immunity 3
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Questions and Answers

Which of the following are types of lymphocytes?

  • Dendritic cells
  • Epithelial cells
  • T cells (correct)
  • Macrophages

    • Where do T cells undergo education to become immunocompetent?

  • Spleen
  • Thymus (correct)
  • Bone marrow
  • Lymph nodes

    • What is the significance of T cell positive selection in the thymus?

  • Eliminating T cells that respond too strongly to antigens
  • Promoting clonal deletion of self-reactive T cells
  • Ensuring T cells do not react to self-antigens
  • Stimulating T cells to develop surface antigen receptors (correct)

    • What is the mechanism by which self-reactive T cells are eliminated in the thymus?

    <p>Clonal deletion (B)</p> Signup and view all the answers

    What is the result of negative selection in T cell development?

    <p>T cells enter a state of self-tolerance, ignoring the body’s own proteins (C)</p> Signup and view all the answers

    What is the term for immunocompetent T cells that have not yet encountered foreign antigens?

    <p>Naive lymphocyte pool (A)</p> Signup and view all the answers

    Where do B cells, that react to self-antigens, undergo clonal deletion or anergy?

    <p>Bone Marrow (C)</p> Signup and view all the answers

    What is the initial site of development for B cells?

    <p>Bone marrow (B)</p> Signup and view all the answers

    How do B cells achieve immunocompetence?

    <p>By synthesizing antigen surface receptors and producing immunocompetent clones (A)</p> Signup and view all the answers

    What is a crucial difference regarding antigen recognition between T cells and antigen-presenting cells?

    <p>T cells require antigens to be presented by antigen-presenting cells (A)</p> Signup and view all the answers

    Which mechanism involves antibodies binding to multiple enemy cells, immobilizing them and enhancing phagocytosis?

    <p>Agglutination (C)</p> Signup and view all the answers

    During a primary immune response, which antibody typically appears first and peaks around 10 days?

    <p>IgM (B)</p> Signup and view all the answers

    What is the hallmark characteristic of a secondary (anamnestic) immune response compared to a primary response?

    <p>Rapid and heightened IgG production (D)</p> Signup and view all the answers

    Which of the following is an example of alloimmunity?

    <p>Reaction to transplanted tissue (D)</p> Signup and view all the answers

    Type I hypersensitivity is characterized by which of the following?

    <p>IgE-mediated reaction with rapid onset (D)</p> Signup and view all the answers

    Which of the following is a typical treatment for anaphylactic shock?

    <p>Epinephrine (B)</p> Signup and view all the answers

    In allergic asthma, what is the primary role of IgE?

    <p>To bind to mast cells in the respiratory mucosa (C)</p> Signup and view all the answers

    Type II hypersensitivity involves:

    <p>IgG or IgM attacking antigens bound to cell surfaces (B)</p> Signup and view all the answers

    What is the underlying mechanism of damage in Type III hypersensitivity reactions?

    <p>Deposition of antigen-antibody complexes and complement activation (D)</p> Signup and view all the answers

    Which type of hypersensitivity involves a delayed cell-mediated reaction?

    <p>Type IV (B)</p> Signup and view all the answers

    What is a key characteristic of autoimmune diseases?

    <p>Failure of self-tolerance (D)</p> Signup and view all the answers

    Cross-reactivity, as a cause of autoimmune disease, refers to:

    <p>Antibodies against foreign antigens reacting with similar self-antigens (A)</p> Signup and view all the answers

    What is the primary defect in Severe Combined Immunodeficiency Disease (SCID)?

    <p>Hereditary lack of T and B cells (C)</p> Signup and view all the answers

    Which of the following is NOT a common mode of HIV transmission?

    <p>Casual contact (B)</p> Signup and view all the answers

    What is a typical indicator of the progression of HIV to AIDS?

    <p>TH cell count below 200 cells/µL (C)</p> Signup and view all the answers

    Which of the following is NOT a typical function of antigen-presenting cells (APCs)?

    <p>Producing antibodies to directly neutralize pathogens. (B)</p> Signup and view all the answers

    What is the primary role of the Major Histocompatibility Complex (MHC) proteins in the context of antigen presentation?

    <p>To serve as 'identification tags' that distinguish self from non-self. (A)</p> Signup and view all the answers

    What happens when a T cell encounters an APC displaying a self-antigen?

