Microbiology Study Guide: Viruses, Bacteriophages, and Viral Evolution

Viruses vs. Eukaryotic and Prokaryotic Cells

Comparison of Fundamental Properties

Viruses differ significantly from both eukaryotic and prokaryotic cells in terms of structure, function, and biological classification. Understanding these differences is essential for studying microbiology and virology.

• Cellular Nature: Viruses are acellular entities, meaning they lack cellular structure and are not considered living cells. Eukaryotes and prokaryotes are cellular and considered alive.

• Size: Viruses are much smaller (20–300 nm) than prokaryotic cells (0.5–5 μm) and eukaryotic cells (10–100 μm).

• Structure: Viruses consist of genetic material (DNA or RNA), a protein coat (capsid), and sometimes an envelope with spikes. Prokaryotes and eukaryotes have complex cellular structures with organelles (eukaryotes) or cell walls (prokaryotes).

• Metabolism: Viruses do not exhibit metabolism and cannot generate energy independently. Prokaryotes and eukaryotes have active metabolic pathways.

• Replication: Viruses replicate only inside host cells using host machinery. Prokaryotes and eukaryotes reproduce independently (binary fission, mitosis, etc.).

• Genome Composition: Viruses may have DNA or RNA genomes, which can be single- or double-stranded. Prokaryotes and eukaryotes have double-stranded DNA genomes.

Example: Influenza virus (acellular, RNA genome) vs. Escherichia coli (prokaryotic cell, DNA genome).

Virus Structure and Main Components

Functions of Viral Parts

Viruses are composed of several key components, each with specific functions essential for infection and replication.

• Genetic Material: Contains the instructions for viral replication; can be DNA or RNA.

• Capsid: Protein shell that protects the genetic material and aids in attachment to host cells.

• Envelope (in some viruses): Lipid membrane derived from host cell; contains viral proteins (spikes) for host recognition.

• Spikes: Glycoproteins that facilitate binding to host cell receptors and entry into the cell.

Example: HIV has an RNA genome, a capsid, an envelope, and spikes (gp120, gp41).

Antigenic Shift vs. Antigenic Drift

Impact on Influenza Virus Evolution and Outbreaks

Antigenic shift and drift are mechanisms by which influenza viruses change their surface proteins, affecting immunity and outbreak patterns.

• Antigenic Drift: Gradual accumulation of mutations in viral genes encoding surface proteins (e.g., hemagglutinin, neuraminidase). Leads to seasonal flu outbreaks.

• Antigenic Shift: Sudden, major change due to reassortment of gene segments between different viral strains. Can result in pandemics.

Example: The 2009 H1N1 pandemic was caused by antigenic shift.

Host Range and Tropism of Viruses

Significance in Viral Infection

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

• Host Range: Determined by the ability of the virus to attach and enter host cells; influenced by viral surface proteins and host cell receptors.

• Tropism: Specificity for certain cell types or tissues within the host, affecting disease manifestation.

Example: Rabies virus has a broad host range but neural tropism.

Bacteriophage Replication

Features of Lytic and Lysogenic Cycles

Bacteriophages (viruses that infect bacteria) can replicate via two main cycles: lytic and lysogenic.

• Lytic Cycle:

  1. Attachment to bacterial cell

  2. Injection of genetic material

  3. Replication and synthesis of viral components

  4. Assembly of new phages

  5. Lysis of host cell, releasing new phages

• Lysogenic Cycle:

  1. Attachment and entry

  2. Integration of phage DNA into host genome (prophage)

  3. Host cell divides, copying prophage DNA

  4. Prophage may later enter lytic cycle

Example: Lambda phage can undergo both lytic and lysogenic cycles.

Lytic vs. Latent Infections in Animal Viruses

Comparison and Examples

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

• Lytic (Acute) Infection: Rapid viral replication, cell lysis, and symptom onset. Example: Influenza virus.

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

Viral Evolution: Selective Pressure and Innovation

Role of Viruses in Driving Evolution

Viruses contribute to evolution by applying selective pressure and facilitating genetic innovation.

• Selective Pressure: Viruses select for host resistance genes, driving genetic diversity.

• Innovation: Horizontal gene transfer via viruses can introduce new genes into populations.

Example: Bacteriophages can transfer antibiotic resistance genes between bacteria.

Phage Conversion in Bacterial Pathogens

Mechanism and Impact

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

• Mechanism: Phage DNA integrates into bacterial genome, expressing new traits (e.g., toxin production).

• Impact: Can increase bacterial virulence and pathogenicity.

Example: Corynebacterium diphtheriae produces diphtheria toxin only after phage conversion.

Laboratory Growth of Bacteriophages and Animal Viruses

Methods and Plaque Assay Explanation

Bacteriophages and animal viruses are grown in the lab using specific techniques to study their properties and quantify infectivity.

• Bacteriophage Growth: Phages are cultured using bacterial lawns on agar plates. Clear zones (plaques) indicate lysis.

• Animal Virus Growth: Viruses are grown in cell cultures, embryonated eggs, or live animals.

• Plaque Assay: Method to quantify viruses by counting plaques formed on a cell or bacterial lawn. Each plaque represents infection by a single virus particle.

Example: T4 phage plaque assay on E. coli lawn.

Antiviral Drugs and Their Modes of Action

Mechanisms of Antiviral Therapy

Antiviral drugs target specific stages of the viral life cycle to inhibit replication and spread.

• Entry Inhibitors: Block viral 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 new influenza viruses (e.g., oseltamivir/Tamiflu).

Example: Oseltamivir inhibits influenza virus neuraminidase, blocking viral release.

Summary Table: Virus vs. Prokaryotic and Eukaryotic Cells

Feature	Virus	Prokaryotic Cell	Eukaryotic Cell
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	Requires host	Independent	Independent