bio 151 lec 14 15 h & iid
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Biology 151 Lectures 14-15 HYPERSENSITIVITIES &
IMMUNITY TO INFECTIOUS DISEASESPARUNGAO-BALOLONG 2011
Thursday, March 3, 2011
WHAT YOU NEED TO KNOW...
4 TYPES OF HYPERSENSITIVITIES
VIRAL INFECTIONS
BACTERIAL INFECTIONS
PROTOZOANS AND HELMINTHS (PARASITIC)
EMERGING AND RE-EMERGING INFECTIONS
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HYPERSENSITIVITIESRECALL!
Inflammatory response - local, eliminates antigen without extensively damaging the host’s tissue
Hypersensitivity - immune & inflammatory responses that are harmful to the host (von Pirquet, 1906)
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IMMEDIATE!!!
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TYPE I HYPERSENSITIVITY REACTION
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Systemic (Anaphylaxis shock)
Symptoms include: labored breathing, drop in blood pressure, smooth muscle contraction, bronchiole constriction (suffocation)
Localized
Examples: Hay fever (allergic rhinitis), asthma (allergic or intrinsic), food allergies, atopic dermatitis (eczema)
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CYTOTOXIC!!!
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EXAMPLES
Transfusion Reactions
Occurs with ABO blood antigen groups
Complement mediated lysis
Drug Induced Hemolytic Anemia
Occurs when an antibiotic forms a complex with red blood cell membrane protein (similar to hapten carrier complex)
Induces formation of antibodies
Complement
Hemolytic Disease of the Newborn
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Transfusion Reactions
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Transfusion Reactions
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Hemolytic Disease of the Newborn
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IMMUNE-COMPLEX MEDIATED!!!
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TYPE III HYPERSENSITIVITY
Occurs when antigen enters bloodstream,
circulating immune complexes form
Symptoms include: Fever ; Weakness;
Rashes; ETC.
Complement initiates mast cell degranulation
Neutrophils are chemotactically attracted to
the site
Neutrophils release lytic enzyme after failed
attempts to endocytose the immune complex
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Hypersensitivity pneumonitis is inflammation of the lungs due to breathing in a foreign substance, usually certain types of dust, fungus, or molds
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DELAYED!!!
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urushiol
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UPDATE ON SCHEDULE
PLAN A
March 7: Immunity and Emerging Diseases
March 14: Vaccines and Special Topics
March 21: Plenary Reports
March 28: Examination 2
PLAN B
Lecture Hand-outs thru FB
Take-Home Examination!
24 hours to complete
Plenary Reports Submitted in PPT format
Parungao-Balolong 2011
Thursday, March 3, 2011
IMMUNITY AND INFECTIOUS DISEASES
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OUR FOCUS...
Overview: Innate and Adaptive Immunity as Response to Infectious Diseases
Viral, Bacterial, Fungal, Parasitic/Helminths/Protozoa
Emerging & Re-emerging Infections
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OUR RESPONSE TO INFECTIOUS AGENTS
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INNATE IMMUNE RESPONSE : forms the initial defense against
pathogens
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OUR RESPONSE TO INFECTIOUS AGENTS
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Humoral and Cell-Mediated Response: for the specific infections may be caused by the host response to the pathogen and its products rather than the pathogen itself response to infectious agents
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OUR RESPONSE TO INFECTIOUS AGENTS
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NOTE:
The survival and pathogenicity of pathogens in a host are critically influenced by their ability to evade or resist protective immunity
Tissue injury and disease consequent to infections may be caused by the host response to the pathogen and its products rather than the pathogen itself
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IMMUNITY AND VIRAL INFECTIONS
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VIRUSES...
•Obligatory intercellular pathogens that replicate within cells
•Use the nucleic acid and protein synthetic machineries of the host cell
•Infect a variety of cell populations by utilizing normal cell surface molecules as receptors to enter cell
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The Outcome of the Infection Depends on How Effectively the Host’s Defensive Mechanisms Resist the Offensive Tactics of the Virus....
