BIO 205 – Microbiology Chapter 6 Study Guide
Virus Structure and Life Cycles
1. Viral Structural Components
Components found in all viruses:
Nucleic Acid Genome: Contains the genetic information, either DNA or RNA (never both), which can be single-stranded (ss) or double-stranded (ds), linear or circular. This is the core genetic material essential for viral replication.
Capsid: A protein coat surrounding the nucleic acid. It's composed of protein subunits called capsomeres. The capsid protects the genome and determines the shape of the virus. It's also involved in attachment to host cells for non-enveloped viruses.
Components found in only some viruses:
Envelope: A lipid bilayer derived from the host cell membrane (plasma membrane, nuclear membrane, endoplasmic reticulum, or Golgi apparatus) during the budding process. Enveloped viruses are generally more susceptible to environmental factors like detergents and alcohol because the envelope is easily damaged.
Spikes (Peplomers): Glycoprotein projections embedded in the viral envelope (or sometimes extending directly from the capsid in non-enveloped viruses). They are crucial for attachment to specific receptor sites on the host cell and can also play a role in host cell penetration (e.g., fusion).
Enzymes: Some viruses carry their own enzymes within the virion, such as reverse transcriptase (retroviruses), RNA-dependent RNA polymerase (negative-sense RNA viruses, dsRNA viruses), or proteases. These enzymes are necessary for specific steps in replication that host cells do not perform.
2. Viral Capsid Shapes
Helical:
Structure: Capsomeres are arranged helically around the nucleic acid, forming a rod-like or filamentous structure. The length of the capsid is determined by the length of the nucleic acid.
Example: Tobacco mosaic virus, Ebola virus, Rabies virus.
Icosahedral (Polyhedral):
Structure: A polyhedron with 20 equilateral triangular faces. This is a very efficient way to enclose a volume, requiring fewer capsomeres. Appears roughly spherical.
Example: Adenovirus, Poliovirus, Herpesvirus.
Complex:
Structure: These viruses have capsids that are neither purely helical nor purely icosahedral, or they possess additional structures. Often have intricate, multi-component architectures.
Example: Bacteriophages (many have an icosahedral head and a helical tail with tail fibers for attachment), Poxviruses (large, brick-shaped structures with complicated internal morphology).
3. Host Range and Its Determinants
Host Range: The spectrum of host cells that a virus can infect. It can be very narrow (e.g., a virus infecting only specific human T-cells) or broad (e.g., a virus infecting multiple species).
Determinants of Host Range:
Specific Host Cell Receptors: The primary determinant. Viral attachment proteins (spikes on enveloped viruses or capsid proteins on non-enveloped viruses) must precisely fit and bind to specific receptor molecules (proteins, carbohydrates, lipids) on the surface of the host cell. This is often described as a "lock-and-key" mechanism.
Presence of Intracellular Factors: Once inside, the virus needs access to specific host cell machinery (enzymes, ribosomes, transcription factors) required for its replication and protein synthesis.
Ability to Penetrate and Uncoat: The host cell must allow the virus to enter (penetration) and release its genetic material (uncoating).
Environmental Conditions: External factors can affect viral stability and ability to reach and infect a host.
4. Basic Steps of Viral Life Cycle
a. Attachment (Adsorption):
The first step where the virus physically binds to the surface of a susceptible host cell. This interaction is highly specific, involving viral attachment proteins (spikes or capsid proteins) recognizing and binding to complementary receptor molecules on the host cell membrane. This specificity is crucial for determining the virus's host range.
b. Penetration (Entry/Uncoating):
Entry: The viral genome (or sometimes the entire virion) enters the host cell. The mechanism depends on the virus type and host cell:
Bacteriophages: Typically inject their nucleic acid into the bacterial cell, leaving the capsid outside.
Animal Viruses: May enter via endocytosis (host cell engulfs the virus in a vesicle) or fusion (enveloped virus's membrane fuses with the host cell membrane, releasing the capsid into the cytoplasm).
Uncoating: The process where the viral nucleic acid is released from its capsid (and envelope, if present) inside the host cell. This can occur in the cytoplasm, at the nuclear membrane, or within endosomes, and is often triggered by changes in pH or proteolytic enzymes.
c. Biosynthesis (Replication and Synthesis):
The viral genome directs the host cell's machinery to synthesize viral components. This involves:
Replication of Viral Nucleic Acid: The viral genome is copied multiple times. This process varies greatly depending on whether the virus has DNA or RNA, and whether it's single- or double-stranded.
Synthesis of Viral Proteins: The host cell's ribosomes, tRNAs, and amino acids are commandeered to translate viral messenger RNA (mRNA) into viral proteins. These proteins include capsid proteins, enzymes needed for replication, and proteins involved in assembly or immune evasion.
d. Maturation (Assembly):
Newly synthesized viral nucleic acids and proteins spontaneously (or with the help of scaffolding proteins) assemble into new, infectious virions. Capsids are formed, and the genome is packaged inside them.
e. Release:
Newly formed virions exit the host cell. The method of release depends on whether the virus is enveloped or non-enveloped, and whether it's a bacteriophage or an animal virus:
Lysis: Non-enveloped viruses and bacteriophages often lyse (burst) the host cell, killing it as progeny virions are released. This is a destructive process.
