Bio 151 lec 14 15 h & iid

Biology 151 Lectures 14-15
HYPERSENSITIVITIES &
IMMUNITY TO INFECTIOUS DISEASES
PARUNGAO-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


HYPERSENSITIVITIES
RECALL!

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)

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 when an antibiotic
forms a complex with red
Occurs with ABO blood
blood cell membrane protein
antigen groups
(similar to hapten carrier
Complement mediated lysis complex)

Drug Induced Hemolytic Induces formation of
Anemia 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!!!


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UPDATE ON SCHEDULE
PLAN A PLAN B

March 7: Immunity Lecture Hand-outs
and Emerging thru FB
Diseases
Take-Home
March 14: Vaccines Examination!
and Special Topics
24 hours to complete
March 21: Plenary
Reports Plenary Reports
Submitted in PPT
March 28: format
Examination 2
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 INNATE IMMUNE RESPONSE :
TO INFECTIOUS forms the initial defense against
AGENTS pathogens


OUR RESPONSE
TO INFECTIOUS
AGENTS

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

OUR 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 CASE: HIV
virus once infection has
Neutralizing antibodies are efficient in
occurred—particularly if the blocking virus particles but poorly
virus is capable of entering a effective against cell-associated virus,
latent state in which its DNA is such as virus-infected cells
integrated into host
CTLs are effective against virus-
chromosomal DNA
infected cells but not against free virus

• Once an infection is particles

established, cell-mediated Neither antibodies nor CTLs are
immune mechanisms are most effective against latently infected cells
important in host defense

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 INFLUENZA
virus

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


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 (a) NK cells can be inhibited by a
viral MHC class I homolog
KILLER CELLS
(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 PLAN B

March 7: Immunity Lecture Hand-outs
and Emerging thru FB
Diseases
Take-Home
March 14: Vaccines Examination!
and Special Topics
24 hours to complete
March 21: Plenary
Reports Plenary Reports
Submitted in PPT
March 28: format
Examination 2
Parungao-Balolong 2011

Bio 151 lec 14 15 h & iid

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