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INTERFERON

PRESENTER- DR. CHINMAYA DASH
INTRODUCTION
•

In 1957 Isaacs and Linderman described a factor that have the
property of viral interference.

• Research has revealed diverse mechanism of action include
antiviral, immune enhancing and cytostatic activities.
Definition
Interferons (IFNs) are naturally occurring cytokines
with antiviral, immunomodulatory and antiproliferative
properties.
• First cytokine to be recognized
CLASSIFICATION
A. In 1980, nomenclature was formally adopted classifying IFNs into
three categories
Based on Antigenic Specificity:IFN categories

Earlier Designation

Alpha

(α)

Leukocyte

Beta

(β)

Fibroblast

Gamma ( )

Immune IFN

B. Their ability to bind to common Receptor Types :(Divided into TWO groups )
IFN
Types

IFN
Categories

Receptors

Prototypic cell of
Origin

Type-I

Alpha (α)

I

Leukocyte

Beta

I

Fibroblast

Omega ( )

I

Leukocyte

Tao ( )

I

Ovine Trophoblast

Gamma-

II

T-Cell
NK-Cell

Type-II

(β)
Properties

Alpha

Beta

Gamma

Current Nomenclature

IFN-α

IFN-β

IFN-

Former Designation

Leukocyte

Fibroblast

Immune
Interferon

Type Designation

Type I

Type I

Type II

No. Of Genes that code for Family

≥20

1

1

Principal Cell Source

Most Cell
Types

Most cell Types Lymphocytes

Inducing Agent

Viruses;
dsRNA

Viruses;
dsRNA

Mitogens

Stability at pH 2.0

Stable

Stable

Labile

Homology with IFN-α

80-95%

30%

<10%

Chromosomal location of genes

9

9

12

Size of secreted protein (Number of
amino acids)

165

166

143

IFN receptors

IFNAR

IFNAR

IFNGR

Chromosomal location of IFN receptor
genes

21

21

6
Important Features :• First recognized by their ability to interfere with viral
infections in cultured cells.
• Does not protect the virus infected cell that produces it.
• Itself is not the antiviral agent.
It moves to other cells where it induces an antiviral
state.(By inhibiting viral replication)

• Almost all cell types produce IFN-α &β and
IFN- are produced in T-cells and NK-Cells
INDUCTION AND ACTIVATION OF IFNs
A. IFN-α & β
(Type-I- IFNs)

When prototypic cell of origin is exposed to
-Viruses
-Double stranded RNA
-Polypeptides And
- Cytokines

B. IFN(Type-II- IFNs)

Following a number of immunological stimuli
including :-T-cell specific antigen
-Staphylococcal enterotoxin -A And
-Mitogens ( Phyto haemagglutinin ,Phorbol Ester
etc)
MODE OF ACTIVATION OF IFN STIMULATED GENES(ISGs):IFN binds with the respective
IFN-Receptors(IFNRs)
Oligomerization of the receptor followed by
phosphorylation of the tail of receptor
molecule
Phosphorylated stat ( Signal Transducers
and activators of transcription ) released from
the receptor molecules and translocate to the
nucleus
Activation of trancription of
IFN-Stimulated gene. This results in
synthesis of several enzymes
 These enzymes instrumental in development of the
antiviral state.
 dsRNA dependent protein kinase, PKRPhosphorylates and inactivates cellular initiation factor elF-2 ,
thus prevents viral protein synthesis
 2-5A synthetase (Oligonuceotide Synthetase)Activates a cellular endonuclease RNase L -» Degrade mRNA
 Phosphodiesterase- inhibits peptide chain elongation

 Nitric oxide synthetase, which is induced by IFN- in
macrophages
Fail to reveal why the antiviral state acts selectively against viral
mRNA and not cellular mRNA
Interferon
BIOLOGICAL PROPERTIES
A. Properties of IFN α & Th1-Differentiation
Growth Inhibition

T-CELLS
IFNproduction
IL-1
Production
Proliferation

NK-CELL/
MACROPHAGES

IFN-α
&

ANTIANGIOGENIC

TUMOR CELLS

 MHC-I
expression
 Tumor
specific
antigenic
expression
Adhession
molecule
expression
Direct
cytostatic effect
B. Properties of IFN- :Increased Activation

T-CELLS
MHC ClassII
upregulation

APC/
MACROPHAGES

IFN-

ANTIANGIOGENIC

TUMOR CELLS

• MHC-I
upregulation.
•Decreased
proliferation
APPLICATIONS
A. Therapeutic Applications:Used to treat several neoplastic and non neoplastic
diseases.
Clinical indications of INF as follows:i.

