Viruses, Viroids, & Prions: Structure, Replication, and Pathogenicity

Viruses, Viroids, & Prions

Overview

This chapter explores the structure, replication, and pathogenic mechanisms of viruses, viroids, and prions. It compares the life cycles of DNA and RNA animal viruses, describes how viral genomes serve as templates, and explains the differences between acute, latent, and persistent infections. The chapter also distinguishes viroids and prions, highlighting their unique properties and roles in disease.

Characteristics of Viruses

General Properties

• Viruses are acellular infectious agents composed of genetic material (DNA or RNA) surrounded by a protein coat (capsid); some possess a lipid envelope.

• They require a host cell for replication and do not carry out metabolic processes independently.

• Viral genomes may be single- or double-stranded, and either DNA or RNA.

Viral Multiplication

General Life Cycle Events

All viral life cycles share four main stages:

1. Recognition & Attachment: Viral capsid proteins, envelope proteins, or glycoproteins bind to specific host cell surface proteins or glycoproteins.

2. Genome Entry: The entire capsid and genome, or only the genome, enters the host cell.

3. Synthesis & Assembly: Genome replication, protein synthesis, and assembly of new virions occur.

4. Exit & Transmission: New virions are released from the host cell, infecting additional cells.

Attachment & Uncoating Mechanisms

• Attachment: Mediated by host protein or glycoprotein receptor sites.

• Entry: Occurs via fusion (for enveloped viruses) or receptor-mediated endocytosis.

• Uncoating: Separation of the viral genome from its capsid, which may occur at the cell membrane, within endosomes, or at the nuclear membrane.

Example: Measles virus enters by membrane fusion; Hepatitis C enters by receptor-mediated endocytosis.

Assembly and Release

• Viruses use host ribosomes for protein synthesis.

• Assembly of new virions occurs in the cytoplasm or nucleus.

• Enveloped viruses insert envelope proteins into host membranes and exit by budding; non-enveloped viruses typically exit by cell lysis.

DNA vs. RNA Animal Virus Life Cycles

DNA Viruses

• Replication and transcription occur in the nucleus using host DNA polymerase.

• Viral proteins are synthesized in the cytoplasm.

• Virion assembly occurs in the nucleus, followed by exit from the cell.

Example: Papovavirus replicates its DNA in the nucleus, synthesizes proteins in the cytoplasm, and assembles new virions in the nucleus.

RNA Viruses

• Replication, protein synthesis, and assembly occur in the cytoplasm.

• Non-retroviral RNA viruses use RNA-dependent RNA polymerase (RDRP) for genome replication.

• (+) ssRNA viruses: Genome serves directly as mRNA for translation.

• (-) ssRNA viruses: Genome must be transcribed into (+) RNA by RDRP before translation.

Example: Poliovirus is a (+) ssRNA virus; Influenza virus is a (-) ssRNA virus.

Retroviruses

• Possess reverse transcriptase (RT) to convert viral RNA into DNA.

• Viral DNA integrates into the host genome, forming a provirus.

• Provirus may remain latent or be transcribed into viral RNA and proteins.

• Exit by budding from the host cell membrane.

Example: HIV infects T helper cells, integrates into host DNA, and may persist in a latent state.

Comparison: Bacteriophage vs. Animal Virus Multiplication

Stage	Bacteriophages	Animal Viruses
Attachment	Tail fibers attach to cell wall proteins	Attachment sites are plasma membrane proteins and glycoproteins
Entry	Viral DNA injected into host cell	Capsid enters by receptor-mediated endocytosis or fusion
Uncoating	Not required	Enzymatic removal of capsid proteins
Biosynthesis	In cytoplasm	In nucleus (DNA viruses) or cytoplasm (RNA viruses)
Chronic infection	Lysogeny	Latency; slow viral infection; cancer
Release	Host cell lysed	Enveloped viruses bud out; nonenveloped viruses rupture plasma membrane

Prions

Structure and Pathogenicity

• Prions are infectious proteins with no nucleic acid component.

• Cause degenerative brain diseases such as "mad cow" disease, Creutzfeldt-Jakob disease, scrapie, and kuru.

• Transmitted via food prepared from infected animals.

• Pathogenesis: Prions convert normal brain cell glycoprotein (PrPC) into the infectious form (PrPSc), which accumulates and forms plaques (spongiform holes) in the brain.

• Disease progresses slowly and prions are highly resistant to physical and chemical agents.

Example: Diagram shows prion-induced conversion and accumulation in nerve cells.

Viroids

Structure and Pathogenicity

• Viroids are naked, circular RNA molecules lacking a capsid; they infect plants.

• Replicated by host RNA polymerase.

• Do not encode proteins; typically 300-400 nucleotides long.

• Some viroids possess catalytic activity (ribozyme function).

Example: Diagram shows secondary structure of a viroid RNA.

Types of Viral Infections

Acute, Latent, and Persistent (Chronic) Infections

• Acute infection: Rapid onset, short duration; virus is cleared quickly.

• Latent infection: Virus infects host cell but remains dormant for long periods; may be reactivated by immunosuppression or stress.

• Persistent (chronic) infection: Virus is continuously released over a long period; often fatal.

Examples:

• Latent: Herpesviruses, Varicella-zoster virus (chickenpox/shingles)

• Persistent: HIV-1, Hepatitis B virus, Papilloma virus

Graph: Shows acute, latent, and persistent infection patterns over time.

Summary Table: Key Differences

Agent	Genetic Material	Capsid	Host Range	Replication	Pathogenicity
Virus	DNA or RNA	Present	Animals, plants, bacteria	Host cell machinery	Acute, latent, persistent infections
Viroid	RNA (circular)	Absent	Plants	Host RNA polymerase	Plant diseases
Prion	None	Absent	Animals	Protein misfolding	Neurodegenerative diseases

Key Equations and Processes

• Reverse Transcription (Retroviruses):

$\text{RNA} \xrightarrow{\text{Reverse Transcriptase}} \text{DNA} \xrightarrow{\text{Host RNA Polymerase}} \text{RNA} \rightarrow \text{Protein}$

• RNA Virus Replication:

$\text{(+)}\text{ssRNA} \xrightarrow{\text{Translation}} \text{Viral Proteins}$ $\text{(-)}\text{ssRNA} \xrightarrow{\text{RDRP}} \text{(+)}\text{ssRNA} \xrightarrow{\text{Translation}} \text{Viral Proteins}$

Summary

• Animal viruses exhibit diverse life cycles depending on their genome type (DNA, RNA, retrovirus).

• Prions and viroids are unique infectious agents lacking conventional viral structures.

• Viral infections may be acute, latent, or persistent, with significant implications for disease progression and treatment.