Viral Infections and Replication
111 Questions
0 Views

Choose a study mode

Play Quiz
Study Flashcards
Spaced Repetition
Chat to lesson

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

What occurs during lytic infections?

  • Release of new virus particles causes host cell lysis (correct)
  • Host cell remains intact
  • Virus enters a latent state
  • Host cell undergoes apoptosis

    • Which type of infection involves viral genetic material remaining in the host cell without immediate replication?

  • Lytic infections
  • Latent infections
  • Persistent infections (correct)
  • Acute infections

    • Which antiviral therapy specifically targets the viral DNA polymerase?

  • Protease inhibitors
  • DNA polymerase inhibitors (correct)
  • Reverse transcriptase inhibitors
  • Neuraminidase inhibitors

    • What is the mode of action of neuraminidase inhibitors like oseltamivir?

    <p>Blocks the neuraminidase enzyme essential for viral release</p> Signup and view all the answers

    What can trigger the release of a latent infection from latency?

    <p>Stress or environmental changes</p> Signup and view all the answers

    Why is the incubation period for viral infections significant?

    <p>Viral replication often occurs before symptoms appear</p> Signup and view all the answers

    Which aspect of antiviral drugs usually allows them to target only infected cells?

    <p>Activation of the drug requires phosphorylation by a viral kinase</p> Signup and view all the answers

    Which of the following is an effect of reverse transcriptase inhibitors?

    <p>They prevent the formation of viral DNA</p> Signup and view all the answers

    What feature distinguishes gram positive bacteria from gram negative bacteria?

    <p>Thicker peptidoglycan coat in the cell wall</p> Signup and view all the answers

    Which of the following correctly describes the role of lipopolysaccharides in gram negative bacteria?

    <p>They form endotoxins when the bacteria dies</p> Signup and view all the answers

    Which of the following bacteria is classified as gram negative?

    <p>Escherichia</p> Signup and view all the answers

    What characteristic of Mycobacteria affects their staining process?

    <p>Waxy outer coat</p> Signup and view all the answers

    Which of the following is a common genus of gram positive bacteria?

    <p>Streptococcus</p> Signup and view all the answers

    What is one of the main survival features of bacteria that can form endospores?

    <p>Survival in adverse conditions</p> Signup and view all the answers

    Which statement is true regarding viral infections?

    <p>Latent viral infections remain unaffected by antiviral medications.</p> Signup and view all the answers

    What cellular structure is NOT typically found in bacteria?

    <p>Nucleus</p> Signup and view all the answers

    What is a characteristic of anaerobic bacteria?

    <p>They can tolerate low oxygen concentrations.</p> Signup and view all the answers

    Which outcome is associated with the release of exotoxins from bacteria?

    <p>Stimulation of cell processes that are harmful to the body.</p> Signup and view all the answers

    What does LPS primarily stimulate in the body?

    <p>Systemic inflammatory response.</p> Signup and view all the answers

    Which antibiotics are known to disrupt peptidoglycan synthesis?

    <p>Penicillin.</p> Signup and view all the answers

    What is a common mechanism of antibiotic resistance in bacteria?

    <p>Alteration of antibiotic target sites.</p> Signup and view all the answers

    What role do quinolones and sulfonamides play in antibiotic therapy?

    <p>They interfere with essential enzyme activity.</p> Signup and view all the answers

    Which of the following scenarios best describes the emergence of superbugs?

    <p>Bacteria acquiring resistance through genetic mutations.</p> Signup and view all the answers

    What is the function of aminoglycosides in bacterial infection treatment?

    <p>They disrupt protein synthesis.</p> Signup and view all the answers

    Which type of bacteria produces potent paralytic toxins?

    <p>Anaerobic bacteria.</p> Signup and view all the answers

    What is a significant concern related to acquired antibiotic resistance?

    <p>Development of new bacterial strains resistant to treatment.</p> Signup and view all the answers

    What is the most common and pathogenic strain of HIV?

    <p>HIV1</p> Signup and view all the answers

    Which groups of HIV2 have grown to epidemic proportions?

    <p>A and B</p> Signup and view all the answers

    Where is HIV2 predominantly seen?

    <p>West Africa</p> Signup and view all the answers

    Which method is NOT a primary mode of HIV transmission?

    <p>Sharing utensils</p> Signup and view all the answers

    What does the P24 antigen indicate early in HIV infection?

    <p>Presence of HIV</p> Signup and view all the answers

    Which cell type does HIV primarily infect?

    <p>CD4+ T cells</p> Signup and view all the answers

    What process leads to the formation of new viral particles in HIV infection?

    <p>Budding</p> Signup and view all the answers

    What is a characteristic of AIDS?