Neoplastic Diseasesa. Lymphoma-

Non Hodgkin’s Lymphoma (NHL)
Follicular Lymphoma
b. Hematopoetic MalignaciesHairy Cell Leukemia
Chronic Myeloid Leukemia(CML)
c. CarcinomaRenal Cell Carcinoma (RCC)
Melanoma
ii. Non Neoplastic Diseasesa. Chronic Hepatitis B InfectionIFN-α / Peg IFN-α with Nucleoside Analogues
(Lamivudin, Adefovir,Tenofovir etc)

b. Chronic Hepatitis C InfectionStandard IFN and the combination of
Peg INF-α2a or 2b with or without Ribavirin therapy
c. Condyloma AcuminataIntralesional INF-α2b in previously resistant to
Podophyllum
TYPE

FDA- APPROVED INDICATIONS

IFN-α2a

-NHL, Hairy Cell Leukemia, CML
-AIDS related KS, Chronic Hepatitis-C

IFN-α2b

-Follicular Lymphoma, Hairy Cell
leukemia, AIDs related KS, Malignant
melanoma,
-Condyloma acuminata, Chronic
hepatitis B, Chronic hepatitis C

IFN-αn3

-Condyloma acuminata

IFN- β1a

-Relapsing remitting Multiple Sclerosis

IFN-β1b

-Relapsing remitting Multiple Sclerosis

IFN-

-Chronic Granulomatous Disease
B. Preventive Application-

Common Cold (Rhinovirus infection)Intranasal IFN-α2
C. Diagnostic Application:-

T Cell based interferon gamma (IFN- ) assay (IGRAs) for
Mycobacterium tuberculosis specific antigens
Helps in screening for Latent (LTBIs) and active tuberculosis
infection.
VIRUS MECHANISMS TO COUNTERACT INTERFERON
 Specific viral proteins may block induction of expression
of IFN
( Herpesvirus, Papilloma virus, Hepatitis C virus, Rota virus)
 May block the activation of the key PKR protein kinase
( Adenovirus, Herpes viruses)
 May activate a cellular inhibitor of PKR
( Influenza, Poliovirus)
 May block IFN induced signal transduction
(Adenovirus, Herpes virus, Hepatitis B Virus)
 May neutralize IFN- by acting as a soluble interferon receptor
( Myxoma virus )
SIDE EFFECTS
 Depending upon the time interval between induction of
therapy and appearance of side effects/toxicities classified as-

 Acute Toxicities ( Occur usually between 3-6Hrs after
receiving IFN )
 Chronic Toxicities
 Clinically there are four major side effect groupsSIDE EFFECTS
I.CONSTITUTIONAL

Fatigue (70%-100%)
Anorexia(40%-70%), Weight loss, Fever, Myalgia,
Headache

II.
• Dizziness/Vertigo
NEUROPSYCHIATRIC •Mood Disorder-( Confusion, pathological depression)
(upto 30%)
•Neuro endocrine disturbance( Perturbation of hypothalamo thyroid adrenalin axis)
III.HEPATIC

Transamnitis

IV.HEMATOLOGICAL

•Thrombocytopenia
•Anemia
•Leukopenia

(The severity of side effects)

α

(Dose and Duration of IFN therapy.)
REFERENCES
• Jonasch E and Haluska FG. Interferon in Oncological Practice:
Review of Interferon Biology, Clinical Applications, and Toxicities.
Oncologist 2001;6(1):34-55.
• Rijckborst V and Janssen Harry L.A. The Role of Interferon in
Hepatitis B therapy. Curr Hepatitis Rep 2010;9:231-238
• Kanda T, Imazeki F and Yokosuka O. New Antiviral Therapies for
Chronic Hepatitis C. Hepatol Int 2010;4:548-561
• Yoshihiro et al .Comparison of T Cell Interferon- y Release Assays
for Mycobacterium tuberculosis – Specific Antigens in Patients with
Active and Latent Tuberculosis. Lung 2010;188:283-287
• Hayden FG and Gwalthey JM jr. Intranasal interferon-alpha 2
treatment of experimental rhinoviral colds. J Infect Dis. 2003
Aug;150(2):174-80.
THANK
YOU

