IMMUNITY

MODERATOR - DR. KALPOJIT SAIKIA

PRESENTERS - ABU ZAMIL IRFAN HUSSAIN

BILKIS SAHIN
DISHA CHETIA
JUGAL RABHA
MENUKA HANSEPI
PRIYA KUMARI
SABANA BEGUM
SIBTAIN MAHMOOD
ZARIR AHMED KHADEM
NUHMAN ROSHID CHOWDHURY
The ability of human body to
resist almost all types of foreign
organisms and toxins that
damage the tissues and organs
is called as IMMUNITY.
 HISTORY

In 1796 - Edward Jenner , an English

physician , also known as the father of
immunology developed first vaccine
by using cowpox to provide
protection against smallpox.
In 1860 - 1880s Louis Pasteur
(France) proved that germs
cause disease , Developed
Vaccines for rabies and
anthrax and introduced the
concept of attenuated
vaccines.
In 1880s - Elie Metchnikoff
(Russia) discovered
phagocytosis and laid the
foundation of innate immunity.
Due to which he won Noble
Prize in 1908.
In 2018 - James Allison and
Tasuko Honjo jointly
recieved noble prize for
development of new kind of
cancer treatment called
immune checkpoint therapy
which helps body's own
immune system to fight
cancer more effectively.
James Allison Tasuko Honjo
CLASSIFICATION OF IMMUNITY
Innate Immunity is the inborn capacity of the body to offer resistance
to pathogens and other toxic products.
Acquired immunity is the resistance that an individual acquires during
his lifetime.
Active Acquired immunity is acquired by synthesis of antibodies
(Humoral immunity) and production of immunoglobulin cells (cell
mediated immunity) by individuals own immune system in response to
antigenic stimulation.
Passive Acquired immunity is acquired by transfer of ready made
antibodies to recipient.
Both active and passive acquired immunity can be induced naturally
and artificially.
 INNATE IMMUNITY

The innate immunity response is the body's first, rapid, and non-
specific defense against pathogens, relying on pre-existing
mechanisms like physical barriers and specialized cells to quickly
detect and eliminate threats, ultimately bridging the gap until the
adaptive immune system can respond.
It is characterized by
PHAGOCYTOSIS and digestion
of the microbes.

It is the first line of defence.

 Innate immunity may be:

(a) Species Immunity- Resistance to a pathogen shown by all

members of a Species.

(b) Racial Immunity- Resistance to a pathogen shown by only a

particular race within a species.

(c) Individual Immunity- Resistance to a pathogen shown by a

particular individual within a race.
 MECHANISMS OF INNATE IMMUNITY

1) Mechanical Barrier: It is against invading microorganisms is

provided by the intact skin and mucosa in the body.

2)Surface Secretions: It includes -

Secretions from the sebaceous glands of skin, which contain both
saturated and unsaturated fatty acids that kill many bacteria and
fungi.
Saliva, constantly produced in the mouth cavity, has an inhibitory
effect on many microorganism.

Gastric juice and highly acidic environment of stomach may

hydrolyse microbial invaders.

Tears poured in the conjunctival sac mechanically wash away

the particles and a hydrolytic enzyme, lysozyme present in the
tears, can destroy most of the microorganisms.
3) Humoral defence mechanisms : Provide innate immunity by the
nonspecific microbicidal substances present in the body fluids. A few
examples are:
Lysozyme is found in high concentration in most tissue fluids
except CSF, sweat and urine. It is a mucolytic enzyme which kills
microorganisms by splitting sugars of the structural mucopeptide
of their cell wall.
Basic polypeptides containing nonspecific microbicidal activity
include leukins, arginine- and lysine-containing proteins
protamine and histone.
 Interferon
Complements have lytic and
several other effects on
foreign substances.
Interferons are antiviral
substances produced by the
cells stimulated by live or
killed viruses. α and β
interferons are part of innate
immunity
4) Cellular mechanisms of defence
Monocyte
which provide nonspecific innate
immunity are:
Phagocytes, i.e. neutrophils
and the monocyte–
macrophage system cells
constitute the most important
nonspecific cellular defence
against the invading
microorganism.
 Natural Killer Cell
Natural killer (NK) cells refer to a
subpopulation of lymphocytes
which provide nonspecific
cellular defence against
viruses, tumour cells and other
infected cells.
 Eosinophil
Eosinophil granules contain
enzymes and toxic molecules
that act against larvae of
helminths.
 STEPS OF PHAGOCYTOSIS

(A)MIGRATION: process of getting

attach to capillary endothelium and
rolling along its surface.