    <p>CD4+ T cell counts below 200 cells/mm</p> Signup and view all the answers

    What is a common opportunistic infection associated with AIDS?

    <p>Candidiasis</p> Signup and view all the answers

    Which phase of HIV infection can last up to 20 years?

    <p>Clinical latency</p> Signup and view all the answers

    What consequence occurs due to HIV's effect on CD4+ T cells?

    <p>Impairment in the immune response</p> Signup and view all the answers

    Which co-infection can increase viral shedding in asymptomatic HIV-infected individuals?

    <p>Other sexually transmitted diseases</p> Signup and view all the answers

    What is the virus's genetic material form in HIV?

    <p>RNA</p> Signup and view all the answers

    What is the role of the gp120 protein in HIV infection?

    <p>Allows fusion with host cell</p> Signup and view all the answers

    What is the primary function of capsids in viruses?

    <p>To protect genetic material</p> Signup and view all the answers

    How do RNA viruses generate mRNA within host cells?

    <p>By synthesizing their own RNA polymerase</p> Signup and view all the answers

    Which of the following methods is a common way for viruses to enter host cells?

    <p>Penetration via fusion</p> Signup and view all the answers

    What role does the Golgi apparatus play in viral infections?

    <p>It helps in the assembly of viral components.</p> Signup and view all the answers

    Which of the following describes the role of retroviruses in infection?

    <p>They integrate their DNA into the host genome.</p> Signup and view all the answers

    What is the result of viral lysis on the host cell?

    <p>The host cell releases viral particles.</p> Signup and view all the answers

    Which type of transmission is responsible for the spread of hepatitis A?

    <p>Oral transmission</p> Signup and view all the answers

    What initiates the viral replication process inside a host cell?

    <p>Recognition and attachment to the host receptor</p> Signup and view all the answers

    What is the primary mechanism responsible for type IV hypersensitivity reactions?

    <p>Sensitized T-lymphocyte activation</p> Signup and view all the answers

    Which condition is classified as an autoimmune disorder?

    <p>Systemic lupus erythematosus</p> Signup and view all the answers

    In type IV hypersensitivity, what is the typical duration for the manifestation of symptoms after allergen exposure?

    <p>Delayed, between 24-72 hours</p> Signup and view all the answers

    Which process prevents the immune system from destroying self-antigens?

    <p>Immunological tolerance</p> Signup and view all the answers

    What occurs during the infiltration of T-lymphocytes in type IV hypersensitivity reactions?

    <p>Direct binding to specific target cells and enzyme release</p> Signup and view all the answers

    What is the main function of central tolerance in the immune system?

    <p>To prevent an immune response to self-antigens and commensal microbes</p> Signup and view all the answers

    Which of the following mechanisms is NOT involved in T lymphocyte central tolerance?

    <p>Development of memory T cells</p> Signup and view all the answers

    What is the purpose of receptor editing in B lymphocyte central tolerance?

    <p>To change the specificity of the B lymphocyte's receptors</p> Signup and view all the answers

    How does peripheral T lymphocyte tolerance typically manifest?

    <p>As anergy or apoptosis upon recognition of self-antigen</p> Signup and view all the answers

    What consequence arises from a reduction in CD4 T helper cell populations?

    <p>Diminished immune response from B and T lymphocytes</p> Signup and view all the answers

    What is a primary function of Treg cells in the context of commensal microbes?

    <p>Suppressing the immune response to commensal microbes</p> Signup and view all the answers

    Which mechanism leads to B lymphocyte tolerance against self-antigens?

    <p>Induction of anergy or apoptosis</p> Signup and view all the answers

    What primarily contributes to the development of autoimmune disease?

    <p>Genetic factors and environmental triggers</p> Signup and view all the answers

    In Systemic Lupus Erythematosus, what is a common clinical consequence?

    <p>Vessel injury and inflammation</p> Signup and view all the answers

    What can trigger a harmful immune/inflammatory response against commensal microbes?

    <p>Self-reactive lymphocytes activation</p> Signup and view all the answers

    What role do APCs play in immune responses related to self-antigens?

    <p>They present self-antigens to T lymphocytes</p> Signup and view all the answers

    What is a potential consequence of infections as environmental triggers for autoimmune diseases?

    <p>Stimulating self-reactive B cells</p> Signup and view all the answers

    In the context of antigen recognition, which of the following is true about mature B lymphocytes?

    <p>They may engage inhibitory receptors upon self-antigen recognition.</p> Signup and view all the answers

    What is the primary characteristic of a Type I hypersensitivity reaction?

    <p>Production of antigen-specific IgE antibodies</p> Signup and view all the answers

    Which of the following is NOT a common allergen associated with Type I hypersensitivity reactions?

    <p>Nuclear antigen</p> Signup and view all the answers

    What occurs during the initial phase of a Type I hypersensitivity reaction?

