Immunology: Immunology By: Bitew T. 1

Immunology
Immunology by: Bitew T. 1

Outline
Basic concepts related with immunology
Types of immunity
Types of hypersensitive reactions

Concepts related with immunity
Immunity: The body’s specific protective response to a

foreign agent or organism; resistance to disease, specifically
infectious diseases
Immune system: is a highly organized system made up of
biological structures and process which are able to detect and
destroy pathogens to protect human beings from diseases.
 Immune response: The coordinated response of the
components of the immune system to a foreign agent or
organism
 Immuno-regulation: Complex system of checks and
balances that regulates or controls immune responses
 Complement: series of enzymatic proteins in the serum
that, when activated, destroy bacteria and other cells
 Opsonization: The coating of antigen–antibody
molecules with a sticky substance to facilitate
phagocytosis

Cytokines: generic term for non antibody soluble
proteins that interact with specific cellular
receptors which involved in :-
regulation of the growth and activation of immune cells
intercellular mediators of normal and pathologic

inflammatory and immune responses.
Chemokine's—soluble molecules that direct and

determine directional movement of leukocytes.
Antigen: Substance that induces the
production of antibodies
 Foreign or self-molecules that are recognized
by immune systems resulting in immune cell
triggering, T cell activation, and/or B cell
antibody production

 Antibody :- Protein substance developed by the body in
response to a specific antigen also called immunoglobulin

 It consist of two subunits, each containing light and
heavy peptide chain held together by a chemical link
composed of disulfide bonds.
 Each subunit has one portion that serves as binding site
for a specific antigen and another portion that allows the
antibody molecule to take part in the complement system.

HC = heavy chain
LC = light chain.
Antigen–antibody binding

The body can produce five different types of
immunoglobulins (Ig).
Each of the five types, or classes, is
identified by a specific letter of the alphabet,
IgA, IgD, IgE, IgG, and IgM.

Major Characteristics of Immunoglobulins

Types of Immunity

1. Natural (innate) immune
Are nonspecific and present at birth
 Provides a broad spectrum of defense against
and resistance to infection

It is considered the first line of host defense
following antigen exposure, because it protects
the host without “remembering” prior contact
with an infectious agent
It include NK cell lymphocytes, DCs,
monocytes/macrophages, neutrophils, basophils,
eosinophil, tissue mast cells, and epithelial cells

2. Acquired Immunity
 Specific immunity develops after birth.
 Usually develops as a result of prior exposure to an

antigen through immunization (vaccination) or by
contracting a disease
 Weeks or months after exposure to the disease or vaccine,
the body produces an immune response that is sufficient
to defend against the disease on re-exposure.
 Relies on the recognition of specific foreign antigens.
Defense mechanism
When the body is invaded or attacked by micro
organisms, it has three means of defense:
 The phagocytic immune response
 The humoral or antibody immune response
The cellular immune response

i. The phagocytic immune response:
Phagocytic cells: cells that engulf, ingest, and

destroy foreign antigen
 Primarily involves the granulocytes &
macrophages, which have the ability to ingest
foreign particles & destroy the invading agent
(phagocytosis)

ii. The humoral immune response
It is also called the antibody response.
Begins with the B lymphocytes, which can
transform themselves into plasma cells that
manufacture antibodies.
 These antibodies are highly specific proteins that are
transported in the bloodstream and attempt to disable
invaders.
iii. Cellular immune response
Involves the T lymphocytes, which can turn into

special cytotoxic (or killer) T cells that can attack
the pathogens
Cellular reactions are initiated, with or without
the assistance of macrophages, by the binding of
an antigen to an antigen receptor located on the
surface of a T cell.
Lymphocytes
Present in lymphoid organs and in blood
T-lymphocytes (grow up in thymus –at neck
vertebra)
B-lymphocytes (grow up in bone marrow)
Each one has receptors for a specific antigen

Recognize millions of different antigens!