(B)EMIGRATION AND DIAPEDESIS:

movement from the blood to the site
of infection by passing through the
junction between endothelial cells of
blood vessel
(C)CHEMOTAXIS: Process by which neutrophils are attracted to the site of
inflammation.

(D)OPSONIZATION: Process of coating of bacteria by opsonins by which

bacteria become tasty.

(E)ENGULFMENT STAGE: Phagocytic vesicles and phagolysome are used.

(F)SECRETION (DEGRANULATION) STAGE: Lysosomes pour enzymes to

vesicles.

(G) KILLING OR DEGRADATION STAGE

 ACQUIRED (ADAPTIVE) IMMUNITY

The resistance that an individual acquires during his lifetime is known as

acquired or adaptive immunity.

It is antigen specific and may be antibody or cell mediated.

It is of two types:
A) Active Immunity
B) Passive Immunity
DIFFERENCE BETWEEN ACTIVE AND PASSIVE IMMUNITY
Active immunity can be induced naturally or artificially.

NATURAL ACTIVE IMMUNITY ARTIFICIAL ACTIVE IMMUNITY

Natural active immunity results Active immunity is induced by
either from a subclinical or clinical introducing antigens in the body
infection. in the form of vaccines.
Eg: Natural active immunity to This process is called active
poliomyelitis due to repeated immunization.
subclinical infections with polio Eg of vaccines:
virus during childhood. Bacterial vaccines
BCG vaccines for tuberculosis
Tetanus toxoid
Passive immunity can also be induced naturally or artificially.

NATURAL PASSIVE IMMUNITY ARTIFICIAL PASSIVE IMMUNITY

It is the transfer of ready-made Artificially, passive immunity can be
antibodies from the mother to the transferred to the recipients by
child. injecting ready-made antibodies.
Examples : This is done by administration of
In a fetus, the IgG antibodies are hyperimmune Sera of men or
transferred from the mother through the animals.
placenta.
Examples :
After birth, immunoglobulins are passed
Antitetanus serum (ATS)
to the newborn through breast milk .
Antidilhtheric serum (ADS)
Antigas gangrene serum(AGS)
 ACTIVE ACQUIRED IMMUNITY

FEATURES HUMORAL RESPONSE CELLULAR RESPONSE

1) Type of response Involves antibodies Involves attacking cells

2) Major cells involved B-Lymphocytes T-Lymphocytes

3) Antigen reacted to Extracellular pathogens: Intracellular pathogens: Viral or

Viruses, fungi or bacterial fungi; parasites infections; (i.e.
infections which are in the which are inside cells) tumours
body fluids i.e. outside the and cancer cells; foreign tissues
cells. such as transplanted organs.
 ANTIGEN

Antigen are substances that can

stimulate an immune response in the
body.
Most antigens are proteins, but some
are carbohydrates, lipids and nucleic
acids.
The specificity of an antigen is due to
specific areas of its molecule called
determinant sites or epitopes.
 The epitopes can bind to specific binding sites called paratopes of the
antibody molecule.
A pure protein can have several epitopes and thus can stimulate
formation of many distinct antibodies.

Some facts about antigenicity:

(1) Immunogenicity
(2) Antigen Specificity
(3) Species Specificity
(4) Isospecificity
 ANTIBODY

Antibodies or Immunoglobulins are

gamma globulins which are
produced in response to an
antigenic stimulation.
These react specifically with the
antigens which stimulated their
production.
All antibodies are Immunoglobulins,
but all Immunoglobulins are not
antibodies.
CLASSES OF ANTIBODIES
MECHANISM OF ACTION OF ANTIBODIES
 FUNCTIONS OF IMMUNOGLOBULINS

IgG protects the body fluids.

