Virology - Host Defense Mechanisms

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Host defense mechanisms

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-natural barriers
-innate immunity
-acquired immunity

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Natural barriers
-types

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-physical/anatomical
-absence of virus receptor
-intracellular barriers that block replication

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Best natural barrier

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-skin

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Innate immunity
-types

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-RNAi
-Interferons/inflammatory cytokines
-Phagocytic cells
-NK cells

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Acquired Immunity
-types

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-TH1 immune response (CTLs)
-TH2 immune response (antibody)

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Good news about innate and adaptive immune responses

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-redundancy
-integration

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Bad news about innate and adaptive immune responses

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-immunity can be exploited by the pathogen to facilitate infection and disease
-immune activation can cause unintended consequences (neoplasia, autoimmunity, inflammation)

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Cells that are active early due to innate immunity

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-IFN-Type 1
-NK cells

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Cells that are active later due to adaptive immunity

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-Antibody (IgM)
-Neutralizing antibody (IgG)
-CTLs

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Initial recognition of infection is due to:

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-Pathogen-associated Molecular Patterns (PAMPs)

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PAMPs
-types

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-dsRNA
-dsDNA in the cytoplasm
-Viral proteins

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How are PAMPs recognized?

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-Toll-like Receptors (TLRs) on the cell surface
-internal cellular receptors

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Danger signals of infection

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-necrotic cell death
-inflammation

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Why do some vaccine adjuvants contain a product that induces some type of danger signal?

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-to strengthen the vaccine potency

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How does RNAi provide host defense?

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the host cell recognizes that there is something wrong in the genes coding for specific proteins so it destroys mRNA, not allowing it to code

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RNAi
-process

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-recognition of dsRNA
-dsRNA cleaved by Dicer into small fragments
-fragments incorporated into RNA-induced silencing complexes (RISCs)
-use a single strand of fragmented RNA to find foreign RNA
-degrades the target RNA

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Distances of Cytokine activity

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-Autocrine (not measurable in body fluids)
-Paracrine (detected in pathological states)
-Endocrine (measured in bodily fluids)

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Cytokine actions

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-innate
-adaptive
-inflammatory

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Interferons (IFN)

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-produced by a virus infected cell to induces a virus-resistant state in surrounding cells (paracrine)

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Type 1 Interferons
-produced by

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Multiple cell types:
-alpha
-beta
-kappa
-delta

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Type 2 Interferons
-produced by

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-NK cells
-T cells

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Primary function of IFN on cell function

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-upregulation of multiple cell pathways

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Proteins upregulated by IFN

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-PKR
-P56
-ADAR
-2-5(A) synthetase

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Main protein upregulated by IFN

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-PKR

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PKR
-antiviral activities

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-activates other antiviral pathways
-induces apoptosis
-inhibits protein synthesis

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P56
-antiviral activities

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-inhibition of cell division

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ADAR
-antiviral activities

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-altered mRNA translation

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2-5(A) synthetase
-antiviral properties

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-apoptosis
-mRNA degredation

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Protein Kinase R (PKR)
-function

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-recognizes dsRNA
-autophosphorylate and dimerizes dsRNA
-eIF2-alpha binds and becomes phosphorylated
-eIF2-alpha is turned off, terminated viral protein synthesis

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Methods viruses can use to subvert PKR

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-inactive PKR
-dimerization inhibition
-sequestration of dsRNA
-active PKR inhibition

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How can viruses make PKR inactive

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-downregulation
-inhibit activation
-dsRNA analogs

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NK cell
-function

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-if a class-I MHC does not bind to the inhibitory receptor of the NK cell, the NK cell will become activated and kill the infected cell through apoptosis

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Function of apoptotic blebs to NK cells

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-increase the expression of activating ligands for NK cells

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Adaptive immunity
-properties

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-recognition and activation by a specific foreign antigen
-effector function (production of cytokines, CTL, antibody)
-memory

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Stages of adaptive immunity

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-recognize antigens
-proliferation of B and T cells
-implement effector functions
-maturation of effector function
-remove unused lymphocytes
-memory

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2 roles of adaptive immunity

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-virus specific antibodies prevent infection of cells
-cell-mediated immunity

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Cell Mediated Immunity
-transfer ability

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-cannot be transfered between animals

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Humoral Immunity
-transfer ability
-ex

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can be transferred between animals
-passive antibody in milk and transplacental
-gamma globulin therapy

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When is it good to use gamma globulin therapy?