    <p>The T cell typically disregards the self-antigen. (D)</p> Signup and view all the answers

    Which type of T cell is responsible for suppressing the immune response to prevent excessive or inappropriate immune activity?

    <p>Regulatory T cells (TR). (C)</p> Signup and view all the answers

    Co-stimulation is crucial in T cell activation to:

    <p>ensure the T cell only attacks foreign antigens. (C)</p> Signup and view all the answers

    What is the immediate outcome of successful co-stimulation of a T cell?

    <p>The T cell undergoes clonal selection. (C)</p> Signup and view all the answers

    Helper T cells (TH) enhance cellular and humoral immunity by:

    <p>secreting interleukins that stimulate other immune cells. (D)</p> Signup and view all the answers

    How do cytotoxic T (TC) cells eliminate infected or cancerous cells?

    <p>By secreting perforin and granzymes to induce apoptosis in the target cells. (D)</p> Signup and view all the answers

    What characteristic distinguishes memory T cells from naive T cells?

    <p>Memory T cells are more numerous and respond more rapidly upon re-exposure to an antigen. (A)</p> Signup and view all the answers

    What is the main function of antibodies in humoral immunity?

    <p>To tag antigens for destruction by other immune cells or mechanisms. (D)</p> Signup and view all the answers

    What triggers the activation of an immunocompetent B cell in humoral immunity?

    <p>Binding of an antigen to multiple surface receptors on the B cell. (C)</p> Signup and view all the answers

    What is the role of helper T cells in the activation of B cells?

    <p>They secrete interleukins that activate B cells after the B cell has processed and displayed an antigen. (C)</p> Signup and view all the answers

    Plasma cells are terminally differentiated B cells that primarily function to:

    <p>secrete large quantities of antibodies. (B)</p> Signup and view all the answers

    Which antibody is produced first during the first exposure to an antigen?

    <p>IgM (D)</p> Signup and view all the answers

    How do memory B cells contribute to long-term immunity?

    <p>By quickly differentiating into plasma cells and producing antibodies upon re-exposure to an antigen. (D)</p> Signup and view all the answers

    Flashcards

    Cells of the Immune System

    Contains lymphocytes and antigen-presenting cells such as macrophages and dendritic cells.

    Lymphocytes

    Key immune cells consisting of NK cells, T cells, and B cells.

    Natural Killer (NK) Cells

    Type of lymphocyte responsible for immune surveillance and eliminating infected or cancerous cells.

    T Lymphocytes

    A type of lymphocyte that matures in the thymus and executes immune responses.

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    Positive Selection of T Cells

    Process in the thymus where T cells learn to recognize foreign antigens.

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    Negative Selection of T Cells

    Elimination of T cells that react to self-antigens, ensuring self-tolerance.

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    Immunocompetent T Cells

    T cells that have receptors for recognizing antigens and are ready to act.

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    Naive Lymphocyte Pool

    Immunocompetent T and B cells that have not yet encountered antigens.

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    B Lymphocytes

    Immune cells that mature in the bone marrow and produce antibodies.

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    Antigen-Presenting Cells

    Cells that present antigens to T cells, crucial for immune responses.

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    Antigen-Presenting Cells (APCs)

    Cells that process and present antigens to T cells, triggering an immune response.

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    MHC Proteins

    Major histocompatibility complex proteins that identify cells as 'self' or 'non-self'.

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    Antigen Processing

    The process where APCs capture, digest, and display antigen fragments to T cells.

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    T Cell Activation

    The process by which T cells recognize and bind to MHC proteins displaying antigens, initiating an immune response.

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    Co-stimulation

    A secondary signal required for T cell activation, preventing an attack on 'self' cells.

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    Clonal Selection

    The process by which activated T cells undergo mitosis to produce a clone responding to the same antigen.

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    Helper T Cells

    T cells that help activate other immune cells, including B cells and cytotoxic T cells.

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    Cytotoxic T Cells

    T cells that directly attack and destroy infected or cancerous cells.

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    Memory T Cells

    Long-lived T cells that respond quickly upon re-exposure to the same pathogen.

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    Humoral Immunity

    Immune response involving B cells that produce antibodies against antigens.

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    B Cell Activation

    B cells become activated when an antigen binds to their receptors and helper T cells assist.

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    Antibody Production

    B cells transform into plasma cells that produce antibodies against antigens.