Budding: Enveloped viruses acquire their envelope by budding through a host cell membrane (plasma membrane, nuclear envelope, or organelle membranes). The host cell is not necessarily immediately killed and can continue to produce viruses for some time.
5. Lytic vs. Lysogenic Cycles of Bacteriophages
Lytic Cycle:
A virulent phage life cycle that culminates in the destruction of the host cell and the release of new phage particles.
Steps: Attachment, penetration (injection), biosynthesis of phage components, maturation/assembly of new virions, and finally, lysis of the host bacterial cell and release of progeny phages.
Outcome: Rapid production of new phage particles and death of the infected bacterial cell.
Lysogenic Cycle:
A temperate phage life cycle where the phage DNA integrates into the host bacterial chromosome, forming a prophage.
Steps: Attachment, penetration (injection), and then integration of the phage DNA into the bacterial genome without immediate replication or lysis.
Outcome: The host bacterium (now called a lysogen) continues to live and reproduce, replicating the prophage along with its own chromosome. The prophage genes are mostly repressed, but one gene, a repressor, keeps the phage in its dormant state. The prophage can be excised from the chromosome and enter the lytic cycle under certain environmental stresses (e.g., UV radiation, certain chemicals), a process called induction.
6. Phage Conversion
Description: Phage conversion (also known as lysogenic conversion) is a phenomenon where a bacterial cell gains new characteristics or traits due to the presence of a prophage integrated into its chromosome. These new traits are encoded by genes carried by the temperate phage.
How it occurs: The prophage's genetic material, even when dormant, can express certain genes that alter the phenotype of the host bacterium. These genes are typically not essential for phage replication but provide an advantage to the bacterial host or contribute to its pathogenicity.
Examples: Many bacterial toxins, such as diphtheria toxin (produced by Corynebacterium diphtheriae), botulinum toxin (produced by Clostridium botulinum), and cholera toxin (produced by Vibrio cholerae), are encoded by prophages. Without the prophage, these bacteria are often non-pathogenic.
7. Consequences of the Lysogenic Cycle for an Infected Bacterial Cell
For a bacterial cell infected by a temperate phage and carrying a prophage (a lysogen), there are three main consequences:
Immunity to Superinfection: The lysogenized bacterial cell becomes immune to subsequent infection by the same type of phage. The phage repressor protein, encoded by the prophage and continuously produced, binds to the operator regions of other incoming phages of the same type, preventing them from entering the lytic cycle and integrating.
Phage Conversion: The host bacterium acquires new genetic properties or traits due to the expression of genes carried by the prophage. These genes can encode proteins that contribute to virulence, alter surface antigens, or provide resistance to antibiotics, as seen in examples like toxin production by pathogenic bacteria.
Specialized Transduction: If the prophage excises imperfectly from the host chromosome during induction (when the phage switches from lysogenic to lytic cycle), it can carry specific, adjacent bacterial genes along with its own DNA. These hybrid phage particles can then transfer these specific bacterial genes to a new bacterial host upon subsequent infection, leading to genetic recombination. This process is generally more precise than generalized transduction.
8. Life Cycles of Bacteriophage vs. Animal Virus: Key Differences
While both bacteriophages and animal viruses follow the general steps of attachment, penetration, biosynthesis, maturation, and release, there are significant differences:
1. Nature of Host:
Bacteriophage: Infects bacterial cells.
Animal Virus: Infects animal cells.
2. Attachment:
Bacteriophage: Tail fibers or other surface structures bind to specific receptors on the bacterial cell wall, outer membrane, or flagella.
Animal Virus: Spikes (enveloped) or capsid proteins (non-enveloped) bind to specific protein or glycoprotein receptors on the animal cell plasma membrane.
3. Penetration & Uncoating:
Bacteriophage: Typically injects only its nucleic acid into the host cell; the capsid remains outside. No uncoating step is required internally. This is due to the rigid bacterial cell wall.
Animal Virus: The entire virion often enters the host cell either through endocytosis (engulfment) or fusion with the plasma membrane (for enveloped viruses). Once inside, uncoating occurs to release the nucleic acid from the capsid (and envelope).
4. Biosynthesis (Location and Machinery):
Bacteriophage: Replication and protein synthesis generally occur in the host cell's cytoplasm.
Animal Virus: Replication can occur in the cytoplasm (e.g., RNA viruses and some DNA viruses like poxviruses) or the nucleus (e.g., most DNA viruses like herpesviruses and adenoviruses), depending on the virus type. They utilize diverse host cell machinery, sometimes including nuclear components.
5. Maturation (Assembly):
Bacteriophage: Assembly typically occurs in the cytoplasm.