IgA protects the body surfaces.
IgM protects the blood stream.
IgE mediates type 1 hypersensitivity.
IgD's role is not clearly known
 LYMPHOCYTES

Lymphocytes are a type of white

blood cell (leukocyte) that play a
central role in the body's immune
response. They are primarily
responsible for recognizing and
responding to specific pathogens
through adaptive immunity.
Nucleus almost completely fills the
cell.
PRODUCTION OF LYMPHOCYTES
Antigen
Recognising
Protein

Antigen
Recognising
Protein
CLASSIFICATION OF LYMPHOCYTES
(A) B Cells (B-Lymphocytes)
Mature in the bone marrow.
On activation, B cells differentiate into plasma cells.
Plasma cells secrete antibodies (immunoglobulins) that help
neutralize and eliminate pathogens — this is known as humoral
immunity.
(B) T Cells (T-Lymphocytes)
Mature in the thymus.
They are part of cell-mediated immunity and are divided
into two main functional types:
1. Helper T Cells
2. Cytotoxic T Cells
Helper T Cells (CD4+T cells)

Identified by CD4 co-receptor.

They recognize antigens presented on MHC Class II
molecules.
Help activate B cells, cytotoxic T cells, and macrophages.
Play a central role in regulating immune responses.
Cytotoxic T Cells (CD8+T cells)

Identified by CD8 co-receptor.

They recognize antigens presented on MHC Class I
molecules.
Their main role is to kill infected cells, tumor cells, or foreign
graft cells.
 LYMPHOCYTE DISTRIBUTION

Blood: ~2% of lymphocytes

Lymphoid tissues: ~98%
Central (Primary): Thymus, Bone marrow
Peripheral (Secondary): Lymph nodes, spleen, tonsils, MALT
(e.g. Peyer’s patches)
 CLINICAL NOTE

HIV targets CD4+ T cells: leading to immunodeficiency.

SCID (Severe Combined Immunodeficiency): defect in both T and
B cell function.
Lymphomas: malignancies of lymphocytes (e.g., Hodgkin’s, Non-
Hodgkin’s)
Autoimmunity: failure of tolerance (e.g., lupus, rheumatoid
arthritis)
 IMMUNE RESPONSE

When a person is exposed to an antigen then our body shows some

response to kill or clear that pathogen, this response is known as
immune response.
This involves antibody production and T cells.
Immune responses to antigens may be categorized as primary and
secondary.
 PRIMARY IMMUNE RESPONSE

When antigens eg microorganisms are encountered for the first

time there is primary response
This response can take upto 14 days to resolve and lead to the
generation of memory cells with a high specificity for the inducing
antigen
Although the response may be sufficient to limit the antigen, the
antibody level then declines
The IgM molecules will be predominant in this primary immune
response
 SECONDARY IMMUNE RESPONSE

The second exposure to the same antigen produces a secondary

response
There is rapid response by memory B cells resulting in marked
increase in antibody production and it declines more slowly
The immune response is
(a) Quicker(within 3 years)
(b) Stronger( 100 to 1000 times more quantity of antibody)
(c) More avid (IgG type)
(d) More prolonged (response last for month)
This response may overcome a potential pathogen before it can
cause the symptoms of infection i.e it provides acquired antibody
mediated immunity.
This principle is used in active immunisation against infectious
disease.
 DIFFERENCE BETWEEN PRIMARY AND SECONDARY IMMUNE
RESPONSE

PRIMARY IMMUNE RESPONSE SECONDARY IMMUNE RESPONSE

1. Initial (first time) response to 1. Response due to repeated

invading organism. exposure to same antigen.
2. Onset: Slow to begin. 2. Fast (by memory B-cells).
3. Duration of effect: few weeks 3. Few months to years and
and declines rapidly. declines slowly.
4. Plasma antibody levels: Low 4. Markedly increased. (consists
(consists mainly of IgM mainly of Ig antibodies)
antibodies)
 CELLULAR IMMUNE RESPONSE

The cellular immunity refers to specific

acquired immunity which is accomplished by
effector T cells and macrophages
 ROLE OF CELLULAR IMMUNITY

1. Protects the host against fungi, most of the viruses and bacterial
pathogens.
2. Participates in allograft rejection and graft vs host reaction.
3. Participates in delayed hypersensitivity reaction.
4. Associated with certain autoimmune diseases.
 TYPES OF CELLULAR IMMUNITY

1) Primary cellular response -

Produced by initial contact with foreign antigen.