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    IgM and IgG Antibodies

    Types of antibodies produced, with IgM being the first response and IgG for later exposures.

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    Attack Phase in Humoral Immunity

    Antibodies bind to antigens, neutralizing them and marking them for destruction.

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    Memory in Humoral Immunity

    Some B cells become memory cells, ensuring rapid response upon future encounters with the same antigen.

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    Neutralization

    Antibodies mask pathogenic region of an antigen.

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    Complement fixation

    IgM or IgG bind to an antigen and initiate complement binding, leading to inflammation and phagocytosis.

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    Agglutination

    Antibodies bind to multiple enemy cells, immobilizing them and enhancing phagocytosis.

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    Precipitation

    Antibodies bind to antigen molecules, creating a precipitate that can be removed.

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    Primary immune response

    Initial immune reaction upon first exposure to an antigen, with a delay of 3 to 6 days.

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    Secondary response

    Rapid plasma cell formation upon re-exposure to an antigen, leading to a quick IgG rise.

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    Hypersensitivity

    Excessive immune reaction against normally tolerated antigens.

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    Type I hypersensitivity

    Immediate reaction (allergies) mediated by IgE within seconds of exposure.

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    Anaphylaxis

    Severe allergic reaction that requires immediate intervention.

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    Type II hypersensitivity

    IgG or IgM attacks antigens on cell surfaces, leading to cell destruction.

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    Type III hypersensitivity

    Immune complex reaction where IgG or IgM forms complexes leading to inflammation.

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    Type IV hypersensitivity

    Delayed cell-mediated response occurring 12 to 72 hours after exposure.

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    Autoimmune diseases

    Conditions where the immune system attacks self-tissues due to loss of self-tolerance.

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    Immunodeficiency

    Failure of the immune system to respond vigorously, leading to increased infections.

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    Study Notes

    Immune System Part III

    • The immune system has major cells: lymphocytes, antigen-presenting cells (APCs), macrophages, and dendritic cells.
    • These cells are concentrated in strategic locations like lymphatic organs, skin, and mucous membranes.

    Lymphocytes

    • Lymphocytes come in three types: natural killer (NK) cells (immune surveillance), T lymphocytes (T cells), and B lymphocytes (B cells).

    T Lymphocytes (T Cells)

    • T cells develop in three stages:

      • Born in bone marrow.
      • Educated in the thymus.
      • Deployed to carry out immune function.

    • Within the thymus:

      • Cortical epithelial cells release chemicals to stimulate maturing T cells developing surface antigen receptors.
      • T cells with receptors are now immunocompetent, recognizing antigens presented to them.

    • Within the thymus (continued):

      • Medullary epithelial cells test T cells presenting self-antigens.
      • T cells failing by reacting to self-antigen are eliminated via negative selection (clonal deletion).
      • Macrophages phagocytize self-reactive T cells.
      • Some self-reactive T cells remain alive but unresponsive (anergy).

    • Negative selection leaves the body in a state of self-tolerance; surviving T cells respond only to suspicious antigens.

    • Only 2% of T cells pass the test; forming the naive lymphocyte pool, T cells not yet encountered foreign antigens.

    • Naive T cells leave the thymus and colonize lymphatic tissues and organs throughout the body.

    B Lymphocytes (B Cells)

    • B cells develop in bone marrow; some fetal stem cells remain differentiating into B cells.
    • Self-tolerant B cells synthesize antigen surface receptors, divide rapidly, and produce immunocompetent clones.
    • B cells leave the bone marrow and colonize the same lymphatic tissues and organs as T cells.

    Antigen-Presenting Cells (APCs)

    • T cells cannot recognize antigens on their own. APCs are needed.

    • Dendritic cells, macrophages, reticular cells, and B cells function as APCs, whose function depends on major histocompatibility (MHC) complex proteins.

    • APCs act as "identification tags" labeling every body cell as belonging to the individual.

    • APCs are structurally unique except for identical twins.

    • Antigen processing:

      • APC encounters antigen.
      • Internalizes it by endocytosis..
      • Digests antigen into molecular fragments.
      • Displays relevant fragments (epitopes) in MHC protein grooves.

    • Wandering T cells inspect APCs for displayed antigens.

    • If APC displays a self-antigen, the T cell disregards it.

    • If APC displays a non-self-antigen, the T cell initiates an immune attack.