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Interferon

  • 2. INTRODUCTION • In 1957 Isaacs and Linderman described a factor that have the property of viral interference. • Research has revealed diverse mechanism of action include antiviral, immune enhancing and cytostatic activities.
  • 3. Definition Interferons (IFNs) are naturally occurring cytokines with antiviral, immunomodulatory and antiproliferative properties. • First cytokine to be recognized
  • 4. CLASSIFICATION A. In 1980, nomenclature was formally adopted classifying IFNs into three categories Based on Antigenic Specificity:IFN categories Earlier Designation Alpha (α) Leukocyte Beta (β) Fibroblast Gamma ( ) Immune IFN B. Their ability to bind to common Receptor Types :(Divided into TWO groups )
  • 5. IFN Types IFN Categories Receptors Prototypic cell of Origin Type-I Alpha (α) I Leukocyte Beta I Fibroblast Omega ( ) I Leukocyte Tao ( ) I Ovine Trophoblast Gamma- II T-Cell NK-Cell Type-II (β)
  • 6. Properties Alpha Beta Gamma Current Nomenclature IFN-α IFN-β IFN- Former Designation Leukocyte Fibroblast Immune Interferon Type Designation Type I Type I Type II No. Of Genes that code for Family ≥20 1 1 Principal Cell Source Most Cell Types Most cell Types Lymphocytes Inducing Agent Viruses; dsRNA Viruses; dsRNA Mitogens Stability at pH 2.0 Stable Stable Labile Homology with IFN-α 80-95% 30% <10% Chromosomal location of genes 9 9 12 Size of secreted protein (Number of amino acids) 165 166 143 IFN receptors IFNAR IFNAR IFNGR Chromosomal location of IFN receptor genes 21 21 6
  • 7. Important Features :• First recognized by their ability to interfere with viral infections in cultured cells. • Does not protect the virus infected cell that produces it. • Itself is not the antiviral agent. It moves to other cells where it induces an antiviral state.(By inhibiting viral replication) • Almost all cell types produce IFN-α &β and IFN- are produced in T-cells and NK-Cells
  • 8. INDUCTION AND ACTIVATION OF IFNs A. IFN-α & β (Type-I- IFNs) When prototypic cell of origin is exposed to -Viruses -Double stranded RNA -Polypeptides And - Cytokines B. IFN(Type-II- IFNs) Following a number of immunological stimuli including :-T-cell specific antigen -Staphylococcal enterotoxin -A And -Mitogens ( Phyto haemagglutinin ,Phorbol Ester etc)
  • 9. MODE OF ACTIVATION OF IFN STIMULATED GENES(ISGs):IFN binds with the respective IFN-Receptors(IFNRs) Oligomerization of the receptor followed by phosphorylation of the tail of receptor molecule Phosphorylated stat ( Signal Transducers and activators of transcription ) released from the receptor molecules and translocate to the nucleus Activation of trancription of IFN-Stimulated gene. This results in synthesis of several enzymes
  • 10.  These enzymes instrumental in development of the antiviral state.  dsRNA dependent protein kinase, PKRPhosphorylates and inactivates cellular initiation factor elF-2 , thus prevents viral protein synthesis  2-5A synthetase (Oligonuceotide Synthetase)Activates a cellular endonuclease RNase L -» Degrade mRNA  Phosphodiesterase- inhibits peptide chain elongation  Nitric oxide synthetase, which is induced by IFN- in macrophages Fail to reveal why the antiviral state acts selectively against viral mRNA and not cellular mRNA
  • 12. BIOLOGICAL PROPERTIES A. Properties of IFN α & Th1-Differentiation Growth Inhibition T-CELLS IFNproduction IL-1 Production Proliferation NK-CELL/ MACROPHAGES IFN-α & ANTIANGIOGENIC TUMOR CELLS  MHC-I expression  Tumor specific antigenic expression Adhession molecule expression Direct cytostatic effect