Animal Virus: Assembly can occur in the cytoplasm or the nucleus, depending on where replication takes place and whether the virus needs to acquire a nuclear envelope as its own.
6. Release:
Bacteriophage: Released by lysis of the bacterial cell wall, destroying the host cell.
Animal Virus: Non-enveloped viruses are released by lysis of the host cell. Enveloped viruses are released by budding, where they acquire their envelope from host cell membranes (plasma membrane, nuclear membrane) and often don't immediately kill the host cell, allowing for persistent infections.
7. Latency/Integration:
Bacteriophage: Can integrate its DNA into the host genome (prophage) during the lysogenic cycle, leading to a dormant state (lysogeny).
Animal Virus: Many animal viruses can establish latent infections where their genome persists in the host cell without actively replicating or causing disease (e.g., herpesviruses). This can involve integration into the host chromosome (e.g., retroviruses) or maintenance as an extrachromosomal element (episome).
9. Penetration (Fusion vs. Endocytosis) and Required Structure for Fusion
There are two main mechanisms of penetration for animal viruses:
1. Endocytosis:
Process: The virus binds to specific receptors on the host cell surface. The host cell membrane then invaginates, forming a vesicle (endosome) that encloses the virus particle. This is a normal cellular uptake process that viruses exploit. The endosome then acidifies, triggering conformational changes in viral proteins that lead to uncoating and release of the viral nucleic acid into the cytoplasm.
Used by: Both non-enveloped and enveloped viruses.
2. Fusion:
Process: After binding to host cell receptors, the viral envelope (the outer lipid layer of the virus) directly fuses with the host cell's plasma membrane. This merges the viral membrane with the cell membrane, releasing the viral capsid and nucleic acid directly into the host cell's cytoplasm. This bypasses the endosomal pathway.
Used by: Only enveloped viruses (e.g., HIV, measles virus, herpesviruses).
Structure a virus must have to undergo fusion: A virus must possess a viral envelope to undergo fusion. The fusion proteins embedded in the viral envelope are critical for mediating this membrane merger.
10. How Viral Replication Works in Different Types of RNA Viruses
RNA viruses are highly diverse in their replication strategies, mainly due to the nature of their RNA genome and the enzymes involved.
a. Single-stranded +RNA Viruses (Positive-Sense RNA):
Genome: The viral RNA genome itself functions directly as messenger RNA (mRNA). It is referred to as "positive-sense" because it can be immediately translated by host ribosomes.
Replication Steps:
Upon uncoating, the +RNA genome is directly translated by host ribosomes to synthesize viral proteins. One of the key proteins produced is an RNA-dependent RNA polymerase (RdRp).
The newly synthesized RdRp uses the original +RNA genome as a template to synthesize a complementary negative-sense (-RNA) strand.
This -RNA strand then serves as a template to produce multiple new +RNA strands. Some of these new +RNA strands are used as mRNA for further protein synthesis, and others are packaged into new virions as genomic RNA.
Example: Poliovirus, Rhinoviruses (common cold), Flaviviruses (Zika, Dengue, West Nile).
b. Single-stranded -RNA Viruses (Negative-Sense RNA):
Genome: The viral RNA genome is "negative-sense," meaning it is complementary to mRNA and cannot be directly translated by host ribosomes. It must first be transcribed into positive-sense mRNA.
Replication Steps:
These viruses carry their own RNA-dependent RNA polymerase (RdRp) within the virion, as the host cell doesn't have an enzyme to synthesize RNA from an RNA template.
Upon uncoating, the viral RdRp uses the -RNA genome as a template to synthesize complementary positive-sense (+RNA) strands.
Some of these newly synthesized +RNA strands act as mRNA for the synthesis of viral proteins (including more RdRp, nucleoproteins, and structural proteins).
Other +RNA strands serve as templates for the RdRp to synthesize new -RNA genomes, which are then packaged into progeny virions.
Example: Influenza virus, Rabies virus, Ebola virus, Measles virus.
c. Double-stranded RNA (dsRNA) Viruses:
Genome: Consists of two complementary RNA strands, one positive-sense and one negative-sense.
Replication Steps:
These viruses also carry their own RdRp within the virion, often packaged within the capsid.
Upon uncoating, the RdRp uses the dsRNA genome (specifically, the negative-sense strand as a template) to synthesize positive-sense (+RNA) strands.
These +RNA strands serve as mRNA for viral protein synthesis and as templates for the synthesis of new complementary -RNA strands.
The newly synthesized +RNA and -RNA strands pair up to form new dsRNA genomes, which are then packaged into progeny virions.
Example: Rotavirus (a major cause of severe diarrhea in infants and young children).
11. Retroviruses and Reverse Transcriptase
What distinguishes retroviruses from other types of RNA viruses?
Retroviruses are unique among RNA viruses because they have a single-stranded +RNA genome, but instead of directly transcribing it into proteins or using it as a template for RNA replication, they convert their RNA genome into a double-stranded DNA copy. This DNA copy then integrates into the host cell's chromosome.
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