T lymphocytes (T Cells)
 Move from the bone marrow to the thymus, where they
mature into several kinds of cells with different
functions
 Thymus-derived lymphocytes that mediate adaptive
cellular immune responses
 Important for producing cellular immune response

Types of T lymphocytes (T cells )
i. Effector T cells,
ii. Suppressor T cells, &
iii. Memory T cells.
The two major categories of effector T cells are

o Helper T cells & Cytotoxic T cells participate in the
destruction of foreign organisms.

Helper T cells are activated on recognition of
antigens & stimulate rest immune system.
When activated, helper T cells secrete cytokines,
which attract & activate B cells, cytotoxic T cells,
NK cells, macrophages, & other cells of immune
system.

 Cytotoxic T cells (killer T cells) attack the antigen
directly by altering the cell membrane & causing cell
lysis (disintegration) & by releasing cytolytic enzymes
and cytokines.
 Destroys tumor cells and cells infected with
intracellular pathogens

Suppressor T cells have the ability to decrease B-cell
production, thereby keeping the immune response at a
level that is compatible with health & life
E.g. Sufficient to fight infection adequately without
attacking the body’s healthy tissues.
Memory cells are responsible for recognizing antigens
from previous exposure & mounting an immune
response

Natural killer (NK) cells are a class of
lymphocytes that recognize infected & stressed cells
 Respond by killing these cells and by secreting
macrophage-activating cytokine that kill target cells
expressing few or no human leukocyte antigen (HLA)
class I molecules, such as malignantly transformed cells
and virally infected cells.

B lymphocytes
 Live in blood, bone marrow, lymphoid tissues
 Basic function: make antibodies (immuno globulins)

 B-cell receptor complex
Recognizes antigens
Binds antigen
Sends signals to T cells

Hypersensitivity reactions

 Hypersensitivity:- is a reflection of excessive or aberrant
immune response to any type of stimulus.
 It is over reactivation of immune response against
foreign antigens or fails to maintain self-tolerance, and
this results in tissue damage.
 Usually does not occur with the first exposure
 Rather, the reaction follows a re-exposure after
sensitization, or buildup of antibodies, in a predisposed
person.
Hypersensitivity reaction classified into four types
 Type I: IgE-Mediated
 Type II: Cytotoxic Reactions
 Type III: Immune-Complex Reactions
 Type IV: Delayed Hypersensitivity Reactions

1.Type I Hypersensitivity
 The most severe hypersensitivity reaction
 It is an immediate reaction beginning within minutes of
exposure to an antigen
IgE-Mediated
 It is characterized by edema, vasodilation, increased
capillary permeability, smooth muscle contraction, and
eosinophilia.

 On the first exposure to the allergen, IgE antibodies are produced
and bind to mast cells and basophils.
 On any subsequent exposures, the allergen links with the IgE
bound to mast cells or basophils and triggers degranulation of
the cells and the release of chemical mediators from the
granules.
 The mediators that are released attack target organs
 Primary chemical mediators are responsible for the symptoms of

type I hypersensitivity because of their effects on the skin, lungs,
and gastrointestinal tract.
If chemical mediators continue to be released, a
delayed reaction may occur and may last for up to
24 hours.
It include both local and systemic anaphylaxis.
local reactions are characterized by rashes
Systemic reactions may involve laryngeal stridor,
hypotension, bronchial spasm;.

Examples :extrinsic asthma, allergic rhinitis,
systemic anaphylaxis, reactions to insect stings.
,people sensitized to penicillin or latex.

2. Type II Hypersensitivity
Occurs when the system mistakenly identifies a

normal constituent of the body as foreign.
For example, in myasthenia gravis, the body
mistakenly generates antibodies against normal
nerve ending receptors
In Good pasture syndrome, it generates antibodies
against lung and renal tissue, producing lung
damage and renal failure.
 Involving the direct binding of IgG or IgM antibodies
to an antigen on the cell surface.
 Antigen-antibody complexes activate the complement

system, which mediates the reaction, lead to eventual
cell and tissue damage
 Cellular tissue is destroyed in one of two ways: (1)

activation of the complement cascade resulting in
cytolysis or (2) enhanced phagocytosis.
 Target cells frequently destroyed in type II reactions are
erythrocytes, platelets, and leukocytes.
 Example ABO incompatibility transfusion reaction, Rh

incompatibility transfusion reaction, hemolytic anemia,
Good pasture syndrome and myasthenia gravis