2) Secondary cellular response

Subsequent exposure to same antigen.
 STAGES OF CELLULAR IMMUNE RESPONSE

1) Antigen processing and presentation :-

Antigen entering the host body is phagocytosed into fragments by
APCs which includes macrophages and dendritic cells. These cells
then associate with MHC antigen and are expressed on the surface of
APC. Two modes of processing are known :
a)Processing of phagocytosed material eg. bacterial antigen
accomplished with MHC II molecules.
b)Processing of antigen derived within the cell eg. virus antigens
accomplished with MHC I molecules.
2)Recognition of antigen by lymphocytes :-
Lymphocytes possess the antigenic recognition receptors called TCRs
which serve as specific surface receptors recognizing and interacting
with single antigen.

3)T lymphocyte differentiation (activation) :-

CD8+ after combining with MHC I complex and differentiate into
Cytotoxic T Cells and Suppressor T Cells.
CD4+ after combining with MHC II complex and differentiate into
helper T cells and delayed type hypersensitivity cells.
T-T cooperation - the differentiation of T lymphocyte into helper,
cytotoxic and suppressor cells are interdependent. This
interdependence is called T-T cooperation.
Release of differentiated T cells - the cells formed are released into the
lymph and then enter the blood through which they are distributed
throughout the body.
T lymphocyte memory cells are formed which spread throughout the
lymphoid tissues of entire body.
4)Attack phase of cell-mediated immunity :-
Role of Cytotoxic T cells- cytotoxic and natural killer cells are
responsible for the attack. Cytotoxic cells have receptor proteins on
their outer membrane which bind with target cells (antigen bearing
cells) and destroy them by:
a)Perforin-mediated killing- secrete a hole forming protein
called perforin which form holes in the membrane of target
cells in presence of calcium and the pores formed cause cell
death.
 b.Lysis through cytotoxic substances- cytotoxic cells after
binding release cytotoxic substances.
c.Induction of apoptosis- cytotoxic cells secrete tumor necrosis
factor which increases calcium permeability of target cell
causing degradation of nucleus producing apoptosis.
Role of Helper T cells- Secrete interleukins and help in activation,
differentiation and apoptosis when required.

Role of Suppressor T cells- They regulate the activity of cytotoxic T

cells and thus cellular immune response is a balance between
cytotoxic and suppressor cells.
STAGES OF HUMORAL IMMUNE RESPONSE

1) Antigen Pocessing And Presentation :-

Once the antigen enters the body, it is phagocytosed by the
macrophages. Phagocytosed material is broken down into
polypeptide fragments. The antigen polypeptide fragments then
combine with the MHC II present in the macrophages and move to
the cell surface. This is called processing of antigen. Macrophages are
also called antigen-presenting cells (APCs). Other antigen-presenting
cells are:
B lymphocytes and
 Dendritic cells present in the skin (Langerhans cells), thymus
(medulla), lymph nodes (cortex and paracortex), spleen and other
secondary lymphoid organs.

2) Recognition Of Antigen by Lymphocytes.

The lymphocytes possess the antigen recognition receptors. These
receptors serve as specific receptors. The process of binding of
processed antigen to specific receptors on the surface of lymphocytes
is called recognition of antigen by lymphocytes.
3) Lymphocyte Activation :-
The lymphocytes that have combined
with antigen are activated, i.e. the
lymphocytes become larger and look
like a lymphoblast. This is known as blast
transformation. Activated B lympocytes
and helper T cells (CD4 cells) play a
major role in humoral immunity. The
macrophages liberate IL-1 and cause
further activation of B lymphocytes and
helper (CD4T) cells.
Activation of T Lymphocytes :
Activation of helper T cells by the processed antigen complex is essential
for humoral immunity. The activated helper T cells secrete two
substances: interleukins 2 (IL2) and B cell growth factor which further
promote proliferation of B lymphocytes and their transformation into
plasma cells. This phenomenon is called T–B cooperation.

Activation of B Lymphocyte :
After T-B cooperation, B lymphoblast proliferate forming clones of cells
that respond to this antigen.
The B lymphocytes proliferate and transform into two types:
Plasma Cell and
Memory B cells

Role of plasma cells : The plasma cells secrete antibodies.

Role of memory B cells : they are responsible for secondary response of

antibodies.
4) Production of Antibodies :-
The plasma cells so formed secrete antibodies [immunoglobulins (Igs)].
The rate of antibody production is very high, i.e. each plasma cell
produces about 2000 molecules of antibodies per second.

