Skip to main content
Back

Study Guide: Viruses and Bacteriophages in Microbiology

Study Guide - Smart Notes

Tailored notes based on your materials, expanded with key definitions, examples, and context.

Viruses: Comparison and Structure

Comparison of Viruses, Eukaryotic Cells, and Prokaryotic Cells

Understanding the differences between viruses, eukaryotic cells, and prokaryotic cells is fundamental in microbiology. These entities differ in cellular structure, metabolic activity, replication, and genetic composition.

  • Cellular Nature: - Viruses are acellular and not considered living organisms. - Eukaryotic cells (e.g., animal, plant cells) and prokaryotic cells (e.g., bacteria) are cellular and alive.

  • Size: - Viruses: 20–300 nm (nanometers) - Prokaryotes: 0.5–5 μm (micrometers) - Eukaryotes: 10–100 μm

  • Structure: - Viruses: Consist of genetic material (DNA or RNA), a protein capsid, and sometimes an envelope with spikes. - Prokaryotes: Cell wall, plasma membrane, cytoplasm, ribosomes, nucleoid region. - Eukaryotes: Plasma membrane, cytoplasm, nucleus, organelles.

  • Metabolism: - Viruses: No metabolism; require host cell machinery for replication. - Cells: Exhibit metabolism and independent replication.

  • Replication: - Viruses: Obligate intracellular parasites; replicate only inside host cells. - Cells: Replicate independently via cell division.

  • Genome Composition: - Viruses: DNA or RNA (single or double-stranded). - Cells: DNA (double-stranded).

Example: Influenza virus (RNA virus) vs. Escherichia coli (prokaryote) vs. human cell (eukaryote).

Virus Structure and Components

Main Components of a Virus

Viruses are composed of several key structural elements that determine their infectivity and host range.

  • Genetic Material: DNA or RNA, single or double-stranded.

  • Capsid: Protein shell that encases the genetic material; made of capsomeres.

  • Envelope (optional): Lipid membrane derived from host cell; present in some viruses.

  • Spikes: Glycoproteins protruding from the envelope or capsid; facilitate attachment to host cells.

Example: HIV has an RNA genome, a capsid, an envelope, and spike proteins (gp120).

Antigenic Shift and Drift

Impact on Influenza Virus Evolution and Outbreaks

Antigenic shift and drift are mechanisms by which influenza viruses evolve, affecting their ability to cause epidemics and pandemics.

  • Antigenic Drift: Gradual accumulation of mutations in viral genes, leading to minor changes in surface proteins (e.g., hemagglutinin, neuraminidase).

  • Antigenic Shift: Abrupt, major change due to reassortment of gene segments, resulting in new viral subtypes.

  • Impact: - Drift leads to seasonal flu outbreaks. - Shift can cause pandemics due to lack of population immunity.

Example: 2009 H1N1 pandemic resulted from antigenic shift.

Host Range and Tropism

Significance of a Virus's Host Range and Tropism

Host range refers to the spectrum of hosts a virus can infect, while tropism describes the specific cells or tissues targeted.

  • Host Range: Determined by virus-receptor interactions; some viruses infect only one species, others multiple.

  • Tropism: Specificity for certain cell types (e.g., HIV targets CD4+ T cells).

  • Significance: Influences disease spread, severity, and control strategies.

Example: Rabies virus infects many mammals; hepatitis B virus is hepatotropic (liver-specific).

Bacteriophage Replication

Features of Bacteriophage Lytic Replication

The lytic cycle is a process by which bacteriophages infect and destroy bacterial cells.

  • Attachment: Phage binds to bacterial surface.

  • Penetration: Phage injects its genetic material.

  • Biosynthesis: Host machinery synthesizes viral components.

  • Assembly: New phage particles are assembled.

  • Release: Host cell lyses, releasing new phages.

Example: T4 phage infecting E. coli.

Features of Bacteriophage Lysogenic Replication

In the lysogenic cycle, the phage genome integrates into the host genome and replicates passively.

  • Integration: Phage DNA incorporates into bacterial chromosome (prophage).

  • Replication: Prophage replicates with host DNA during cell division.

  • Induction: Environmental triggers can activate the lytic cycle.

Example: Lambda phage in E. coli.

Animal Virus Infections

Lytic vs. Latent Infections

Animal viruses can cause either acute (lytic) or latent infections, with distinct outcomes.

  • Lytic (Acute) Infection: Rapid virus production, cell death, and symptom onset. Example: Influenza virus.

  • Latent Infection: Virus remains dormant in host cells, reactivating later. Example: Herpes simplex virus.

Virus-Driven Evolution

Selective Pressure and Innovation

Viruses drive evolution in host populations by exerting selective pressure, leading to genetic innovation and adaptation.

  • Selective Pressure: Hosts evolve resistance; viruses adapt to overcome defenses.

  • Gene Spreading: Viral infection can facilitate horizontal gene transfer.

Example: Bacterial CRISPR systems evolved as defense against phages.

Phage Conversion

Impact on Bacterial Pathogens

Phage conversion occurs when a bacteriophage introduces new genes into a bacterium, altering its phenotype.

  • Lysogenic Conversion: Acquisition of virulence factors (e.g., toxins).

  • Impact: Can transform non-pathogenic bacteria into pathogens.

Example: Corynebacterium diphtheriae produces diphtheria toxin only when lysogenized by a phage.

Virus and Bacteriophage Cultivation

Growth in the Laboratory and Plaque Assay

Viruses and bacteriophages are cultivated in labs using host cells and quantified by plaque assays.

  • Bacteriophage Growth: Inoculate bacteria with phage; observe lysis.

  • Animal Virus Growth: Use cell cultures, embryonated eggs, or live animals.

  • Plaque Assay: Method to quantify viruses; clear zones (plaques) indicate cell lysis by viruses.

Example: Counting plaques on an agar plate to determine phage concentration.

Antiviral Drugs

Mechanisms of Action

Antiviral drugs inhibit various stages of the viral life cycle to prevent infection and replication.

  • Entry Inhibitors: Block virus attachment or fusion with host cell.

  • Reverse Transcriptase Inhibitors: Prevent synthesis of viral DNA from RNA (e.g., AZT for HIV).

  • Protease Inhibitors: Block viral protein processing.

  • Neuraminidase Inhibitors: Prevent release of influenza viruses (e.g., oseltamivir).

Example: Acyclovir inhibits herpesvirus DNA polymerase.

Summary Table: Comparison of Viruses, Prokaryotes, and Eukaryotes

Feature

Viruses

Prokaryotes

Eukaryotes

Cellular Structure

Acellular

Cellular

Cellular

Considered Alive?

No

Yes

Yes

Size

20–300 nm

0.5–5 μm

10–100 μm

Genome

DNA or RNA

DNA

DNA

Metabolism

None

Present

Present

Replication

Host-dependent

Independent

Independent

Pearson Logo

Study Prep