Summary

This document provides an overview of the structure, replication, and evolution of viruses. It includes information on viral classifications and replication cycles. The document also explores the origins and rapid evolution of viruses.

Full Transcript

Viruses A 2.3 Viruses: Definition: Viruses are non-living infectious agents that require a host cell to replicate. Unique Characteristics: Small size (20 to 300 nanometers). Genetic material (DNA or RNA) surrounded by a protein coat (capsid). Lack cellular structure and metabolism. Replication occ...

Viruses A 2.3 Viruses: Definition: Viruses are non-living infectious agents that require a host cell to replicate. Unique Characteristics: Small size (20 to 300 nanometers). Genetic material (DNA or RNA) surrounded by a protein coat (capsid). Lack cellular structure and metabolism. Replication occurs inside Structural Features Common to Viruses Capsid: Protein coat that protects the viral genetic material. Provides shape and structural integrity to the virus. Genetic Material: Can be either DNA or RNA. Carries the necessary instructions for viral replication and protein synthesis. Envelope (optional): Some viruses have an outer lipid envelope derived from the host cell membrane. Diversity of Structure in Viruses Helical Symmetry: Viral capsid forms a helical structure around the genetic material. Ex: Tobacco mosaic virus. Icosahedral Symmetry: Viral capsid forms a symmetrical icosahedron shape. Ex: Adenovirus. Complex Structure: Combination of helical and icosahedral components, often with additional structures. Ex: Bacteriophage T4. Lytic Cycle of a Virus Attachment: Viruses recognize and attach to specific receptors on the host cell surface. Entry: The virus injects its genetic material into the host cell. Replication: Viral genetic material takes control of the host cell machinery. It replicates its own genetic material and synthesizes viral proteins. Assembly: New viral particles are assembled inside the host cell. Release: The host cell is lysed (ruptured), and the newly formed viruses are released to infect other cells. Lysogenic Cycle of a Virus Integration: Viral genetic material integrates into the host cell genome. Dormancy: The viral DNA, known as a prophage, remains inactive and is replicated along with the host DNA during cell division. Activation: Environmental cues or stressors may trigger the prophage to become active. Initiation of Lytic Cycle: The prophage is excised from the host genome, initiating the lytic cycle and producing new viral particles. Multiple Origins of Viruses Escape Hypothesis: Viruses originated from fragments of cellular genetic material that gained the ability to infect other cells. Regressive Hypothesis: Viruses originated from parasitic cellular organisms that lost unnecessary cellular components over time. Coevolution Hypothesis: Viruses and cells coevolved, with viruses evolving alongside cellular life forms. Rapid Evolution in Viruses High Mutation Rate: Viruses have high mutation rates due to error-prone replication and lack of proofreading mechanisms. Genetic Recombination: Viruses can undergo genetic recombination when multiple strains infect the same host cell. Selective Pressure: Environmental factors, host immune responses, and antiviral treatments exert selective pressure, favoring the survival of viral variants with advantageous mutations. Implications of Rapid Evolution Antigenic Drift: Accumulation of mutations leads to changes in viral surface proteins, allowing evasion of immune responses. Antigenic Shift: Genetic reassortment between different viral strains can lead to the emergence of novel viruses with new antigenic properties. Challenges for Vaccination: Rapid evolution poses challenges in developing effective vaccines against certain viral diseases.

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