5) Inactivation of Antigen or Attack Phase or

Effector Phase of Immune Response :-
This is the last phase of immune response and involves the inactivation
of antigen by the antibodies. Antibodies act on the invading antigen
in two ways:
A) Direct attack on the invading agents-
Antibodies can inactivate the invading agent by the following
reactions:
Agglutination. By this reaction, large number of particles (bacteria
or red cells) with antigens on their surface are bound together to
form a clump. Clumping increases the susceptibility to
phagocytosis.
Precipitation. In this reaction, the antigen–antibody complex forms
an insoluble precipitate.
Neutralization. Antibodies cover the toxic sites of antigen and
neutralize them.
 Cytolysis. Antibodies attach to the membranes of cellular agents
thereby causing rapture of cells.

B) Attack on antigen through complement system-

The complement system includes 11 enzymatic proteins which are
named as C1 to C9, B and D. All these are present in the blood as
plasma proteins. These are also present in the tissue fluid.
 COMPLEMENT SYSTEM

“Complement” is a collective term that describes a system of

about 20 proteins, many of which are enzyme precursors. The
principal actors in this system are 11 proteins designated C1
through C9, B, and D.
 CLASSICAL PAYHWAY

This is activated by an antigen–antibody reaction. When an antibody

binds with an antigen, a specific reactive site on the constant portion of the
antibody becomes uncovered where the protein C1 binds and thus gets
activated. The activated C1 in turn activates the other complements in a
series of cascade reactions. The products of complement activation cause
the following effects:
Opsonization. Opsonization is the coating of antigen by antibody and
complement. It helps the neutrophils and macrophages to phagocytose
the antigen. The activated C3a product acts as an opsonin.
Lysis, i.e. destruction of bacteria by rupturing the cell membrane. A
membrane attack complex is formed by C5b–C6–C7–C8–C9. The
cell lysis is brought about by the complement system by inserting
proteins called perforins into the cell membrane. Perforins make
holes in the cell membranes, resulting in free flow of ions and
disrupting membrane permeability.
Agglutination, i.e. clumping of bacteria and RBCs.
Chemotaxis, i.e. attraction of leucocytes to the site of antigen–
antibody reaction. Chemotaxis is enhanced by C5b–C6–C7
complex.
Neutralization, i.e. covering the toxic sites of antigenic products.
 Activation and degranulation of mast cells and basophils is caused
by C4b. This releases factors producing vasodilatation and
chemotaxis. Vasodilatation increases capillary permeability;
therefore, plasma proteins enter the tissues and antigenic products
are inactivated.

The antibodies which can fix and thereby activate complements are
IgM and IgG.
 ALTERNATIVE PATHWAY

Activated without Ag-Ab reaction. It is initiated by binding of factor

I with polysaccharide present in the cell wall of invading organism.
Activated C3 and C5 ultimately attack the antigenic products of
invading organis.
 APPLIED PHYSIOLOGY
Impaired immune function, characterised by hyperactivity,
hypoactivity or abnormal responses can results in diseases.

Examples : a)Autoimmune Disease

b)Hypersensitivity
c)AIDS
d)Graft rejection
 AUTOIMMUNITY

Sometimes body starts producing antibodies or T cells against self-

antigen (own cells or tissue) leading to an autoimmune disease.
Therefore autoimmunity may be defined as immune response to self-
antigen.
 MECHANISM OF AUTOIMMUNITY

The possible mechanisms involved in development of autoimmunity are:

1) Forbidden Clones.
According to clonal selection theory, antibody-forming lymphocytes are
formed against different antigens. The clones of these cells are called
forbidden clones and hence an immune response does not occur
against self-antigen. However, persistence of these clones or their
development in later life by some mutations leads to autoimmunity
2) Hidden antigen or sequestration antigen.
Certain self-antigens are present in the close system and never exposed
to the immune system during fetal life. These are known as hidden
antigens or sequestrated antigens. When such antigens in later life are
somehow exposed to the immune system this leads to an immune
response. Another example of a hidden antigen is sperm antigen. Injury
to testes or viral infections (mumps) leads to leakage of sperm proteins
into the circulation and thus evokes an immune response against one’s
own testes and orchitis occurs.
3) Neoantigen or altered antigen.
Certain cells of the body undergo alterations due to exposure to
irradiations, drugs, sunlight, etc. and start producing an immune
response.