3. Immune Complex (Type III) Hypersensitivity
 Involves immune complexes that are formed when

antigens bind to antibodies.
 Marked by acute inflammation resulting from formation
and deposition of immune Complexes (antigen-antibody
complexes) combine with immunoglobulins of the IgG
and IgM classes
 As a result, there is an increase in vascular permeability
and tissue injury.
 The complexes are cleared from the circulation by
phagocytic action.
 If these type III complexes are deposited in tissues or
vascular endothelium, cause injury due to increased
amount of circulating complexes and the presence of
vasoactive amines.

The joints and kidneys are particularly susceptible to
injury
Common sites for deposit are the kidneys, skin, joints,
blood vessels, and lungs.
Example: systemic lupus erythematous, nephritis, and
rheumatoid arthritis.
Some signs and symptoms include urticaria, joint pain,
fever, rash, and adenopathy (swollen glands).
4. Delayed-Type (Type IV) Hypersensitivity
 Also known as cellular hypersensitivity (cell-mediated

immune response),
 Occurs 24 to 72 hours after exposure to an allergen.
 It is mediated by sensitized T cells and macrophages
rather than antibodies.
 Involves activity by lymphokines, macrophages, and
lysozymes.
 Erythema and itching are Common
Sensitized T lymphocytes attack antigens or
release cytokines.
Some of these cytokines attract macrophages into

the area.
The macrophages and enzymes released by them

are responsible for most of the tissue destruction.

 Symptoms include itching, erythema, and raised
lesions.
 Examples: Contact dermatitis

Management of patients with HIV /AIDS

Outlines
Definitions
 Epidemiology
Pathogenesis
 MOT
Clinical stages
Management of HIV/AIDS

The human immunodeficiency virus (HIV) is a virus
that infects humans & weakens the immune system
HIV infection targets the immune system and
weakens a person’s defense systems against
infections
The collection of diseases that results from HIV
infection is called Acquired Immunodeficiency
Syndrome (AIDS).
AIDS: is defined by the development of certain
infections, or other severe clinical manifestations.
Most advanced stage of HIV infection

Historical background of HIV/AIDs
AIDS was first recognized in the United States in

the summer of 1981
The first evidence of HIV epidemic in Ethiopia was
detected in 1984, and AIDS cases1986.

Historical…
 Since then, AIDS has claimed the lives of
millions & has left behind hundreds of thousands
orphans
 Free Anti Retroviral (ARV) drugs was launched
in January 2005 & public hospitals started
providing free ARTs in March 2005.

Etiologic Agent
Human Immunodeficiency virus (HIV) is the

etiologic agent of AIDS
HIV belongs to a group of viruses known as

retroviruses, which carry their genetic material
in the form of ribonucleic acid (RNA) rather than
deoxyribonucleic acid (DNA).
Types of HIV
HIV-1:- is the virus responsible for the majority
of HIV infections in most countries, including
Ethiopia.
HIV-1 is more infectious & has a much greater
ability to be transmitted between people than
HIV-2.

 HIV-2:- infection is mainly prevalent in West
African countries
 It’s thought to induce progression to HIV-
associated diseases and AIDS more slowly than
HIV-1.

Morphology of the Virus

Modes of transmission of HIV
 HIV is transmitted in body fluids that contain free virions and
infected CD4-T cells.
 These fluids include blood, seminal fluid, vaginal secretions,

amniotic fluid, & breast milk.
1.Sexual intercourse
 Unsafe sex (sexual intercourse without a condom) is responsible

for the majority of HIV infections worldwide.
 HIV is primarily considered as a sexually transmitted infection

(STI).
 Is the major mode of transmission worldwide 90
%
 STIs increase risk of HIV transmission due to the
presence of lesions in the genital mucosa.