    <p>Vasodilation and increased capillary permeability</p> Signup and view all the answers

    Which immune cells are primarily involved in the late phase of a Type I hypersensitivity reaction?

    <p>Eosinophils</p> Signup and view all the answers

    What is a clinical consequence of Type I hypersensitivity?

    <p>Anaphylaxis</p> Signup and view all the answers

    In Type II hypersensitivity reactions, target cells are primarily destroyed by which mechanism?

    <p>Complement-mediated lysis</p> Signup and view all the answers

    Which of the following describes a mechanism of Type II hypersensitivity involving NK cells?

    <p>Antibody-dependent cell-mediated cytotoxicity (ADCC)</p> Signup and view all the answers

    Type III hypersensitivity reactions are primarily characterized by the formation of what?

    <p>Immune complexes in circulation</p> Signup and view all the answers

    What can be a consequence of immune complex deposition in Type III hypersensitivity?

    <p>Vasculitis</p> Signup and view all the answers

    Which agent is often responsible for the antibody-mediated destruction in Type II hypersensitivity?

    <p>Tissue-specific antigens</p> Signup and view all the answers

    What happens to eosinophils during a Type I hypersensitivity reaction?

    <p>They are recruited by cytokines.</p> Signup and view all the answers

    What is the role of Th2 cells in Type I hypersensitivity reactions?

    <p>Producing cytokines that stimulate IgE production</p> Signup and view all the answers

    Which response best describes the degranulation of mast cells?

    <p>Release of histamines and newly formed mediators</p> Signup and view all the answers

    Which clinical sign is associated with local responses in Type I hypersensitivity?

    <p>Urticaria (hives)</p> Signup and view all the answers

    What mechanism is primarily responsible for the deletion of auto-reactive T lymphocytes during central tolerance?

    <p>Apoptosis</p> Signup and view all the answers

    Which of the following occurs in central B lymphocyte tolerance in response to exposure to self-antigens?

    <p>Receptor editing</p> Signup and view all the answers

    What effect does a reduction in CD4 T helper cell population have on the immune response?

    <p>Weakens B and T lymphocyte response</p> Signup and view all the answers

    Which of the following is not a mechanism of peripheral T lymphocyte tolerance?

    <p>Increased cytokine production</p> Signup and view all the answers

    What is one of the outcomes when immature T lymphocytes encounter self-antigens during central tolerance development?

    <p>Apoptosis of auto-reactive T cells</p> Signup and view all the answers

    What is the main characteristic of type IV hypersensitivity reactions?

    <p>They are delayed hypersensitivity reactions mediated by T-lymphocytes.</p> Signup and view all the answers

    What best describes the process of immunological tolerance?

    <p>It allows the immune system to recognize self-antigens without mounting a response.</p> Signup and view all the answers

    What occurs during the pathophysiology of type IV hypersensitivity skin reactions?

    <p>Sensitized T-lymphocytes infiltrate the site and release damaging enzymes.</p> Signup and view all the answers

    Which of the following conditions is an example of autoimmunity?

    <p>Systemic lupus erythematosus</p> Signup and view all the answers

    Which factor primarily triggers the release of immune complexes in Raynaud disease?

    <p>Temperature-dependent immune complexes</p> Signup and view all the answers

    What is the impact of mature B lymphocytes recognizing self-antigens?

    <p>They undergo anergy or apoptosis.</p> Signup and view all the answers

    What is the estimated number of bacteria and viruses in the human body?

    <p>Approximately $10^{11}$</p> Signup and view all the answers

    Which of the following describes the role of Treg cells in relation to commensal microbes?

    <p>They suppress the immune response to prevent inflammation.</p> Signup and view all the answers

    What genetic factor is commonly associated with an increased risk of autoimmune diseases?

    <p>Inheritance of multiple susceptibility genes, particularly those affecting MHC.</p> Signup and view all the answers

    What triggers the activation of self-reactive lymphocytes during infections?

    <p>Antigen presenting cells activating through foreign antigen recognition.</p> Signup and view all the answers

    Which autoimmune disease is known to affect multiple tissues, including skin and joints?

    <p>Systemic lupus erythematosus.</p> Signup and view all the answers

    What role do environmental triggers play in the development of autoimmune diseases?

    <p>They can stimulate immune responses that may lead to activation of autoreactive lymphocytes.</p> Signup and view all the answers

    How does the body typically respond to self-antigens to prevent autoimmune reactions?

    <p>Through the process of anergy or apoptosis of reactive lymphocytes.</p> Signup and view all the answers

    What characterizes Type I hypersensitivity reactions?

    <p>IgE-mediated reactions</p> Signup and view all the answers

    Which of the following is a common trigger for Type I hypersensitivity reactions?