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-if you don't have 2 weeks to wait for a vaccination to take effect

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TH1 is what kind of immunity

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Cell-Mediated Immunity

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TH1 Cell-Mediated Immunity
-process

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-NK-cell causes virus infected cell to undergo apoptosis
-APC takes up the apoptotic bleb
-Inflammatory cytokines are produced by the APC to alert of infection
-The APC processes the antigen and presents it as MHC-II to a T-Cell receptor on TH1 (trimolecular complex)
-Th1 will make IL-2 to drive the proliferation of more THC and make IFN through the paracrine response of IL-2
-IL-2 will also drive the proliferation of CTLs
-a virus infected cell presents antigen as MHC-I to a CTL with a T-cell receptor, forming a trimolecular complex
-the CTL kills the virus infected cell

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TH2 is what kind of immunity

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Humoral Immunity

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TH2 Humoral Immunity
-process

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-antibody on the resting B-cell is the receptor for antigen
-B-cell takes up antigen
-antigen is presented by the B-cell as MHC-II to the TCR of TH2 (trimolecular complex)
-TH2 cell produces B-cell cytokines
-cytokines cause: B-cell proliferation, B-cell differentiation into plasma cells, and B-cell production of antibody

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MHC-I
-location

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-target cell

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MHC-II
-location

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-presenting cells

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Trimolecular complex
-components

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-MHC I/II
-Ag
-TCR

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CD4
-purpose

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stabilize the trimolecular complex of Helper T-cells

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CD8
-purpose

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stabilize the trimolecular complex of CTLs

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What is the effect of a virus trying to downregulat MHC-I on the surface of the virus infected cell, in order to not be recognized by the CTLs?

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-NK cells will recognize the missing MHC-1 and kill the cell

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What is the end stage of CTL killing of a virus infected cell?
Why is this important?

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-the end stage is apoptosis
-it is important because it avoids an inflammatory response, and it provides apoptotic blebs with antigen to be recognized by APC

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3 ways that the CTL causes apoptosis

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-granzymes
-perforin
-FAS ligand

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What type of apoptotic signal is FAS ligand?

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-extrinsic

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How is apoptosis activated within the virus-infected cell?

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caspase cascade activated by granzymes

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2 regions of antibody

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-Fab
-Fc

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Fab antibody region
-function

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-recognition

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Fc antibody region
-Function

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-Function

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How are the heavy and light chains of antibody held together?

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-disulfide bond

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Antibody type found in circulation

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-IgG

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Antibody type from naive B cells

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-IgD

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Antibody type responsible for allergies

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-IgE

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Antibody type that is found at mucosal surfaces

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-IgA

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Antibody type with high avidity

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-IgM

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Why is IgA important?

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-most viruses enter the body through mucosal surfaces

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Antibody
-actions

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-neutralize the virus infectivity of cells
-opsonize virus and virus-infected cells
-complement-mediated lysis of enveloped viruses
-antibody-dependent cell-mediated cytotoxicity

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Antibody
-bad effects

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-can facilitate infection with antibody-dependent enhancement of infection

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Virus-neutralizing antibody
-function

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-bind to virus so that it cannot bind with the cell surface receptor

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Opsonization antibody
-function

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-the ability to bind to the Fc receptor of a cell so that the virus gets taken up into a phagosome and degraded

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Antibody Dependent Enhancement
-Function

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-virus uses the Fc receptor on a cell surface to facilitate infection
-the virus enters a cell endosome and replicates eventually resulting in infection

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Complement-Mediated membrane attack complex
-function

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remove the envelope from the virus making it unstable

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Antibody-dependent cell-mediated cytotoxicity (ADCC)
-function

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-Fc receptors on the surface of NK cells recognize antibod bound to a virus infected cell
-When bound the NK cell releases granzymes and perforins, causing apoptosis