    • APCs alert the immune system to the presence of foreign antigens.

    • Successful defense relies on quickly mobilizing immune cells against the antigen with chemical messengers coordinating activities (interleukins).

    Cellular Immunity

    • Cellular immunity is a form of specific defense where T lymphocytes directly attack and destroy diseased or foreign cells.
    • The immune system remembers antigens preventing future disease.
    • It employs four classes of T cells: cytotoxic, helper, regulatory, and memory T cells.

    Cellular Immunity 2

    • Cytotoxic T (Tc) cells: killer T cells (T8, CD8, or CD8+). They are the "effectors" of cellular immunity and attack target cells.
    • Helper T (TH) cells: help promote Tc and B cell action and innate immunity.
    • Regulatory T (TR) cells: (T-regs) inhibit multiplication and cytokine secretion by other T cells limiting immune response. They are also called T4, CD4, CD4+.
    • Memory T (TM) cells: descend from cytotoxic T cells, responsible for memory in cellular immunity.

    Cellular Immunity 3

    • Both cellular and humoral immunity occur in three stages:
      • Recognition
      • Attack
      • and Memory

    Recognition (Cellular)

    • Antigen presentation and T cell activation are crucial in cellular immunity recognition. APCs encounter and process antigens, migrating to the nearest lymph node, and displaying antigens to T cells. T cells encounter the antigen displayed on MHC proteins initiating the immune response.

    T Cell Activation 1

    • T cell activation begins when a T cell binds to an MHC protein displaying an epitope (portion of the antigen).
    • The T cell also binds to another APC protein, related to interleukins.
    • A T cell must verify that it is bound to a foreign antigen—co-stimulation.
    • Co-stimulation prevents the immune system from attacking the body's own tissues falsely.

    T Cell Activation 2

    • Successful co-stimulation initiates clonal selection; the activated T cell undergoes repeated mitosis creating a clone of identical T cells programmed against the same epitope.
    • Some cells in the clones become effector cells carrying out the attack, and other cells become memory T cells.

    Attack (Cellular)

    • Helper and cytotoxic T cells have different roles in the attack phase.
    • Helper T cells play a central role in coordinating cellular and humoral immunity. They recognize Ag-MHC protein complexes producing and releasing interleukins with three effects:
      • Attract neutrophils and NK cells.
      • Attract macrophages, stimulate phagocytosis, and inhibit their movement from the area.
      • Stimulate T and B cell mitosis and maturation.
    • Cytotoxic T (Tc) cells are the only T cells directly attacking other cells.
      • When a Tc cell recognizes a complex of antigen and MHC-I protein on a foreign or diseased cell, it docks on the cell.
      • Cytotoxic T cells deliver lethal chemicals: perforin and granzymes acting like NK cells, interferons inhibiting viral replication, recruiting macrophages, activating them for killing cancer cells.

    Memory (Cellular)

    • Immune memory follows the primary response.
    • Following clonal selection, some Tc and TH cells become long-lived memory cells.
    • They are more numerous than naive T cells, requiring fewer activation steps leading to rapid response upon re-exposure to the same antigen.

    T-Cell Recall Response

    • Upon re-exposure to a pathogen, memory cells launch a swift attack avoiding noticeable illness.
    • The individual becomes immune to the disease.

    Humoral Immunity

    • Humoral immunity is a more indirect defense method than cellular immunity.
    • B lymphocytes produce antibodies binding to antigens for destruction by other means.
    • Humoral immunity works in three stages similar to cellular immunity (recognition, attack, and memory).

    Recognition (Humoral)

    • Immunocompetent B cells have thousands of surface receptors for a single antigen.
    • Antigen binding to several receptors links them together for endocytosis within the B cells.
    • Small molecules aren't antigenic because they can't link many receptors together.
    • B cells process (digest) the antigen linking some epitopes to its MHC-II proteins then displaying themselves on the cell surface.

    Recognition 2 (Humoral)

    • A B cell response does not continue without a helper T cell binding to the Ag-MHC protein complex.
    • The bound T helper cell secretes interleukins to activate the B cell. This triggers clonal selection which is important.
    • B cells reproduce to produce many identical B cells. They are programmed against the same antigen.
    • Most differentiate into plasma cells bigger than B cells with rough ER.
    • Plasma cells secrete antibodies. This occurs at a rate of 2,000 molecules per second for a lifespan of 4-5 days.
    • First exposure to antigen triggers IgM production and later exposures are IgG. Antibodies travel in blood and other body fluids.