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VIRUS NEUTRALIZATION : ANTIBODIES
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Antibodies: effective in protecting against localized infection (site of viral entry)
SURFACE RECEPTOR MOLECULES: enable them to initiate infection = binding to specific host-cell membrane molecules
EXAMPLES:
Influenza: binds to sialic acid residues in cell membrane glycoproteins and glycolipids
Rhinovirus: binds to intercellular adhesion molecules (ICAMs)
Epstein-Barr virus: binds to type 2 complement receptors on B cells
NOTE: If antibody to the viral receptor is produced, it can block infection altogether by preventing the binding of viral particles to host cells
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Oseltamivir was developed through modifications to the sialic acid analogue
A: Rhinovirus binds to ICAM-1 on cell surface
B: ICAM-1 binding triggers a conformational change of virus, and leads to a release of RNA, which is transported into the inside of cells
C: Use the first domain of ICAM-1 to neutralize virus = inhibit rhinovirus infection
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VIRUS NEUTRALIZATION : ANTIBODIES
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Secretory IgA in mucous secretions plays an important role in host defense against viruses by blocking viral attachment to mucosal epithelial cells
EXAMPLE: attenuated oral polio vaccine
induces production of secretory IgA
effectively blocks attachment of poliovirus along the gastrointestinal tract
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CELL-MEDIATED IMMUNITY: VIRAL CONTROL & CLEARANCE
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• ANTIBODIES: contain the spread of a virus in the acute phases of infection
• BUT, cannot eliminate the virus once infection has occurred—particularly if the virus is capable of entering a latent state in which its DNA is integrated into host chromosomal DNA
• Once an infection is established, cell-mediated immune mechanisms are most important in host defense
CASE: HIV
Neutralizing antibodies are efficient in blocking virus particles but poorly effective against cell-associated virus, such as virus-infected cells
CTLs are effective against virus-infected cells but not against free virus particles
Neither antibodies nor CTLs are effective against latently infected cells
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CELL-MEDIATED IMMUNITY: VIRAL CONTROL & CLEARANCE
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In most viral infections, specific CTL activity arises within 3–4 days after infection, peaks by 7–10 days, and then de- clines
Within 7–10 days of primary infection, most virions have been eliminated, paralleling the development of CTLs
CTLs specific for the virus eliminate virus-infected self-cells and thus eliminate potential sources of new virus
INFLUENZA
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EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)
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EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)
PARUNGAO-BALOLONG 2011Thursday, March 3, 2011
EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)
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EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)
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To prolong cell viability and facilitate their own replication, viruses have evolved multiple mechanisms to inhibit the host apoptotic response
Cellular proteases such as caspases and serine proteases are instrumental in promoting apoptosis
Thus, these enzymes are logical targets for virus-mediated modulation to suppress cell death
Thursday, March 3, 2011
EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)
PARUNGAO-BALOLONG 2011Thursday, March 3, 2011
EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)
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EVASION OF NATURAL KILLER CELLS
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(a) NK cells can be inhibited by a viral MHC class I homolog
(b) Viruses can inhibit expression of HLA-A and HLA-B, resulting in a relative increase in HLA-C and HLA-E on the surface of the target cell; these inhibit NK cells
(c) Virus-encoded proteins can function as cytokine binding proteins that block the action of NK cell activating cytokines
(d) NK cell activities can also be avoided by decreased expression of NK cell−activating ligands in virus-infected target cells, which prevent signal transduction via NK cell−activating receptors.
(e) Viruses can also directly inhibit NK cells by infecting them or using envelope proteins to ligate NK cell inhibitory receptors
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NEXT MEETING:SPECIAL IMMUNOLOGY CASES
INFLUENZA & HIV etc......
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PLS. CHOOSE YOUR PREFERENCE
PLAN A
March 7: Immunity and Emerging Diseases
March 14: Vaccines and Special Topics
March 21: Plenary Reports
March 28: Examination 2
PLAN B
Lecture Hand-outs thru FB
Take-Home Examination!
24 hours to complete
Plenary Reports Submitted in PPT format
Parungao-Balolong 2011
Thursday, March 3, 2011