Viruses, Prions, and Host–Microbe Interactions: Key Concepts and High-Yield Themes

Chapter 6 – Viruses & Prions

Classifying & Naming Viruses

Viruses are classified based on several structural and genetic factors. The International Committee on Taxonomy of Viruses (ICTV) provides a hierarchical system for naming and organizing viruses.

• Classification factors: Nucleic acid type, capsid symmetry, envelope presence, genome architecture, host range, tropism.

• ICTV system: Phylum → Order → Family → Genus → Species.

Host Range & Tropism

Viruses exhibit specificity for their hosts and the types of cells or tissues they infect.

• Host range: Species infected (e.g., measles infects humans only).

• Tropism: Tissue/cell preference (e.g., HIV targets CD4 T cells; Zika virus has a wide range of tissue tropism).

Persistent Viral Infections

Some viruses can persist in the host for extended periods, either with ongoing replication or in a dormant state.

• Chronic: Slow-release, long-term infection (e.g., HIV).

• Latent: Dormant with periodic flare-ups (e.g., Herpes Simplex Virus [HSV], Varicella-Zoster Virus [VZV]).

Oncogenic Viruses

Certain viruses can cause cancer by integrating into the host genome and disrupting normal cellular regulation.

• Oncoviruses: Account for 10–15% of cancers.

• Mechanisms: Genome integration, chronic inflammation.

• Examples: Human Papillomavirus (HPV), Epstein-Barr Virus (EBV), Hepatitis B Virus (HBV).

Diagnostics

Laboratory methods are used to detect viral proteins or antibodies in patient samples.

• Protein detection: Antigen tests, agglutination, ELISA.

• Antibody detection: Evidence of past or current infection.

Prions

Prions are infectious proteins that lack nucleic acids and cause neurodegenerative diseases.

• Nature: Infectious proteins, no nucleic acids.

• Diseases: Creutzfeldt-Jakob Disease (CJD), Fatal Familial Insomnia (FFI), Gerstmann-Sträussler-Scheinker syndrome (GSS).

• Mechanism: Misfolded protein → brain damage, spongy tissue.

• Non-infectious misfolding parallels: Alzheimer’s, Parkinson’s, Amyotrophic Lateral Sclerosis (ALS).

High-Yield Themes

• Antigenic drift vs shift: Mechanisms of viral genetic variation, especially in influenza.

• Why prions are unique: Lack DNA/RNA; propagate by protein misfolding.

Key Concepts to Know

• Pathogens: Prions, viruses, bacteria, protozoa, fungi, helminths.

• Pathogen types: Opportunistic vs true pathogens.

• Patterns of occurrence: Sporadic, endemic, epidemic, pandemic.

• Emerging vs re-emerging pathogens: Examples: SARS-CoV-2, MRSA, MDR-TB.

Disease Transmission

Understanding how diseases spread is crucial for prevention and control.

• Reservoir vs Source: Reservoir = natural habitat; Source = direct origin.

• Endogenous vs Exogenous sources: Endogenous (e.g., E. coli UTI), Exogenous (e.g., Salmonella food poisoning).

• Direct vs Indirect transmission: Direct (contact, droplets, vectors), Indirect (fomites).

• Vector transmission: Biological (mosquito, tick) vs Mechanical (fly).

Stages of Infection

Infections progress through distinct stages, each with characteristic features.

• Incubation → Prodromal → Acute → Decline → Convalescent

• Latent infections: Pathogens persist but dormant (e.g., HSV).

• Carrier states: Chronic or asymptomatic carriers (e.g., Typhoid Mary, Hepatitis B).

Epidemiology

Epidemiology is the study of disease patterns in populations.

• Definition: Study of disease in populations.

• Epidemiological triangle: Host, agent, environment.

• Public health tools: Surveillance, contact tracing, vector control.

• HAIs (Healthcare-associated infections): Sources = hands, devices. Examples: C. diff, MRSA, catheter UTIs, ventilator-associated pneumonia.

• Key HAI caution: Antimicrobial resistance.

Chapter 10 – Host–Microbe Interactions & Pathogenesis

Key Concepts to Know

• Normal microbiota roles: Vitamin synthesis, pathogen competition, immune maturation.

• Dysbiosis: Antibiotic disruption → C. difficile infection.

• Same microbe, different outcome: GBS harmless in adults, deadly to newborn.

• Tropism: Pathogen’s tissue/host preference (influenza = respiratory tract; Plasmodium = RBCs, liver).

Pathogenicity & Virulence

Pathogenicity is the ability to cause disease; virulence is the degree of severity.

• Pathogenicity vs Virulence: Ability vs severity of disease.

• Virulence factors: Adhesion, toxins, enzymes, immune evasion.

• Exotoxins: Types I (superantigens), II (membrane-damaging), III (A-B toxins).

• Endotoxin (Lipid A): Released when Gram-negatives die → septic shock.

Five Steps to Infection

1. Entry: Portals (mucous membranes, parenteral, transplacental).

2. Adhesion: Biofilms, adhesins.

3. Invasion/Nutrient acquisition: Intracellular vs extracellular pathogens.

4. Immune evasion: Hiding (latency, mimicry, variation; undermining: suppress phagocytosis).

5. Transmission to new host: Symptoms aid spread.

Infection Control

• Standard precautions: Hand hygiene, gloves, sharps disposal.

• Transmission-based precautions: Contact, droplet, airborne.

High-Yield Themes

• Endotoxin vs exotoxin distinction: Endotoxins are part of Gram-negative cell wall; exotoxins are secreted proteins.

• Antigenic variation vs latency: Mechanisms for immune evasion.

• Biofilm contribution to chronic infection: Biofilms protect microbes from immune response and antibiotics.

• R0 vs Re: $R_0$ = basic reproductive number; $R_e$ = effective reproductive number.

Table: Comparison of Exotoxins and Endotoxins

Feature	Exotoxins	Endotoxins
Chemical Nature	Proteins (often enzymes)	Lipopolysaccharide (Lipid A component)
Source	Gram-positive and Gram-negative bacteria	Gram-negative bacteria only
Heat Stability	Heat labile (destroyed by heat)	Heat stable
Toxicity	Highly toxic (small amounts)	Low toxicity (large amounts needed)
Mode of Action	Specific targets (e.g., nerves, GI tract)	General effects (fever, shock)
Fever Production	Usually no	Yes

Example: Tetanus toxin (exotoxin) vs Lipid A (endotoxin from E. coli).