2. Blood & blood products
Transfusion of an infected blood or blood products
Sharing contaminated needles & syringes to inject
illegal drugs
Accidental puncturing of the skin by contaminated
instruments during healthcare

3. Mother to child transmission - Infected mother
to her child through the placenta during pregnancy
(in utero), or delivery(more often) , through breast
feeding
i. Pregnancy:-10 % before the 3rd Trimester
ii. Labor and Delivery:- 70 % late pregnancy and

during labor
iii. Breast Feeding :- 10-15 %

Pathophysiology (Replication Cycle of HIV)
 All viruses target specific cells.
 HIV targets cells with CD4 receptors, which are expressed on

the surface of T lymphocytes, monocytes, dendritic cells,
and brain microglia.
 Mature T cells are composed of two major subpopulations
that are defined by cell surface receptors of CD4 or CD8.

 Approximately 2/3 of peripheral blood T cells are CD4+, and
approximately 1/3 is CD8+.
 During acute/recent infection, most varieties of HIV-1 use
the chemokine receptor CCR5 (R5 virus) for entry to T cells
in addition to the CD4 receptor

 The glycoproteins of HIV (GP120 and GP41) must
attach to both the CD4 and the CCR5 binding sites
in order to bind to the CD4 cell membrane, which
results in fusion of HIV with the T cell.

 Once HIV has attached to the host cell, the virus
can replicate.
 The HIV life cycle is complex and consists of the
following steps

07/16/2022 Immunology by Bitew T.
1. Attachment
 The GP120 & GP41 of HIV bind with the host’s
uninfected CD4+ receptor & chemokine coreceptors,
usually CCR5, which results in fusion of HIV with the
CD4+ T cell membrane.

2. Uncoating:- the contents of HIV’s viral core (two single
strands of viral RNA and three viral enzymes: reverse
transcriptase, integrase, and protease) are emptied into
the CD4+ T cell.
3. DNA synthesis:- HIV changes its genetic material from
RNA to DNA through action of reverse transcriptase,
resulting in double-stranded DNA that carries
instruction for viral replication.

4. Integration
 New viral DNA enters the nucleus of the CD4+ T cell &
through action of integrase is blended with the DNA of
the CD4+ T cell, resulting in permanent, lifelong
infection.
 Prior to this step, the uninfected person has been only
exposed to, not infected with, HIV.
 With this step, HIV infection is permanent.

5. Transcription:- then the CD4+ T cell is activated, the
double-stranded DNA forms single-stranded
messenger RNA (mRNA), which builds new viruses.
6. Translation: the mRNA creates chains of new

proteins & enzymes (polyproteins) that contain the
components needed in the construction of new
viruses.

7. Cleavage: the HIV enzyme protease cuts the
polyprotein chain into the individual proteins that
make up the new virus.
8. Budding: New proteins and viral RNA migrate to
the membrane of the infected CD4+ T cell, exit
from the cell, and start the process all over.

HIV TEST(Investigations )
 Demonstration of antibodies to HIV by Rapid test using
the National HIV test algorism.
ELISA (Enzyme-linked Immunosorbent Assay)
Western blot: also detects antibodies to HIV; used to

confirm EIA

Three HIV rapid tests
i. Algorism 1 (A1) :- STAT PACK- 5 microliter of
whole blood with 3 drop of running buffer /15-20’/
ii. Algorism 2 (A2) :- ABON-10 microliter of blood
/2drop/ with 2 drops of running buffer/10-20’/
iii. Algorism 3 (A3) :- SD-BIOLINE-20 microliter of
blood with 4 drops of running buffer /10-20’/

First Response HIV 1 and 2

DNA – PCR : Viral replication(load)
 Detection of the viral antigens using PCR- Viral load;
Measures HIV RNA in the plasma; CD4/CD8 count.
 Is an extremely sensitive test -can detect 1-10 copies of
HIV proviral DNA per ml of blood
 It uses PCR technology to amplify proviral DNA
 It is highly sensitive and the chance of false positivity is
high.
CD4 T cell count
 CD4 cells play a crucial role in the body defense mechanism
 Measuring the amount of CD4 cells is an important indicator
of the level of immune suppression that a patient infected
with HIV
 Normally CD4 count of a normal person is in the range of500
to 1500 cells/mm3
 In patients with HIV CD4 count drops by an average of 50 -
100 cells per year
 Tells you the level of immune damage inflicted by HIV
WHO HIV clinical stages in adults & adolescents
 The WHO HIV clinical staging system is a staging
system developed for PLHIV to help healthcare providers
to estimate the degree of immune deficiency that an
HIV patient presents.