4) Cross-reacting antigen.
Although antibodies are highly specific for a particular antigen, but in
some cases they cross-react with other cells or body tissue. This
phenomenon is called as molecular mimicry and these antigens are
called cross-reacting antigens. For example, in rheumatic heart disease,
the heart is damaged by antibodies formed against streptococci.
5) Mutations.
The body immune system becomes competent for self-antigen by
certain mutations.

6)Unbalanced activity of helper and suppressor T cells.

Overactivity of TH cells and underactivity of Ts cells, then it may result in
autoimmunity.
 AUTOIMMUNE DISEASES

Common autoimmune diseases include:

1) Autoimmune anaemia. For example:

Haemolytic anaemia. Antibodies react with one’s own RBCs.
Pernicious anaemia. Antibodies react against gastric mucosa.

2) Thrombocytopenic purpura. Autoantibodies react with self-platelets.

3) Graves’ disease. Autoantibodies bind to thyroid cells and stimulate
them.

4) Hashimoto’s disease. T cells react against the antigen on the thyroid

cells.

5) Insulin-dependent diabetes mellitus. Antibodies damage the β cells

(insulin producing cells) of pancreas.

6) Rheumatoid arthritis. Antibodies damage the joints.

 HYPERSENSITIVITY

Hypersensitivity is an abnormal response which produces physiological

or histopathological damage in the host. There are five types of
hypersensitivity reactions:
1. Type I (anaphylaxis or IgE mediated)
2. Type II (antibody-mediated cytotoxicity),
3. Type III (immune complex-mediated disorders),
4. Type IV (delayed type or T cell-mediated hypersensitivity) and
5. Type V (stimulatory).
 HYPERSENSITIVITY REACTIONS

TYPE I TYPE II TYPE III TYPE IV

3 - 8 hrs
Type of Onset of (peak 48-72
1/2 - 8 hrs 5 - 12 hrs 24 - 48 hrs
Reaction hrs)

IgG, IgM, T-
IgE,
IgG, IgM and Neutrophils, Lymphocytes
Reaction Mediators Histamine,
and
complement Lysosomal
Serotonin,etc
enzymes Macrophages
 TYPE I TYPE II TYPE III TYPE IV

Response to
Erythema Erythema
Intradermal Injection Wheal and
- and and
Flare
of Antigens Oedema Induration

Transfusion
Arthur’s
Anaphylaxis, reaction, Tuberculin
reaction,
Examples Hay fever, Haemolytic test, Contact
Serum
Asthma disease of dermatitis
sickness
newborn
 AIDS
Acquired deficiencies of immunological response mechanisms can
occur secondarily to number of diseases. Acquired
immunedeficiency syndrome (AIDS) is the most important. AIDS, i.e.
acquired immune deficiency syndrome is characterized by reduction
in the number of helper T cells because of infection by human
immuno deficiency virus (HIV). AIDS was first of all detected in the USA
in 1981. HIV is of two types, HIV-1 and HIV-2.
 SPREAD OF DISEASE

AIDS is a major worldwide life-threatening disease spreading rapidly.

Daily about 8500 persons get infected with HIV. The high-risk groups
include: sex workers, drug addicts, homosexual males, persons with
extramarital relations and recipients of unscreened blood
transfusion.
 TRANSMISSION

There are mainly three routes of transmission:

1. Parenteral route - is through blood contact involving:
Unscreened blood transfusion
Tattooing
Use of infected razors, syringes, needles, etc.
Use of poorly sterilized dental instruments and
Organ transplants.
2. Sexual route - accounts for about 85% of HIV infection due to
multiplesex partners, sex workers, homosexuality and artificial
insemination. The virus is present in sufficient concentration in the
semen and vaginal secretions of the infected person.

