BackMicrobiology Study Guide: Viruses, Bacteriophages, and Viral Evolution
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Viruses vs. Eukaryotic and Prokaryotic Cells
Comparative Overview
Viruses are distinct from both eukaryotic and prokaryotic cells in several fundamental ways. Understanding these differences is crucial for grasping the nature of viral life and its impact on living organisms.
Cellular Status: Viruses are not considered true cells; they lack cellular structure and cannot carry out independent metabolism. Eukaryotic and prokaryotic cells are living cells with complete cellular machinery.
Alive or Not: Viruses are generally considered non-living outside a host; they require host cells for replication. Eukaryotic and prokaryotic cells are 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. Cells have cytoplasm, organelles, and membranes.
Replication: Viruses replicate only inside host cells using host machinery. Cells replicate independently by binary fission (prokaryotes) or mitosis/meiosis (eukaryotes).
Metabolism: Viruses do not exhibit metabolism; cells do.
Genome Composition: Viral genomes can be DNA or RNA, single- or double-stranded. Cellular genomes are always double-stranded DNA.
Example: Influenza virus vs. Escherichia coli (prokaryote) vs. human cell (eukaryote).
Virus Structure and Functions
Main Components of a Virus
Viruses are composed of several key structural elements, each with specific functions essential for infection and replication.
Genetic Material: DNA or RNA, encoding viral proteins.
Capsid: Protein shell that protects the genetic material.
Envelope (in some viruses): Lipid membrane derived from host cell, containing viral proteins.
Spikes: Glycoproteins on the envelope or capsid, facilitating 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 change over time, affecting their ability to cause epidemics and pandemics.
Antigenic Drift: Gradual accumulation of mutations in viral genes, leading to minor changes in surface proteins.
Antigenic Shift: Abrupt, major change due to reassortment of gene segments, resulting in new viral subtypes.
Impact: Drift causes seasonal flu outbreaks; shift can lead to pandemics.
Example: 2009 H1N1 pandemic resulted from antigenic shift.
Host Range and Tropism
Significance in Viral Infection
The host range and tropism of a virus determine which organisms and cell types it can infect, influencing disease spread and severity.
Host Range: The spectrum of hosts a virus can infect (e.g., humans, animals, plants).
Tropism: Specificity for certain cell types or tissues within a host.
Significance: Determines transmission, pathogenesis, and epidemiology.
Example: Rabies virus infects many mammals; HIV targets CD4+ T cells.
Bacteriophage Replication
Lytic and Lysogenic Cycles
Bacteriophages (viruses that infect bacteria) can replicate via two main cycles: lytic and lysogenic.
Lytic Cycle:
Phage attaches to bacterium and injects DNA.
Phage DNA replicates, new phages are assembled.
Bacterium lyses, releasing new phages.
Lysogenic Cycle:
Phage DNA integrates into bacterial genome (prophage).
Prophage is replicated with host DNA.
Can later enter lytic cycle.
Example: Lambda phage exhibits both cycles in E. coli.
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 virus production, cell death, and symptoms (e.g., influenza).
Latent Infection: Virus remains dormant in host cells, can reactivate (e.g., herpes simplex virus).
Example: Herpes simplex virus causes latent infections; rhinovirus causes acute infections.
Viral Evolution: Selective Pressure and Innovation
Role of Viruses in Evolution
Viruses drive evolution by exerting selective pressure and facilitating genetic innovation, such as gene transfer and mutation.
Selective Pressure: Viruses select for host resistance genes.
Innovation: Viral genes can be incorporated into host genomes, spreading new traits.
Example: Endogenous retroviruses in mammalian genomes.
Phage Conversion in Bacterial Pathogens
Mechanism and Impact
Phage conversion occurs when a bacteriophage introduces new genes into a bacterium, altering its phenotype and pathogenicity.
Mechanism: Lysogenic phage integrates genes encoding toxins or other factors.
Impact: Can make bacteria more virulent (e.g., diphtheria toxin in Corynebacterium diphtheriae).
Laboratory Growth of Bacteriophages and Animal Viruses
Methods and Plaque Assay
Bacteriophages and animal viruses are grown in the lab using specific techniques to quantify and study them.
Bacteriophages: Grown on bacterial lawns; plaques indicate lysis.
Animal Viruses: Grown in cell cultures, embryonated eggs, or live animals.
Plaque Assay: Method to quantify viruses by counting clear zones (plaques) formed by cell lysis.
Example: Plaque assay used to determine phage titer in E. coli cultures.
Antiviral Drugs
Mechanisms of Action
Antiviral drugs inhibit viral replication by targeting specific stages of the viral life cycle.
Example Drug: Acyclovir
Mode of Action: Inhibits viral DNA polymerase, preventing replication of herpesviruses.
Other Mechanisms: Entry inhibitors, protease inhibitors, reverse transcriptase inhibitors.
Summary Table: Viruses vs. Cells
Feature | Viruses | Prokaryotic Cells | Eukaryotic Cells |
|---|---|---|---|
Cellular Structure | Non-cellular | Cellular | Cellular |
Alive? | No (outside host) | 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 | Binary fission | Mitosis/meiosis |