Immune Memory and Protection Quiz

Immune Memory and Protection

• Following an infection, the host immune system develops memory cells that remember the specific pathogen, providing protection against subsequent infections and forming the basis for vaccination strategies.

Molecular Mechanisms of Pathogenesis

• These mechanisms refer to the specific biological processes and interactions between a pathogen and its host that contribute to the development and progression of disease.
• They vary depending on the type of pathogen (bacteria, viruses, fungi, parasites) and the specific characteristics of the host-pathogen interaction.

Common Molecular Mechanisms of Pathogenesis

• Adhesion and colonization
• Invasion
• Immune evasion
• Toxin production
• Immune system modulation
• Intracellular survival
• Molecular mimicry
• Genetic variation

Adhesion and Colonization

• Pathogens possess surface molecules that allow them to adhere to specific host cells or tissues.
• These adhesion molecules interact with receptors on host cells, facilitating initial attachment and colonization.

Immune System Modulation

• Pathogens manipulate the host immune response to their advantage.
• They may suppress or evade immune recognition, inhibit immune cell activation or function, or induce an excessive or dysregulated immune response.

Intracellular Survival

• Some pathogens survive and replicate inside host cells.
• They can manipulate host cellular processes to create a favorable intracellular environment and evade immune detection.

Molecular Mimicry

• Pathogens produce molecules that mimic or resemble host molecules.
• This molecular mimicry can confuse or deceive the host immune system, leading to a diminished immune response against the pathogen.

Innate Immune Response to Viral Infection

• Type I Interferons (INF-α and β) are proteins produced in response to virus infection, stimulating cells to make proteins that block viral transcription and protecting them from infection.

Biologic Actions of Type I Interferons

• Type I interferons inhibit viral replication in infected cells (autocrine manner).
• They act on other cells to prevent the spread of viral infection (paracrine manner).

Anti-Viral Activity of Type I Interferons

• INF-α inhibit intracellular replication of viruses.
• They activate NK-cells and CD8+ CTLs to kill virus-infected cells.
• They promote the differentiation of naive T cells to TH1.
• They upregulate the expression of MHC I.

NK Cells

• Destroy some virus-infected cells and are not MHC restricted.
• Natural killer cells lyse virally infected cells when Class I MHC expression is shut off.

Mechanisms of Defense Against Intracellular Bacteria

• Inhibition of phagolysosome formation (e.g., M. tuberculosis).
• Escape from phagolysosome (e.g., L. monocytogenes).
• Inhibition of ROS & NO (e.g., M. leprae).

Injurious Effects of Immune Response

• Chronic inflammation (DTH) and granuloma formation (e.g., tuberculosis).

Host Immune Responses to Bacterial Infections and Bacterial Evasion Mechanisms

• Host immune responses include humoral and cell-mediated immunity.
• Bacterial evasion mechanisms include adhesion and colonization, immune system modulation, and molecular mimicry.

Immune Response to Fungal Infections

• Fungal infections are normally only a superficial nuisance.
• Concomitant immunity or premunition is a state of partial immunity acquired after a previous infection, where the individual remains persistently infected but asymptomatic or experiences milder symptoms.

Premunition

• A host response that protects against high numbers of parasites and illness without eliminating the infection.
• Premunition is relatively rapid, progressively acquired, short-lived, and partially effective.

Concomitant Immunity (CI)

• Describes a state of effective anti-larval immunity coupled with persistent adult infection.
• CI occurs during an ongoing infection, where the immune system partially controls the pathogen, limiting disease progression.

Laboratory Tests

• Can include bacteriological diagnosis, parasitological diagnosis, immunological and serological diagnosis, and molecular diagnosis.