3. Transplacental route - Infection can be transmitted from infected

mother to her fetus (vertical transmission) across the placenta and
also to the infant through breast milk (perinatal transmission).
 STRUCTURE OF HIV

HIV is a retrovirus having rounded

outline and consists of :
The core has two single strands
of genomic RNA, enzyme
reverse transcriptase and
protein P-15 associated with
genomic RNA. Genomic RNA is
surrounded by two coverings:
1. Inner covering is cone shaped consisting of P-24, and
2. Outer covering of P-17

Genome has two types of genes—overlapping and split genes

(8 in HIV-1 and 9 in HIV-II). Virus is surrounded by host-derived
envelop with spikes containing protein components
complementary to CD4 or T4 receptors present on the surface
of helper T cells, monocytes, macrophage and some other
nerve cells.
 VIRUS MULTIPLICATION

When virus comes in contact with the cells having receptors of T4

antigen(helper T cells, monocytes, macrophages and some nerve cells),
it sticks to the receptor site and then passes into the cell. Then free
genomic RNA synthesizes a copy DNA with help of enzyme reverse
transcriptase and biochemicals of the host.
The copy DNA forms complement strand and the duplex attaches to
the host DNA in the form of provirus. Provirus may multiply with
hostcell and ultimately forms genomic RNA and messenger RNA.
The messenger RNA synthesizes viral proteins. Then genomic RNA and
viral proteins are packed to form virions and these bud off from the
host cell, get covered by an envelope and attack a new host cell.

The infected host cell ultimately gets killed leading to reduction in

number of cells belonging to the immune system.
 INCUBATION PERIOD

Varies from 2 to 10 years (commonly 27–28 months). The first 2–6 months
are called window period because in this period tests are negative.
Then onwards HIV positivity is indicated by:
Presence of P24,
Antiviral antibodies and
Reduction in number of T cells.
 SIGNS AND SYMPTOMS

Signs and symptoms are mostly of opportunistic infections due to

decreased immunity. They include:
Repeated episodes of diarrhoea,
Unexplained weight loss,
Prolonged cough, night sweating, continuous fever for more than 1
month,
Tuberculosis, candidiasis of mouth and oesophagus, and
Ulcers, Kaposi sarcoma (cancer of skin and lymph nodes).
 HIV TEST

Laboratory tests employed for diagnosis of HIV infection may be

classified into three groups:
A) Screening tests are used to screen antibodies against HIV. The most
commonly used test is ELISA (enzyme-linked immune sorbent assay).
B)Supplement tests. These tests also detect antibodies against HIV and
are recommended for validation of positive tests on screening. The
commonly employed test is western blot assay.
C)Confirmatory tests. These tests confirm HIV infection in an individual
who is seropositive.
 PREVENTION

Preventive measures against HIV infection include:

Education. National AIDS Control Organization (NACO) has been

setup under the Ministry of Health and Family Welfare. Awareness is
being imparted through all means of publicity and by NGOs
inschools, colleges, factories, farms, etc
 GRAFT REJECTION
Graft rejection occurs when the immune system identifies a transplanted
organ or tissue (the graft) as foreign and mounts an immune response
against it. Here's a brief overview of the immune physiology involved:

innate immunity
1. Recognition: The innate immune system recognizes the graft as foreign
through pattern recognition receptors (PRRs) that bind to pathogen-
associated molecular patterns (PAMPs) or damage-associated molecular
patterns (DAMPs).
2. Activation: This recognition activates immune cells, such as dendritic
cells, macrophages, and natural killer cells, which produce pro-
inflammatory cytokines and chemokines.

Acquired Immunity
1. T-cell activation: T-cells (CD4+ and CD8+) are activated by antigen-
presenting cells (APCs), such as dendritic cells, which present graft
antigens to T-cells.
2. T-cell proliferation: Activated T-cells proliferate and differentiate into
effector cells, such as cytotoxic T-cells and helper T-cells.
3. Antibody production: B-cells are activated to produce antibodies
against graft antigens.
 EFFECTOR MECHANISMS

1.Cell-mediated immunity: Cytotoxic T-cells and natural killer cells

directly kill graft cells.

2.Antibody-mediated immunity: Antibodies bind to graft cells, marking

them for destruction by complement or immune cells.
 TYPES OF GRAFT REJECTION

1. Hyperacute rejection: Immediate rejection due to pre-existing

antibodies.
2. Acute rejection: Rejection that occurs within days to months after
transplantation.
3. Chronic rejection: Gradual rejection that occurs over months to
years.
 PREVENTION AND TREATMENT

1. Immunosuppressive therapy: Medications that suppress the immune

system, such as calcineurin inhibitors, corticosteroids, and
monoclonal antibodies.
2. HLA matching: Matching the graft to the recipient's human
leukocyte antigen (HLA) type to reduce the risk of rejection.