Clinical Stage 1
 Asymptomatic infection
 Persistent generalized lymphadenopathy
 Acute retroviral (HIV) Syndrome
 Performance status 1: asymptomatic, normal activity
Clinical Stage 2
 Unintentional weight loss < 10% body weight
 Skin manifestation (e.g., Pruritic Papular Eruptions (PPE), seborrhic
dermatitis,
 fungal nail infections,
 Herpes zoster within previous 5 years

Mouth/throat problems- angular cheilitis, recurrent
mouth ulcers
Recurrent upper respiratory tract infections- (repeated
throat infections, sinusitis, or ear infections)
Performance Status 2: symptoms, but nearly fully
ambulatory

Figure: Scaly skin rash on the face, mainly
around the nose, caused by seborrhoea.
Figure:- Small sores and cracks, at the corners of the
mouth caused by angular chelitis.
Herpes zoster
HZ scar(left)

Clinical Stage 3
 Unintentional weight loss > 10% body weight
 Chronic diarrhoea > 1 month
 Prolonged fever > 1 month (constant or intermittent)
 Mouth/throat problems:- oral thrush, oral hairy

leukoplakia, acute necrotising ulcerative
gingivitis/periodontitis (severe gum disease accompanied
by ulcers)
 Pulmonary tuberculosis within the previous 2 years
 Severe bacterial infections (e.g. pneumonia, pulmonary
TB.
 vaginal candidiasis
 Unexplained anemia, Neutropenia or chronic
thrombocytopenia
 Performance Status 3: in bed more than normal but < 50%
of normal daytime during the previous month.

Figure(left): Recurrent aphtous ulcers on the upper part of
the mouth.
Figure (right): White patches in the mouth cause oral
thrush.
figure Oral Candidiasis

Clinical Stage 4
o HIV wasting syndrome
o Pneumocystis jiroveci pneumonia

o Non typhoid salmonella septicemia
o Oesophageal thrush/ candiasis of the esophagus, throat,

bronchi, trachea/lung
o Herpes simplex ulcerations (large and chronic painful
wounds on the genitals and/or anus for more than 1 month)

Lymphoma (cancer of the immune system)
Kaposi’s sarcoma (dark lesions on the skin and/or
mouth, eye, lungs, intestines)
Extra pulmonary TB
Cryptococcal meningitis (meningitis caused by a
fungus)
Toxoplasma brain abscess (infection of the brain by a
parasite)

Visceral leishmaniasis
HIV encephalopathy (neurological impairment).
Performance Status 4: in bed >50% of normal
daytime during the previous month

Figure Wasting syndrome
 Note that if the patient has clinical conditions that fall into
more than one WHO clinical stage, the patient will be placed
in the highest WHO clinical stage that fits the symptoms.
 However, staging of a person living with HIV is not a
permanent fixture.
 For example, a PLHIV who has been successfully treated
for, and recovered from, Pneumocystis pneumonia may be
downgraded from stage 4 to stage 3 if no other severe
conditions are present.

Treatment
 The treatment used for HIV-positive people is called
antiretroviral therapy (ART)
Objective of ART
 To reduce viral replication to undetectable level- HIV RNA
<50copies/ml or “undetectable” within 4-6 months of ART
initiation.
To prevent Opportunistic infections(OIs)
To rehabilitate the patient & allow full function

Reduce HIV transmission
Prolongs life & improves Immunology
qualityby:of life.
Bitew T. 103
Non pharmacological treatment
 Psychological support
 Nutritional support
 Socioeconomic support

Pharmacological treatment
 Management of HIV disease includes prevention and
treatment of OIS & controlling viral replication with Highly
Active Antiretroviral Therapy (HAART).