    <p>Pollens and molds</p> Signup and view all the answers

    What is the role of Th2 cells in Type I hypersensitivity reactions?

    <p>Helper cells that produce cytokines</p> Signup and view all the answers

    Which factor is associated with 'atopy' in individuals?

    <p>Higher IgE production</p> Signup and view all the answers

    What occurs during the initial phase of a Type I hypersensitivity reaction?

    <p>Vasodilation and increased capillary permeability</p> Signup and view all the answers

    Which of the following accurately describes the clinical consequence of anaphylaxis?

    <p>Systemic bronchospasm and hypotension</p> Signup and view all the answers

    What is the common outcome of Type II hypersensitivity reactions?

    <p>Destruction of target cells by antibody-mediated mechanisms</p> Signup and view all the answers

    Which mechanism results in complement-mediated lysis in Type II hypersensitivity reactions?

    <p>Activation of complement proteins</p> Signup and view all the answers

    What triggers the formation of immune complexes in Type III hypersensitivity reactions?

    <p>Antigen-antibody interactions</p> Signup and view all the answers

    Which tissue is commonly affected by immune complex diseases in Type III hypersensitivity reactions?

    <p>Kidneys</p> Signup and view all the answers

    What distinguishes Type III hypersensitivity from other types?

    <p>Involves immune complex formation in circulation</p> Signup and view all the answers

    What can result from the degranulation of mast cells in Type I hypersensitivity?

    <p>Release of histamine and other mediators</p> Signup and view all the answers

    How do natural killer (NK) cells contribute to Type II hypersensitivity reactions?

    <p>By releasing toxic molecules to destroy target cells</p> Signup and view all the answers

    Study Notes

    Viruses and Viral Infections

    • Viruses are made up of genetic material (DNA or RNA) and a protein capsule (capsid), they may also contain an outer envelope or membrane.
    • Viruses require a host cell for replication and use the host's cellular machinery for this process.
    • Viral transmission can occur through routes such as inhaled droplets, oral transmission, direct transfer from other hosts, or bites from vector arthropods.
    • Once a virus enters a host cell, it recognizes and attaches to cell receptors, penetrates the cell through fusion or endocytosis, and uncoats its genome.
    • The viral genome then replicates using host enzymes and translates viral structural proteins in the host's endoplasmic reticulum and Golgi apparatus.
    • Following assembly, the virus is released through budding, exocytosis, or lysis of the host cells.

    Viral Replication

    • Viral replication involves the synthesis of mRNA, which leads to the creation of new viral genomes and protein shells.
    • DNA viruses make mRNA using the host's DNA polymerase; RNA viruses must produce their own RNA polymerase to form mRNA.
    • Retroviruses use the viral reverse transcriptase enzyme to convert RNA into DNA, then this DNA is incorporated into the host cell's genome.

    Outcomes of Viral Replication

    • The replication process results in the creation of viral proteins, such as enzymes and regulatory molecules.
    • Lytic infections lead to the release of new virus particles and the destruction of the host cell.
    • Persistent infections involve the ongoing presence of the virus, with viral genetic material remaining within the host cell.
    • Latent infections do not replicate until activated by specific signals.

    Principles of Antiviral Therapy

    • Many viral infections lack effective treatments.
    • Antiviral drugs target specific steps in viral replication.
    • DNA polymerase inhibitors, like acyclovir and ganciclovir, block viral DNA polymerase but do not affect cellular DNA polymerase.
    • Reverse transcriptase inhibitors, like AZT, interfere with viral DNA formation in retroviruses.
    • Protease inhibitors disrupt protein synthesis needed for HIV replication.
    • Neuraminidase inhibitors, like oseltamivir, block the activity of the influenza virus neuraminidase enzyme.

    Issues in Antiviral Therapy

    • Viral infections often have long incubation periods, meaning that antiviral treatments may be ineffective once symptoms appear.
    • Latent viral infections are typically not affected by antiviral medications.
    • Viruses mutate rapidly, making them prone to developing resistance to antiviral medications.

    Bacteria and Bacterial Infections

    • Bacteria are single-celled organisms with circular DNA and no defined nucleus.
    • Most bacteria have cell walls, and some contain capsules, flagella, or pili.
    • Some bacteria can form endospores for survival in harsh conditions.

    Bacterial Classification

    • Gram Staining: This laboratory technique classifies bacteria based on their cell wall structure.
      • Gram-positive bacteria: Have a thicker peptidoglycan layer in their cell wall, which stains purple.
      • Gram-negative bacteria: Have a thinner peptidoglycan layer and an outer membrane containing lipopolysaccharides (LPS) that stains pink.
    • Aerobes vs. Anaerobes:
      • Aerobic bacteria: Require oxygen for cellular respiration.
      • Anaerobic bacteria: Can tolerate low oxygen concentrations and may produce enzymes that break down tissue and toxins.

