Unit XIV Exam 1 Review: Viruses, Disease & Epidemiology, Innate & Adaptive Immunity

Chapter 13: Viruses, Viroids, and Prions

Viral Structure and Classification

Viruses are acellular infectious agents that require a host cell for replication. They are classified based on their structure, genetic material, and host range.

• Basic Structure: All viruses possess a nucleic acid core (DNA or RNA) surrounded by a protein coat (capsid). Some have an additional lipid envelope derived from the host cell membrane.

• Host Range: The spectrum of host cells a virus can infect. Determined by specific host attachment sites and cellular factors.

• Viral Shapes: Common shapes include helical, polyhedral, enveloped, and complex.

• Classification: Based on nucleic acid type (DNA or RNA), replication strategy, and morphology.

Example: Influenza virus is an enveloped RNA virus with a helical nucleocapsid.

Viral Multiplication

Viruses replicate by hijacking host cell machinery. The replication cycle differs between bacteriophages and animal viruses.

• Lytic Cycle: Virus attaches, penetrates, replicates, assembles, and lyses the host cell to release progeny.

• Lysogenic Cycle: Viral genome integrates into host DNA and replicates with it without causing immediate lysis.

• Animal Virus Replication: Involves attachment, entry (often by endocytosis or fusion), uncoating, biosynthesis, maturation, and release (budding or lysis).

Example: Bacteriophage lambda can undergo both lytic and lysogenic cycles in Escherichia coli.

Prions and Viroids

Prions are infectious proteins causing neurodegenerative diseases; viroids are small, circular RNA molecules infecting plants.

• Prion Diseases: Include Creutzfeldt-Jakob disease and mad cow disease.

• Viroids: Cause diseases in plants, such as potato spindle tuber disease.

Chapter 14 & 15: Principles of Disease, Epidemiology, and Microbial Mechanisms of Pathogenicity

Pathogenesis and Disease Terminology

Pathogenesis is the process by which microbes cause disease. Understanding disease terminology is essential for epidemiology and clinical practice.

• Pathology: Study of disease, including etiology (cause), pathogenesis (development), and effects on the body.

• Infection: Invasion and multiplication of pathogens in the body.

• Disease: Abnormal state in which the body is not functioning normally.

• Symptoms vs. Signs: Symptoms are subjective (e.g., pain), signs are objective (e.g., fever).

• Communicable vs. Non-communicable Diseases: Communicable diseases can be spread from person to person; non-communicable cannot.

Stages of Disease

• Incubation Period: Time between infection and appearance of symptoms.

• Prodromal Period: Early, mild symptoms.

• Period of Illness: Disease is most severe.

• Period of Decline: Signs and symptoms subside.

• Period of Convalescence: Body returns to pre-diseased state.

Transmission of Disease

• Contact Transmission: Direct (person-to-person), indirect (fomites), droplet (coughing/sneezing).

• Vehicle Transmission: Transmission by an inanimate reservoir (food, water, air).

• Vector Transmission: Arthropods, especially fleas, ticks, and mosquitoes.

Nosocomial (Healthcare-Associated) Infections

Infections acquired in healthcare settings. Major factors include compromised host, chain of transmission, and presence of microorganisms in hospital environment.

Epidemiology

• Incidence: Number of new cases in a population during a specific time period.

• Prevalence: Total number of cases at a given time.

• Mortality Rate: Number of deaths from a disease in a population.

• Morbidity Rate: Number of people affected by a disease in a population.

Chapter 16: Innate Immunity – Nonspecific Defenses of the Host

Overview of Innate Immunity

Innate immunity provides immediate, nonspecific defense against pathogens. It includes physical, chemical, and cellular barriers.

• First Line of Defense: Skin, mucous membranes, secretions (tears, saliva, mucus), normal microbiota.

• Second Line of Defense: Phagocytic cells (neutrophils, macrophages), inflammation, fever, antimicrobial substances.

Phagocytosis

• Steps: Chemotaxis, adherence, ingestion, digestion, and exocytosis of pathogens.

• Phagocytes: Neutrophils, macrophages, dendritic cells.

Inflammation

• Purpose: Confines and destroys microbes, initiates tissue repair.

• Signs: Redness, heat, swelling, pain, and sometimes loss of function.

• Cytokines: Chemical messengers that regulate immune responses.

Fever

• Role: Systemic response to infection; increases body temperature to inhibit pathogen growth and enhance immune function.

Antimicrobial Substances

• Complement System: Group of proteins that enhance immune responses (opsonization, inflammation, cytolysis).

• Interferons: Proteins produced by virus-infected cells that inhibit viral replication.

• Iron-Binding Proteins: Sequester iron to inhibit microbial growth (e.g., transferrin, lactoferrin).

Chapter 17: Adaptive Immunity – Specific Defenses of the Host

Overview of Adaptive Immunity

Adaptive immunity is a specific response to antigens, involving lymphocytes (B and T cells) and the production of antibodies. It has memory and specificity.

• Humoral Immunity: Mediated by B cells and antibodies; effective against extracellular pathogens.

• Cell-Mediated Immunity: Mediated by T cells; effective against intracellular pathogens and cancer cells.

Antigens and Antibodies

• Antigen: Substance that provokes an immune response.

• Antibody Structure: Y-shaped proteins with variable regions for antigen binding.

• Classes of Antibodies: IgG, IgM, IgA, IgD, IgE (each with distinct roles).

Major Histocompatibility Complex (MHC)

• MHC I: Present on all nucleated cells; present endogenous antigens to CD8+ T cells.

• MHC II: Present on antigen-presenting cells; present exogenous antigens to CD4+ T cells.

Activation of B and T Cells

• B Cell Activation: Leads to plasma cells (antibody production) and memory B cells.

• T Cell Activation: Helper T cells (CD4+) coordinate immune response; cytotoxic T cells (CD8+) kill infected cells.

Types of Adaptive Immunity

Type	How Acquired	Example
Naturally acquired active	Infection	Recovery from measles
Artificially acquired active	Vaccination	MMR vaccine
Naturally acquired passive	Maternal antibodies	Antibodies from placenta or breast milk
Artificially acquired passive	Injection of antibodies	Antitoxin administration

Summary Table: Innate vs. Adaptive Immunity

Feature	Innate Immunity	Adaptive Immunity
Specificity	Nonspecific	Specific
Memory	None	Present
Response Time	Immediate	Slower (days)
Main Cells	Phagocytes, NK cells	B and T lymphocytes

Additional info: These notes expand on the outline provided, adding definitions, examples, and tables for clarity and completeness.