    Attack and Memory (Humoral)

    • Attack in humoral immunity: antibodies bind to antigens rendering them harmless.
    • Memory in humoral immunity: some B cells differentiate into memory cells.

    Clonal Selection and Ensuing Events of the Humoral Immune Response

    • Antigen recognition initiates the process where antigens bind to B cells with matching receptors.
    • Antigen presentation where the B cell internalizes the antigen, displays the processed epitope, and helper T cell binding stimulates interleukin secretion.
    • Clonal selection occurs leading to B cell division of many identical B cells directed at the same antigen.
    • Differentiation occurs with some cells becoming memory B cells, and most differentiate into plasma cells.
    • Plasma cells produce antibodies.

    B Cell and Plasma Cell

    • B cells (a) and plasma cell (b) are illustrated with electron microscope images showing their cellular structure.

    Humoral Attack 1

    • Antibodies have four mechanisms to attack antigens:
      • Neutralization: antibodies mask pathogenic regions of the antigen.
      • Complement fixation: IgM or IgG binding changes shape triggering complement binding leading to inflammation, phagocytosis, immune clearance, or cytolysis. Primary defense against foreign cells, bacteria, mismatched RBCs.

    Humoral Attack 2

    • Agglutination: antibodies with multiple binding sites bind to many enemy cells; immobilizing them from spreading. Enhancing phagocytosis through creating bigger "bites".
    • Precipitation: antibody binds antigen molecules (not cells); creating antigen-antibody complexes, precipitating and making them removable, cleared by immune system or phagocytized by eosinophils.

    Humoral Memory 1

    • Primary immune response: Immune reaction to first exposure; protective antibodies appear after several days.
    • Plasma cells form after B cell multiplication and differentiation, producing antibodies like IgM first peaking around 10 days. Then IgM levels decline, IgG levels rise and then drop to low within a month.
    • Antibodies enter the bloodstream via plasma.

    Humoral Memory 2

    • Primary response leads to immune retention of the antigen.
    • Clonal selection creates memory B cells in germinal centers of lymph nodes.
    • They readily mount fast secondary responses.

    Humoral Memory 3

    • Secondary (anamnestic) response; if re-exposed.
      • Plasma cells form within hours of re exposure to antigen.
      • IgG titer sharply rises and peaks within days. Rapid response, no illness.
      • Low levels of IgM also secreted then quickly decline. IgG rises and stays elevated for weeks to years conferring long-lasting protection; memory does not last as long in humoral as in cellular immunity.

    Disorders of the Immune System

    • Immune responses can be too vigorous, too weak, or misdirected against the wrong targets.

    Hypersensitivity

    • Hypersensitivity is an excessive immune reaction against antigens typically tolerated by most.
    • Alloimmunity: reaction to transplanted tissue from another person.
    • Autoimmunity: abnormal reactions to one's own tissues.
    • Allergies: reactions to environmental antigens (allergens)-dust, mold, pollen vaccines , venom, poison ivy, plant, food (nuts, milk, eggs, shellfish), drugs (penicillin, tetracycline, insulin).
    • Four kinds of hypersensitivity:
      • Type I (acute, immediate): very rapid response.
      • Type II and III (subacute): slower onset (1-3 hours after exposure) lasting longer, quicker antibody-mediated responses.
      • Type IV (delayed): cell-mediated, signs 12-72 hours after exposure.

    Type I Hypersensitivity 1

    • Includes most common allergies.
    • IgE-mediated reaction occurring within seconds of exposure usually subsiding within 30 minutes, severe to fatal.
    • Allergens bind to IgE on basophils and mast cells.
    • Stimulating release of histamine and other inflammatory chemicals.

    Type I Hypersensitivity 2

    • Clinical signs include local edema, mucus hypersecretion and congestion, watery eyes, runny nose, hives, and sometimes cramps, diarrhea, vomiting.
    • Examples include food allergies, and asthma (local inflammatory reaction to inhaled allergens).

