This ppt includes the immune response to the infections

1. IMMUNE RESPONSE TO
INFECTIOUS DISEASE
By: Erin Anthony
Yasmin Deliz
Jasminia Nuesa

2. INTRODUCTION
 Despite innate and
adaptive immune
responses to pathogens,
infectious diseases which
have plagued human
populations throughout
history still cause millions
of deaths per year.
 There are 4 main types of
pathogens that cause
infectious disease
 1. Viruses
 2. Bacteria
 3. Protozoa
 4. Helminths

3. VIRAL INFECTIONS
 One of the 4 main pathogens responsible for infectious diseases
 Responsible for smallpox, the common cold, chickenpox, influenza,
shingles, herpes, polio, rabies, Ebola, hanta fever, and AIDS.
 Several specific immune effector & nonspecific defense
mechanisms
 Viruses act to subvert one or more of these mechanisms to prolong
their survival

4. VIRAL INFECTIONS
 Viruses: Structure &
Function
 Viruses depend on host cells
for reproduction
 Outside of host cells, the
viruses remain metabolically
inert
 They exist as a protein coat or
capsid, sometimes enclosed
within a membrane
 The capsid encloses either DNA
or RNA which codes for the virus
elements

5. VIRAL INFECTIONS
 Viruses: Structure &
Function (cont.)
 In contact with a cell, the
virus, with help from
surface molecules, will
inject it’s genetic material
into the cell
 Thus taking over the cell’s
functions
 The infected cell
produces more viral
proteins and genetic
material rather than it’s
usual products
 In the cell, the virus has
two phases:
 1. The lysogenic phase
 2. The lytic phase

6. VIRAL INFECTIONS

7. VIRAL INFECTIONS
 Innate Immune Response
- 2 primary events:
1. Induction of Type I Interferons
2. Activation of NK cells

8. VIRAL INFECTIONS
 Induction of Type I Interferons:
 The double-stranded RNA (dsRNA) of the
virus induces the expression of the interferons
by the infected cell.
 The bound IFN’s will activate the JAK/STAT
pathway responsible for the synthesis of
several genes
 One encodes 2-5(A) synthetase an enzyme that
activates ribonuclease (RNAse L)

9. VIRAL INFECTIONS
 IFN’s and NK Cells
 In addition, IFN-α & IFN-β binding induces a
specific protein kinase called RNA-dependent
protein kinase (PKR)
 The binding of IFN-α & IFN-β to NK cells
induces lytic activity
 Effective in killing virally infected cells
 Enhanced by IL-12

10. VIRAL INFECTIONS

11. VIRAL INFECTIONS
 Viral Neutralization by Humoral Antibody
 What is crucial to the preventing of the spread of the virus
during acute infection and in protecting against
reinfection?
 ANTIBODIES
 If antibody is produced to the viral receptor, it can block
infection altogether by preventing viral binding to the host
cells
 i.e. Secretory IgA in mucous secretions
 Viral Neutralization by antibody sometimes occurs after viral
attachment
 Some may block viral penetration by binding to epitopes necessary to
mediate fusion of the viral envelope with the plasma membrane
 Some cause the lysis of the enveloped virions
 Some agglutinate viral particles and function as an opsonizing agent

12. VIRAL INFECTIONS
 Cell-Mediated Antiviral Mechanisms
 Antibodies, although crucial in containing the
spread of the virus, are not able to eliminate
the virus once infection has occurred
 Once infection occurs, cell-mediated immune
mechanisms become the most important
 2 main components of cell-mediated antiviral
defense
 1. CD8+ Tc cells
 2. CD4+ Th1 cells (CD4+ Tc cells)

13. VIRAL INFECTIONS
Cell-Mediated Antiviral Mechanisms (Cont.)
Activated Th1 cells
produce several cytokines
IL-2
Acts indirectly by assisting
in the recuitment of CTL
precursors
Activates NK cells
IFN-γ
Directly induces an antiviral
state in cells
Activates NK cells
TNF
CTL activity
Arises within 3-4 days after
infections
 Peaks by 7-10 days, and
then declines
Have viral specificity
Eliminites specific virus-
infected cells, thus getting
rid of potential new sources
of new virus

14. VIRAL INFECTIONS
 Viral Invasion of Host-Defense Mechanisms
 Viruses encode proteins that interfere at various
levels with specific or nonspecific host defenses
 Some develop strategies to avade the action of IFN-α & IFN-
β
 Some inhibit the antigen presentation by infected hosts by
preventing antigen delivery to class I MHCs
 Some reduce levels of class II MHCs on cell surface
 Others evade complement-mediated destruction
 Some cause generalized immunosuppression-direct viral
infection of lymphocytes or macrophages
 Some constantly change their antigens
 i.e. Influenza

15. VIRAL INFECTIONS
 Properties of the
Influenza Virus
 Virions are roughly
spherical or ovoid in shape
with an ave. diameter of
90-100nm
 Virions are surrounded by
an outer envelope
 2 proteins are inserted into
this envelope
 1. Hemagglutinin (HA)
 2. Neuraminidase (NA)
 Inside the envelope:
 Matrix protein surrounds
the nucleocapsid
 Consists of 8 different
strands of ssRNA
associated with protein
and RNA polymerase

16. VIRAL INFECTIONS
 Influenza
 3 major types– A, B, &C
 Distinguished by
differences in their
nucleoprotein and matrix
proteins
 Distinguishing feature of
influenza virus is its
variability
 Two different mechanisms
for variation in HA & NA
 1. Antigenic Drift
 2. Antigenic Shift

17. VIRAL INFECTIONS
 Influenza (Flu) Symptoms:
 Fever
 Muscle aches and pain
 Headache
 Fatigue
 Dry cough
 Sore throat
 Runny nose
 What makes this different
from a cold?

18. VIRAL INFECTIONS
 Host Response to
Influenza Infection
 Humoral Antibody specific
for the HA molecule is
produced during infection
 Serum antibodies
antibodies imporant for
resistance to reinfection by
the same strain, but not
required for recovery
 In addition, CTLs also play
a role

19. VIRAL INFECTIONS
 Epstein-Barr
(Infectious Mono)
 Herpes virus family
 Life-long dormant
infection in some cells
 Symptoms:
 Fever
 Sore Throat
 Swollen Lymph glands
 Swollen liver/spleen
 *Age Group*