  • 13. B. Properties of IFN- :Increased Activation T-CELLS MHC ClassII upregulation APC/ MACROPHAGES IFN- ANTIANGIOGENIC TUMOR CELLS • MHC-I upregulation. •Decreased proliferation
  • 14. APPLICATIONS A. Therapeutic Applications:Used to treat several neoplastic and non neoplastic diseases. Clinical indications of INF as follows:i. Neoplastic Diseasesa. Lymphoma- Non Hodgkin’s Lymphoma (NHL) Follicular Lymphoma b. Hematopoetic MalignaciesHairy Cell Leukemia Chronic Myeloid Leukemia(CML) c. CarcinomaRenal Cell Carcinoma (RCC) Melanoma
  • 15. ii. Non Neoplastic Diseasesa. Chronic Hepatitis B InfectionIFN-α / Peg IFN-α with Nucleoside Analogues (Lamivudin, Adefovir,Tenofovir etc) b. Chronic Hepatitis C InfectionStandard IFN and the combination of Peg INF-α2a or 2b with or without Ribavirin therapy c. Condyloma AcuminataIntralesional INF-α2b in previously resistant to Podophyllum
  • 16. TYPE FDA- APPROVED INDICATIONS IFN-α2a -NHL, Hairy Cell Leukemia, CML -AIDS related KS, Chronic Hepatitis-C IFN-α2b -Follicular Lymphoma, Hairy Cell leukemia, AIDs related KS, Malignant melanoma, -Condyloma acuminata, Chronic hepatitis B, Chronic hepatitis C IFN-αn3 -Condyloma acuminata IFN- β1a -Relapsing remitting Multiple Sclerosis IFN-β1b -Relapsing remitting Multiple Sclerosis IFN- -Chronic Granulomatous Disease
  • 17. B. Preventive Application- Common Cold (Rhinovirus infection)Intranasal IFN-α2
  • 18. C. Diagnostic Application:- T Cell based interferon gamma (IFN- ) assay (IGRAs) for Mycobacterium tuberculosis specific antigens Helps in screening for Latent (LTBIs) and active tuberculosis infection.
  • 19. VIRUS MECHANISMS TO COUNTERACT INTERFERON  Specific viral proteins may block induction of expression of IFN ( Herpesvirus, Papilloma virus, Hepatitis C virus, Rota virus)  May block the activation of the key PKR protein kinase ( Adenovirus, Herpes viruses)  May activate a cellular inhibitor of PKR ( Influenza, Poliovirus)  May block IFN induced signal transduction (Adenovirus, Herpes virus, Hepatitis B Virus)  May neutralize IFN- by acting as a soluble interferon receptor ( Myxoma virus )
  • 20. SIDE EFFECTS  Depending upon the time interval between induction of therapy and appearance of side effects/toxicities classified as-  Acute Toxicities ( Occur usually between 3-6Hrs after receiving IFN )  Chronic Toxicities
  • 21.  Clinically there are four major side effect groupsSIDE EFFECTS I.CONSTITUTIONAL Fatigue (70%-100%) Anorexia(40%-70%), Weight loss, Fever, Myalgia, Headache II. • Dizziness/Vertigo NEUROPSYCHIATRIC •Mood Disorder-( Confusion, pathological depression) (upto 30%) •Neuro endocrine disturbance( Perturbation of hypothalamo thyroid adrenalin axis) III.HEPATIC Transamnitis IV.HEMATOLOGICAL •Thrombocytopenia •Anemia •Leukopenia (The severity of side effects) α (Dose and Duration of IFN therapy.)
  • 22. REFERENCES • Jonasch E and Haluska FG. Interferon in Oncological Practice: Review of Interferon Biology, Clinical Applications, and Toxicities. Oncologist 2001;6(1):34-55. • Rijckborst V and Janssen Harry L.A. The Role of Interferon in Hepatitis B therapy. Curr Hepatitis Rep 2010;9:231-238 • Kanda T, Imazeki F and Yokosuka O. New Antiviral Therapies for Chronic Hepatitis C. Hepatol Int 2010;4:548-561 • Yoshihiro et al .Comparison of T Cell Interferon- y Release Assays for Mycobacterium tuberculosis – Specific Antigens in Patients with Active and Latent Tuberculosis. Lung 2010;188:283-287 • Hayden FG and Gwalthey JM jr. Intranasal interferon-alpha 2 treatment of experimental rhinoviral colds. J Infect Dis. 2003 Aug;150(2):174-80.