drift: Minor mutations causing vaccine strains to lose efficacy.
    • Antigenic Shift: Major genomic rearrangements leading to new virulent strains (e.g., A/H1N1).
  2. HIV: A chronic infection leading to AIDS, characterized by gradual immune system deterioration.
  3. Herpesviruses: Can establish latent infections with periodic reactivation in response to triggers (e.g., stress).
  4. Cancer-related Viruses: HPV can lead to cervical and other cancers by subverting normal cell cycle controls.
Emerging and Re-emerging Diseases
  • Emerging diseases appear in populations for the first time or with increased incidence, while re-emerging diseases return after a period of decline (e.g., Ebola outbreak).

26.5 Prions and Viroids

Learning Outcome
  1. Explain how prion replication and transmission violates traditional notions of heredity.
Prions
  • Pathogenic prion proteins (PrPSc) cause transmissible spongiform encephalopathies (TSEs). They convert normal proteins into abnormal forms, disrupting cellular function.
Viroids
  • Infectious RNA molecules lacking a protein coat. They replicate using the host cellular machinery and can impact plant growth significantly.
Conclusion
  • Understanding viruses, prions, and viroids challenges existing biological paradigms regarding life, replication, and disease pathology.

Chapter Review Summary

  • Viruses are obligate intracellular parasites with diverse structures and life cycles.
  • Classification of viruses is complex, involving taxonomy, disease, host range, and genome expression.
  • Both acute and persistent infections have different implications for health and treatment strategies, particularly in the context of emerging diseases and viral ecology.
  • Prions and viroids present unique challenges, highlighting the complexity of pathogenic organisms.