bio 151 lec 14 15 h & iid

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

PARUNGAO-BALOLONG 2011Thursday, March 3, 2011

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)


PARUNGAO-BALOLONG 2011

IMMEDIATE!!!



TYPE I HYPERSENSITIVITY REACTION



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)



CYTOTOXIC!!!


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


Transfusion Reactions


Hemolytic Disease of the Newborn



IMMUNE-COMPLEX MEDIATED!!!


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



Hypersensitivity pneumonitis is inflammation of the lungs due to breathing in a foreign substance, usually certain types of dust, fungus, or molds



DELAYED!!!



urushiol


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


IMMUNITY AND INFECTIOUS DISEASES


OUR FOCUS...

Overview: Innate and Adaptive Immunity as Response to Infectious Diseases

Viral, Bacterial, Fungal, Parasitic/Helminths/Protozoa

Emerging & Re-emerging Infections


OUR RESPONSE TO INFECTIOUS AGENTS


INNATE IMMUNE RESPONSE : forms the initial defense against

pathogens




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




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


IMMUNITY AND VIRAL INFECTIONS


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


The Outcome of the Infection Depends on How Effectively the Host’s Defensive Mechanisms Resist the Offensive Tactics of the Virus....


VIRUS NEUTRALIZATION : ANTIBODIES


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


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


VIRUS NEUTRALIZATION : ANTIBODIES


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


CELL-MEDIATED IMMUNITY: VIRAL CONTROL & CLEARANCE


• 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


CELL-MEDIATED IMMUNITY: VIRAL CONTROL & CLEARANCE


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


EVASION: VIRUSES (Antonio Alcami and Ulrich H. Koszinowski, 2000. IMMUNOLOGY TODAY. Vol.21 No.9 447)




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


EVASION OF NATURAL KILLER CELLS


(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


NEXT MEETING:SPECIAL IMMUNOLOGY CASES

INFLUENZA & HIV etc......


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


bio 151 lec 14 15 h & iid

Documents

viral control

immunity lecture

transfusion

fb diseases

balolong 2011thursday

antonio alcami

vaccines examination

immunology