When to start treatment ART?
According to national (Ethiopia) guidelines for

comprehensive HIV prevention, care and treatment
2018
 It is critical for people living with HIV to initiate
ART as early as possible
 All HIV positives are eligible for ART irrespective
of their WHO clinical staging and/or CD4 count
When to start treatment …….
 Rapid ART initiation should be offered to all people

living with HIV following a confirmed HIV diagnosis
 ART initiation should be offered on the same day to
people who are ready to start
 For women identified at labor and delivery, provide ART
with in the same hour of HIV diagnosis with brief
counseling and provide detailed counseling on ARV and
adherence after delivery

Treatment regimens
Classes of Antiretroviral Drugs
1.Nucleoside reverse transcriptase inhibitors
Zidovudine (ZDV, AZT) Lamivudine (3TC)
Stavudine (D4T) Didanosine (DDI)
Abacavir (ABC) Emtricitabine (FTC)
Tenofovir disoproxil fumarate (TDF)
Mechanism of Action: Structurally these drugs resemble
naturally occurring nucleosides and break the formation of
viral DNA by breaking the chain ( chain breakers )
2.Non Nucleoside reverse transcriptase inhibitors(NNRTI)
Neverapine (NVP)
Efavirenz (EFV)
Delavirdine*
Etravirine*
Mechanism of Action: inhibit the active site of
Reverse transcriptase enzyme

3.Protease Inhibitors
 Lopinavir
 Nelfinavir
 Saquinavir-
 Indinavir
 Atazanavir
 Ritonavir
Mechanism of Action: Inhibit viral assembly

Treatment regimens
First-line regimens
Is a combination of drugs that will be given to HIV
positive patient who has never taken any ARV
drugs before.
Commonly consist two NRTIs and one NNRTI.
A therapy with only one or two agents allows HIV

to overcome therapy through resistance mutation.
Recommended first line antiretroviral regimens in adults and adolescents

Note that:
3TC is included in all of the first-line regimens
According to the current Ethiopian ART guidelines,

new adult and adolescent patients started on a AZT or
TDF-containing regimens.
First-line drug regimens commonly include ARVs in
fixed dose combinations, meaning combinations of
three ARV drugs in fixed doses in the same tablet

Second-line ARV combination regimens for adults
and adolescents
Second line regimen is the combination of ARVs given
for a patient who has been taking ART and developed
treatment failure, or severe side effects.
Usually, the second-line regimen will consist of two
NRTIs and one PI drug in combination.
Even a second-line regimen can fail, if not taken
consistently and correctly.
Second-line ARV…
 2H=TDF-3TC-ATV/r
 2F=AZT-3TC-ATV/r
 2G=TDF-3TC-LPV/r
 2E=AZT-3TC-LPV/r
 2I=AZT-3TC-LPV/r

Monitoring ARV Treatment
1.Treatment Adherence
 Patient and attendant or family education
and counseling before initiation of therapy is
mandatory to maximize future adherence.
 Ongoing attention and counseling is crucial
to enforce adherence throughout the entire
course of treatment
2.Clinical monitoring for toxicity of ART
 All patients require clinical evaluation every month in
the first 6 months for ARV related toxicity.
 Subsequent follow-up can be done every 3months.
Laboratory monitoring for toxicity of ART:
 Baseline: Hemoglobin/hematocrit, white blood cell
count and differential, organ function test , serum
creatinine and/or blood urea nitrogen.