    Outcomes of Bacterial Infection

    • Exotoxin Release: Exotoxins can inhibit protein synthesis, damage host cells, or disrupt cell function.
    • Endotoxin Release (LPS): Gram-negative bacteria release LPS, which acts as a pyrogen and stimulates an inflammatory response.

    Targets for Antibacterial (Antibiotic) Therapy

    • Cell Wall: Antibiotic drugs that interfere with peptidoglycan synthesis, like penicillin and cephalosporins, weaken bacterial cell walls.
    • Cell Membrane: Polymixins, like Polysporin, target LPS and damage the bacterial cell membrane, affecting gram-negative bacteria more strongly.
    • Bacterial Enzymes: Antibiotics like quinolones, sulfonamides, rifamycins, and lipiarmycins interfere with essential bacterial enzyme activity.
    • Bacterial Protein Synthesis: Macrolides, lincosamides, and tetracyclines generally inhibit bacterial protein synthesis.

    Antibiotic Resistance

    • Widespread antibiotic use has led to the emergence of bacteria that are resistant to these drugs.
    • Antibiotic resistance can arise from spontaneous genetic mutations or acquired resistance through transmissible plasmids.
    • Mechanisms of resistance include altered antibiotic target sites, altered antibiotic uptake, and production of enzymes that inactivate or destroy the antibiotic.
    • Superbugs are bacterial strains resistant to multiple antibiotics.

    Human Immunodeficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS)

    Strains of HIV

    • HIV is a retrovirus belonging to the lentivirus genus.
    • HIV-1 is the most common and pathogenic strain, with multiple subtypes.
    • HIV-2 is less widespread and found primarily in West Africa.

    Epidemiology

    • Over 39 million people globally are living with HIV, with 1.3 million new cases in 2022.
    • Most HIV cases occur in eastern and southern Africa, followed by western and central Africa.
    • In the United States, the majority of new cases are due to male-to-male sexual contact, followed by high-risk heterosexual activity and injected drug use.
    • Globally, heterosexual transmission is the main mode of HIV spread.

    Viral Transmission

    • HIV is primarily transmitted through blood (IV drug use, blood transfusions) or sexual intercourse.
    • Vertical transmission (from mother to child) is also possible during pregnancy, delivery, or breastfeeding.
    • Viral load (amount of virus in the body) is a significant factor in transmission risk.

    Pathogenesis

    • HIV is a retrovirus that uses reverse transcriptase to convert RNA into DNA.
    • It targets cells with CD4 receptors, including helper T cells, dendritic cells, monocytes, and macrophages.
    • HIV utilizes a fusion protein (GP41) to fuse with host cells and release its capsid into the cytoplasm.

    HIV Infection and Replication Cycle

    • HIV enters the body and initially infects CD4+ cells.
    • The viral core enters the cytoplasm and the RNA genome undergoes reverse transcription to produce viral DNA.
    • This DNA integrates into the host cell's genome, becoming a provirus.
    • Activation of the host cell can lead to provirus transcription, resulting in the formation of new viral particles.
    • The virus buds from the host cell, acquiring its outer envelope from the cell membrane.

    Mechanisms of Immunodeficiency

    • HIV replication leads to lysis of infected CD4+ cells.
    • The bone marrow initially replaces dying CD4+ cells, but over time, these cells become depleted.
    • Lymphoid tissues are destroyed, impacting the formation of new CD4+ cells.
    • Uninfected CD4+ cells undergo significant apoptosis, further decreasing their numbers.
    • These events result in reduced production of cytotoxic T cells and plasma cells, increasing susceptibility to infections.

    Disease Progression

    • Acute Infection (Acute HIV): This phase features mild, flu-like symptoms.
    • Clinical Latency: This stage is generally asymptomatic, with viral replication continuing at low levels.
    • AIDS: This stage occurs when CD4+ T cell counts drop below 200 cells/mm3, leading to opportunistic infections, secondary neoplasms, and neurological dysfunction.