    Type I Hypersensitivity 3

    • Anaphylaxis is an immediate and severe type I reaction, widespread, relieving local anaphylaxis with antihistamines.
    • Anaphylactic shock is severe with bronchoconstriction, dyspnea, widespread vasodilation, circulatory shock, and, occasionally, death.
    • Antihistamines are insufficient and epinephrine is needed dilating bronchioles, increasing cardiac output, restoring blood pressure, with fluid therapy and respiratory support sometimes being required.

    Type I Hypersensitivity 4

    • Asthma is common, especially in children.
      • Allergic (extrinsic) asthma is frequently seen.
      • Respiratory crisis often triggered by inhaled allergens.
      • Stimulating plasma cell IgE binding to respiratory mucosa; mast cells releasing inflammatory chemicals intense airway inflammation.
      • Nonallergic (intrinsic) asthma can be triggered by infections, drugs, air pollutants, cold dry air, exercise or emotions but effects are similar to allergic asthma.

    Type I Hypersensitivity 5

    • Asthma effects include bronchospasms within minutes; severe coughing, wheezing, potentially fatal suffocation.
    • A second respiratory crisis can occur 6-8 hours later.
    • Interleukins attract eosinophils, leading to bronchial tissue damage , edema, and plugging with thick sticky mucus.
    • Treatment involves epinephrine and other ẞ-adrenergic stimulants to dilate the airway and corticosteroids to control inflammation.

    Type II Hypersensitivity

    • Antibody-dependent cytotoxic reactions. IgG or IgM attack antigens bound to cell surfaces, activating complement, lysing or opsonizing target cells
    • Macrophages destroy opsonized platelets, erythrocytes, etc. This includes blood transfusion reactions and certain drug reactions.

    Type III Hypersensitivity

    • Immune complex reactions forming IgG or IgM antigen antibody complexes. These complexes deposit in tissues beneath blood vessel endothelium activating complement triggering intense inflammation.
    • Examples include acute glomerulonephritis and systemic lupus erythematosus.

    Type IV Hypersensitivity

    • Cell-mediated, delayed reactions, signs appear 12-72 hours after exposure.
    • Activation begins with APCs in lymph nodes displaying antigens to helper T cells; triggering the secretion of interferons and cytokines activating cytotoxic T cells, and macrophages.
    • The result is a mixture of innate and immune responses like cosmetics, poison ivy, graft rejection, TB skin test, beta cell destruction causing type 1 diabetes mellitus.

    Autoimmune Diseases 1

    • Autoimmune diseases result from immune system failure to distinguish self from non-self antigens producing autoantibodies attacking body tissues.
    • Cross-reactivity, with antibodies that attack foreign antigens sometimes targeting similar self-antigens plays a part.

    Autoimmune Diseases 2

    • Three reasons for self-tolerance failure include:
      • Abnormal exposure of self-antigens in the blood.
      • Changes in self-antigen structure due to factors like viral infections or drugs may make them perceived as foreign.
      • Self-reactive T cells that are not eliminated in the thymus remain in check by regulatory T cells.

    Immunodeficiency Diseases 1

    • Immune system fails to respond strongly enough leading to severe combined immunodeficiency disease (SCID) .
    • Hereditary lack of T and B cells and vulnerability to opportunistic infections that require protective enclosures.

    Immunodeficiency Diseases 2

    • Acquired immunodeficiency syndrome (AIDS) is a group of conditions severely depressing the immune response.
    • Caused by infection with the human immunodeficiency virus (HIV).

    Acquired Immunodeficiency Syndrome 3

    • Early symptoms: Flu-like symptoms with progressive chills, night sweats, fatigue, headache, extreme weight loss, lymphadenitis.
    • Lowered TH count (600-1,200 cells/μL) in AIDS being less than 200 cells/μL.
    • Increased susceptibility to opportunistic infections (Toxoplasma, Pneumocystis, herpes simplex virus, cytomegalovirus, tuberculosis, Candida infections, Kaposi sarcoma).

    Acquired Immunodeficiency Syndrome 4

    • HIV transmission: blood, semen, vaginal secretions, breast milk, or across the placenta.
    • Most common transmission methods are: sexual contact (vaginal, anal, oral), contaminated blood products, and contaminated needles.
    • Undamaged latex condoms are an effective HIV barrier.

    HIV Transmission

    • HIV is transmitted through blood, semen, vaginal secretions, breast milk, or across the placenta.
    • Most common methods of transmission are sexual intercourse (vaginal, anal, oral), contaminated blood products, and contaminated needles.

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