3.Monitoring Effectiveness of ART
Response to ART is monitored using both clinical
and laboratory parameters.
The concentration of HIV - RNA in plasma (the
"viral load")
The desirable "virologic" endpoint is a plasma
viral load that is: "below the limits of detection",
within 3 to 4 months of starting treatment.
Table: Definitions of treatment failure in adults and adolescents
Clinical Adults and adolescents

Failure  New or recurrent clinical event indicating
severe immunodeficiency
 (WHO clinical stage 4 condition and
 certain WHO clinical stage 3 conditions
after 6 months of effective treatment

Immunologic Adults and adolescents

Failure  Fall of CD4 count to pre-therapy baseline
 (or below); 50% fall from the on-treatment peak value
 CD4 count at or below 250 cells/mm3
 following clinical failure Or Persistent CD4 levels
below 100 cells/mm3
Children
 Younger than 5 years Persistent CD4 levels
 below 200 cells/mm3 or <10%
 Older than 5 years Persistent CD4 levels below 100
cells/mm3

Virological Failure  Viral load above 1000 copies/mL

based on two consecutive viral load
measurements in 3 months, with
adherence support following the first
viral load test

Post exposure Prophylaxis for Health Care Providers
Low risk exposure
 Exposure to a small volume of blood or blood

contaminated with fluids from asymptomatic HIV positive
patients or the patient is not in an advanced stage of HIV
disease.
 Following an injury with a solid needle.
 Any superficial injury or muco-cutaneous exposure.

If the exposure is onto mucus membranes, not
deeply penetrating or involves body fluids other
than blood; and also if the device is dry
 The amount of blood transferred is very small
 Gloves are worn

High risk exposure
 Exposure to a large volume of blood or other potentially
infectious fluid
 Exposure to a large volume of blood or blood
contaminated with fluids from a patient with clinical
AIDS or early sero-conversion phase of HIV.
 Injury with a hollow needle.
 Deep and extensive injuries

Timing of initiation of treatment
 Should be given in the shortest time possible (within
the first 1-2 hours of exposure)
 Do not consider PEP beyond 72 hours
 The recommends regimen for PEP is AZT Or TDF +
3TC + EFV for 28 days..

Prevention of opportunistic infections
 Isoniazid is a chemoprophylaxis drug used to
prevent TB infection in children and PLHIV.
 The most commonly used prophylactic drug for
HIV/AIDS is cotrimoxazole, a wide-spectrum
antibiotic that targets the pathogens causing the
most common opportunistic infections.

Criteria for starting cotrimoxazole prophylaxis by
adult PLHIV
 All HIV-positive people at WHO clinical stages 2, 3, 4,
or with a CD4 count less than 350 cells/mm³, should
start cotrimoxazole prophylaxis.
 The drug regimen for cotrimoxazole prophylaxis is two
480 mg tablets, or one 960 mg tablet daily.

Duration of cotrimoxazole prophylaxis for adult PLHIV
 If a person living with HIV has no access to HIV

treatment, cotrimoxazole prophylaxis should be taken
for the rest of the patient’s life.
 If the patient has access to antiretroviral therapy (ART)

for HIV, cotrimoxazole prophylaxis should be stopped
when the CD4 count has increased to 350 cells/mm³
and remains above that level for at least 6 months.
THANK YOU!!!

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Immunology by: Bitew T. 1

Types of hypersensitive reactions

Immunology by: Bitew T. 2

Immunity: The body’s specific protective response to a

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intercellular mediators of normal and pathologic

Chemokine's—soluble molecules that direct and

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response to a specific antigen also called immunoglobulin

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 Provides a broad spectrum of defense against

and resistance to infection

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 Usually develops as a result of prior exposure to an

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Phagocytic cells: cells that engulf, ingest, and

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Involves the T lymphocytes, which can turn into

Each one has receptors for a specific antigen

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The two major categories of effector T cells are

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 Live in blood, bone marrow, lymphoid tissues

 Basic function: make antibodies (immuno globulins)

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 Type II: Cytotoxic Reactions

 Type III: Immune-Complex Reactions

 Type IV: Delayed Hypersensitivity Reactions

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 Primary chemical mediators are responsible for the symptoms of

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Occurs when the system mistakenly identifies a

 Antigen-antibody complexes activate the complement

 Cellular tissue is destroyed in one of two ways: (1)

 Example ABO incompatibility transfusion reaction, Rh

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 Involves immune complexes that are formed when

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 Also known as cellular hypersensitivity (cell-mediated

Some of these cytokines attract macrophages into

The macrophages and enzymes released by them

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AIDS was first recognized in the United States in

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