    Hypersensitivity Reactions

    • Altered immunologic reaction, resulting in a pathologic response

    Type I Hypersensitivity Reaction

    • IgE-mediated reaction
    • Characterized by production of antigen-specific IgE after exposure to an antigen
    • Common allergens: pollens, dusts, molds, food, drugs, bee venom
    • Genetic predisposition and atopy: mutations affecting IL-4 receptors, levels, IgE, Class II MHC proteins
    • Atopic individuals tend to produce higher IgE and more IgE receptors on mast cells
    • They also display increased eosinophil response leading to hyperactive immune responses

    Type I Hypersensitivity Reaction - Pathophysiology

    • Dendritic cells present allergens to Th2 cells
    • Th2 cells produce IL-4 and IL-5, stimulating IgE-producing B cells
    • IgE binds to mast cell membrane receptors, activating the mast cell
    • Degranulation of histamine and release of arachidonic acid metabolites occur
    • Eosinophils are recruited by Th2 cytokines and mast cell eosinophil chemotactic factor

    Type I Hypersensitivity - Phases

    • Initial phase (5 to 30 minutes): vasodilation, increased capillary permeability, and non-vascular smooth muscle constriction
    • Late phase (2 to 8 hours): similar responses to the initial phase with intensified granulocyte infiltration (eosinophils, neutrophils) and mucosal damage

    Type I Hypersensitivity - Clinical Consequences

    • Allergic reactions (Local response): itching, urticaria (hives), rhinitis, conjunctivitis
    • Anaphylaxis (Systemic response): bronchospasm, bronchoconstriction, hypotension, edema, GI cramping

    Type II Hypersensitivity Reactions

    • Destruction of a target cell through antibody action against cell plasma membrane antigens
    • Common antigens: tissues with HLA or tissue-specific antigens (autoimmune), drugs or drug metabolites bound to cell membranes (often RBCs or platelets), transplanted tissues or organs
    • Pathophysiology: Mechanisms of Antigen Destruction

    Type II Hypersensitivity - Pathophysiology: Mechanisms of Antigen Destruction

    • Complement-mediated lysis: IgM or IgG reacts with cell surface antigen activating complement, leading to plasma membrane damage and cell injury
    • Phagocytosis by macrophages: macrophages bind to the Fc portion of antibody on opsonized target cells and phagocytose them
    • Antibody-dependent cell-mediated cytotoxicity (ADCC): NK cells bind to the Fc portion of antibody and release toxic molecules destroying the target
    • Inducing target cell malfunction: antibodies binding to target cell receptors alter cell function resulting in changes (example: hyperthyroidism in Graves disease)

    Type III Hypersensitivity Reactions

    • Immune complex diseases
    • Common antigens: viral, bacterial and parasitic antigens, pollens, vaccines, plasma/serum, nuclear antigens

    Type III Hypersensitivity - Pathophysiology

    • Antigen-antibody complexes form in circulation and deposit on capillary endothelium or extravascular tissues
    • Complement proteins are activated
    • Neutrophils ingest the deposited complexes causing tissue damage

    Type III Hypersensitivity - Common Target Tissues/Disease Examples

    • Kidneys: glomerulonephritis
    • Blood vessels: vasculitis
    • Arthus reaction: repeated exposure to antigen forms immune complexes in vessel walls causing local inflammatory skin lesions
    • Raynaud disease: temperature-dependent immune complexes (cryoglobulins) precipitate at below-normal temperatures
    • Systemic lupus erythematosus: Immune reaction to nuclear antigen

    Type IV Hypersensitivity Reactions

    • Delayed hypersensitivity reaction, mediated by sensitized T-lymphocytes (Tc or Th)
    • Examples: tissue graft rejection, contact dermatitis, tuberculin reaction, diabetes type 1, rheumatoid arthritis, multiple sclerosis, Crohn disease, toxic shock

    Type IV Hypersensitivity Skin Reactions - Pathophysiology

    • Allergen binds to epidermal cell membrane proteins
    • T lymphocytes and macrophages infiltrate the site
    • T lymphocytes bind to target cells and release enzymes (granzymes), damaging or destroying the target cell
    • Manifestations are delayed for 24-72 hours, and no dermatitis occurs from the primary contact with the allergen

    Autoimmunity

    • Altered immunologic reaction involving B and T lymphocyte response against the body's own cells

    Immunological Tolerance

    • Prevents the immune system from destroying self-antigens
    • Immunocompetent B and T lymphocytes capable of recognizing all antigens are produced
    • Mechanisms exist to prevent immune responses to self-antigens and commensal microbes

    Generation of Central Tolerance

    • Immunocompetent (immature) B and T lymphocytes migrate to the bone marrow and thymus
    • They are exposed to self antigens and develop tolerance
    • Central T lymphocyte tolerance:
      • Immature T lymphocytes migrate to the thymus, encountering self antigens
      • Recognition induces apoptosis (negative selection) of CD4 (Th) and CD8 (Tc) lymphocytes or development of regulatory cells (T reg)
    • Central B lymphocyte tolerance:
      • Immature B cells migrate to or stay in the bone marrow, interacting with self antigens
      • Recognition induces receptor editing, apoptosis (“deletion”), or anergy (reduced antigen receptor expression)

    Generation of Peripheral Tolerance

    • Central tolerance generation is imperfect
    • Reduction in CD4 Th cell population minimizes the response

    Peripheral T lymphocyte Tolerance

    • Mature T cells recognizing self-antigens undergo anergy or apoptosis
    • APCs secrete fewer signaling molecules
    • Mature T cells are susceptible to the effects of Treg cells

    Peripheral B lymphocyte tolerance

    • Mature B cells recognizing self-antigens undergo anergy or apoptosis
    • Mature B cells engaging self-antigens activate inhibitory receptors

    Generation of Tolerance to Commensal Microbes

    • Human body harbors ~ 10^14 bacteria and viruses
    • Abundance of Treg cells secrete interleukins suppressing immune responses to microbes

    Development of Autoimmune Disease

    • Affects 1 out of 5 Americans
    • Involves inheritance of susceptibility genes and environmental triggers
    • Susceptibility genes: interfere with self-tolerance pathways, mainly affecting MHC (HLA) genes
    • Environmental triggers:
      • Infections: stimulate APCs activating self-reactive lymphocytes, microbes produce antigens similar to self-antigens
      • Sunlight (UV radiation)

    Systemic Lupus Erythematosus

    • Autoimmune disease affecting skin, joints, kidneys, heart, liver, and other tissues
    • Etiology: Genetic susceptibility and environmental triggers
    • Pathophysiology:
      • Immune complexes deposit in blood vessels, joints, and other tissues
      • Complex deposition activates complement and inflammatory cascade
    • Clinical Consequences: Vessel injury and inflammation
    • Diagnosis: Based on clinical manifestations, autoantibodies (ANA), and exclusion of other disorders

    Hypersensitivity Reactions

    • An altered immunologic reaction resulting in a pathologic response
    • 4 types of hypersensitivity reactions

    Type I Hypersensitivity Reaction

    • IgE mediated reaction
    • Characterized by production of antigen-specific IgE after exposure to an antigen
    • Most responses are to environmental antigens (allergens)
    • Common allergens:
      • Pollens, dusts, molds
      • Food
      • Drugs
      • Bee venom
    • Genetic Predisposition and Atopy
      • Mutations in genes affecting IL-4 receptors, IL-4 levels, IgE receptors, Class II MHC proteins
      • Individuals with atopy produce higher amounts of IgE, more IgE receptors on mast cells, and an increased eosinophil response

    Type I Hypersensitivity Reaction - Pathophysiology

    • Dendritic cells present allergens to Th2 cells
    • Th2 cells produce cytokines (IL-4, IL-5) which stimulate IgE-producing B cells
    • IgE binds to receptors on the mast cell's plasma membrane, which activates the mast cell
    • Result is degranulation of histamine from the mast cell and the release of newly formed mediators (arachidonic acid metabolites)
    • Eosinophils are recruited by cytokines from Th2 cells and eosinophil chemotactic factor from the mast cell

    Type I Hypersensitivity Reaction - Clinical Consequences

    • Two defined phases:
      • Initial phase (5-30 minutes): vasodilation, increased capillary permeability, and non-vascular smooth muscle constriction
      • Late phase (occurs 2-8 hours): more intense infiltration of tissues with granulocytes (eosinophils, neutrophils), and mucosal damage
    • Allergic Reactions: itching, urticaria (hives); rhinitis; conjunctivitis
    • Anaphylaxis:
      • Bronchospasm, bronchoconstriction
      • Hypotension
      • Edema
      • GI cramping

    Type II Hypersensitivity Reactions

    • Destruction of target cells due to antibodies against cell surface antigens
    • Common Antigens:
      • Tissues with HLA and/or tissue-specific antigen (autoimmune reactions)
      • Drugs or metabolites bound to plasma membrane of cells (often RBCs or platelets)
      • Transplanted tissues/organs (including blood transfusions)
    • Mechanisms of antigen destruction:
      • Complement-mediated lysis: IgM/IgG react with cell surface antigens, activating compliment proteins (C5-9) which cause plasma membrane damage and cell injury
      • Phagocytosis by macrophages: macrophages recognize and bind to Fc portion of antibody on opsonized target cells and phagocytose the target
      • ADCC: NK cells bind to Fc portion of antibody on opsonized target cell and release toxic molecules that destroy the target
      • Inducing target cell malfunction: antibody binding to target cell receptors alters normal cellular function

    Type III Hypersensitivity Reactions

    • Immune complex diseases
    • Common Antigens:
      • Viral, bacterial, and parasitic antigens
      • Pollens
      • Vaccines
      • Plasma/Serum
      • Nuclear antigens
    • Pathophysiology:
      • Antigen-antibody (immune) complexes form in circulation and deposit on endothelium of capillaries or extravascular tissues
      • Compliment proteins are activated
      • Neutrophils ingest the deposited antigen-antibody complexes and cause tissue damage
    • Common Tissues/Disease Examples:
      • Kidneys: Glomerulonephritis
      • Blood vessels: Vasculitis
      • Arthus reaction: repeated local exposure to antigen causes immune complex formation in blood vessel walls leading to local skin lesions
      • Raynaud's Disease: Temperature-dependent immune complexes (cryoglobulins) precipitate at below-normal body temperatures
      • Systemic Lupus Erythematosus: Immune response to nuclear antigen

    Type IV Hypersensitivity Reactions

    • Delayed hypersensitivity reaction mediated by sensitized T-lymphocytes (Tc or Th)
    • Examples:
      • Tissue graft rejection
      • Contact dermatitis
      • Tuberculin reaction
      • Other diseases: diabetes type 1, RA, MS, Crohn disease, toxic shock
    • Pathophysiology of Type IV Hypersensitivity skin reactions:
      • Allergen binds to proteins on membranes of epidermal cells
      • Infiltration of site by T lymphocytes and macrophages
      • T lymphocytes bind to target cells and release enzymes (granzymes) that damage/destroy the target cell
    • Manifestations delayed by 24-72 hours

    Autoimmunity

    • Altered immunologic reaction resulting in B and T lymphocyte response against self-cells

    Immunological Tolerance

    • How the immune system is prevented from destroying self-antigen
    • Mechanisms prevent the immune system from mounting an immune response to self-antigen (and commensal microbes)

    Generation of Central Tolerance

    • Immunocompetent B and T lymphocytes develop 'tolerance' in bone marrow and thymus by exposure to self-antigens
    • Central T Lymphocyte Tolerance:
      • Immunocompetent T lymphocytes are exposed to self-antigen in the thymus
      • Recognition of self-antigen induces:
        • Apoptosis (negative selection) of CD4 (Th) and CD8 (Tc) lymphocytes
        • Development of Regulatory T lymphocytes (Treg)
    • Central B Lymphocyte Tolerance:
      • Immunocompetent B lymphocytes are exposed to self-antigen in the bone marrow
      • Recognition of self-antigen induces:
        • Receptor editing
        • Apoptosis
        • Anergy

    Generation of Peripheral Tolerance

    • Central tolerance is imperfect
    • Peripheral T Lymphocyte Tolerance:
      • Mature T lymphocytes recognize self-antigen, causing anergy or apoptosis
      • Antigen presenting cells (APCs) secrete fewer signaling molecules
      • Mature T lymphocytes are sensitive to the effects of Treg cells
    • Peripheral B Lymphocyte Tolerance:
      • Mature B lymphocytes recognize self-antigen, causing anergy or apoptosis
      • Mature B lymphocytes that recognize self-antigen engage inhibitory receptors

    Generation of Tolerance to Commensal Microbes

    • Human body contains ~10^14 bacteria and viruses
    • Treg cells suppress immune response to commensal microbes

    Development of Autoimmune Disease

    • Immune response against self-antigen affecting approximately 1/5 Americans
    • Associated with inheritance of susceptibility genes and environmental triggers
    • Susceptibility Genes: Interfere with self-tolerance pathways, most affecting MHC (HLA) genes
    • Environmental Triggers:
      • Infections: Infections stimulate antigen presenting cells (APCs) that activate self-reactive lymphocytes, and infectious microbes produce antigens similar to self-antigens
      • Sunlight (UV radiation)

    Systemic Lupus Erythematosus

    • Autoimmune disease that affects the skin, joints, kidneys, heart, liver, and other tissues
    • Etiology: Genetic susceptibility with environmental triggers
    • Pathophysiology: Unclear, but associated with vessel injury and inflammation
    • Clinical Consequences: Associated with vessel injury and inflammation

    Studying That Suits You

    Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

    Quiz Team

    Related Documents

    NURS 7053 Advanced Pathophysiology I for DNP Students PDF
    NURS 7053 Advanced Pathophysiology I - Infection Class Notes PDF

    Description

    Explore the intricate world of viruses, their structure, and the process of viral replication. This quiz covers key concepts, including how viruses attach, enter host cells, and utilize the host's machinery for their reproduction. Test your understanding of viral transmission and the life cycle of viruses.

    More Like This

    Viruses medium
    27 questions

    Viruses medium

    WiseTropicalIsland4758 avatar
    WiseTropicalIsland4758
    Introduction to Viruses and Viral Infections
    96 questions

    Introduction to Viruses and Viral Infections

    SumptuousSugilite7063 avatar
    SumptuousSugilite7063
    Viral Infections and Replication Quiz
    32 questions

    Viral Infections and Replication Quiz

    DistinguishedBarbizonSchool avatar
    DistinguishedBarbizonSchool
    Use Quizgecko on...
    Browser
    Open
    Browser
    Browser