Acquired Immunodeficiency

Syndrome (AIDS)

Faridha S Ilyas

Dermatovenereology Dept
Hasanuddin University /
Dr. Wahidin Sudirohusodo,
General Hospital

1
Copyright © 2005 by Garland Science Publishing
Immune
RETROVIRAL
Tolerance
Respon

DISEASES

SICK
HIV
HEALTH
AIDS
 Topics

Acquired Immunodeficiency Syndrome

• Introduction AIDS
• Pathogenesis AIDS
• Laboratory examination
• Clinical manifestation AIDS
• Treatment of AIDS

2
Introduction

Human
Immunodeficiency
Virus

3
 What is AIDS? (1)

• Acquired (not genetic)

• Immune (host immune system)
• Deficiency (decreased of immune function)
• Syndrome (severe many diseases)
4
 What is AIDS? (2)
Transmission from other
A - Acquired people
Damage host immune system.
Immune system as host
I - Immune protection to maintain the body
against infection

D - Deficiency Decreased host immune

system
AIDS patients suffer many
S - Syndrome opportunistic infection and
other diseases
5
 What is AIDS? (3)
• AIDS: syndrome caused by decreased immune system
that acquired due to HIV infection so people has
susceptible to suffer opportunistic infection and
malignancy.

• Transmission via 3 ways, namely:

(1) From mother to child/ breast feeding
(2) Sexual intercourse (homosexual or heterosexual)
(3) Contact with infected blood/ contaminated needle
Saliva  no evidence ? 6
7
HIV not transmited via
Social contact

8
Virus against immune system

9
HIV infections caused millions of morbidity and
mortality around the world

10
 Cases of HIV in Indonesia
1987-2017

Source : Laporan Sistem Informasi HIV/AIDS (SIHA 2017)

Cases of AIDS in Indonesia
1987-2017

Source : Laporan Sistem Informasi HIV/AIDS (SIHA 2017)

 Cases of HIV Reported
Sulawesi Selatan 1987- 2016

Sumber : Laporan Sistem Informasi HIV/AIDS (SIHA 2017)

 Cases of AIDS Reported
Sulawesi Selatan 1987- 2016

Source : Laporan Sistem Informasi HIV/AIDS (SIHA 2017)

• Manifestation of AIDS raised in 10 years after
infection.

• Patient with immunocompromised CD4 cell

level is low & loss function of CD4 cell 
systemic opportunistic infection.

• > 90% HIV patients suffer opportunistic

infection (bacteria, fungal, virus, parasite).

12
 AIDS Characteristics
• Susceptibility to infection with opportunistic pathogens or by
the occurrence of aggressive form of certain malignancies

• CD4+ T cells ↓

• Spread by contact with body fluid

• Transmission:
– Sexual intercourse
– Contaminated needles/infected blood
– Breast feeding
13
 Topics
Acquired Immunodeficiency Syndrome

• Introduction
• Pathogenesis AIDS
• Clinical manifestation AIDS
• Treatment of AIDS

14
HIV is a retrovirus that infects CD4 T cells, dendritic cells
and macrophages through their chemokine receptors
CCR5 (R5 virus) and CXCR4 (X4 virus)

virus: - blood - vaginal fluid 15

- semen - mother’s milk
HIV Receptor Co-receptor Cell- Requirement
Variants lines of entry

R5 CCR5 CCL3 DC Low level of

CCL4 MØ CD4
CCL5 T cells
R4 CXCR4 CXCL12 T cell High level of
CD4

16
HIV structure

• Envelop
– gp 120
– gp41

• Enzym
– Reverse transcriptase
– Integrase
– Protease

• Nucleus
– P17 (matrix)
– P24 (capsid)
– P7/P9 (nucleocapsid)

17
18
 Immune response to HIV 19

CD4 T cells declines, CD8 T

cells and antibody titer high CD4 low, CD8 low,
antibody low
 Viral Entry
• Mucosal epithelia
– Exposed to foreign antigens
– Provide a milieu of immune system activity in which HIV
replication occurs readily

• 2 types of epithelial cell lining

– Vagina, penis, cervix, anus (stratified squamous epithelium)
• DC with DC-sign – bind viral gp 120  HIV is internalized 
brought to lymph tissue  present it to CD4 T cells
– Rectum, endocervix (single layer of epithelial cells)
• Epithelium express CCR5  translocate R5 variants to
submucosal CD4 T cell and DC

20
21
 Late in infection…
• 50% of cases
• Viral phenotype switches to X4 type
• Usage of CXCR4
• Associate with rapid decline of CD4 count
• Mechanism loss of CD4
– Direct viral killing of infected cells
– ↑ susceptibility to induction of apoptosis in infected cells
– Killing of infected CD4 T cells by CTL

22
 Five phases :

•Binding & entry

•Reverse transcription

•Replication

•Budding

•Maturation
23
Source: thefutureofthings.com/articles.php?itemId=21/60
HIV structure
• Envelop
– gp 120
– gp41
• Enzym
– Reverse transcriptase
– Integrase
– Protease

• Inti
– P17 (matrix)
– P24 (kapsid)
– P7/P9 (nucleocapsid)

24
 The infection of CD4 T cells caused by HIV

CXCR4 or CCR5

25
Tat: transcription regulator
Rev: export transcr from nucleus
Gag: core & matrix
Pol: RT, protease, integrase

26
 Variety of
opportunistic
infections and
cancers can kill
AIDS patients.
27
 Topics
Acquired Immunodeficiency Syndrome

• Introduction
• Pathogenesis AIDS
• Laboratory Examination
• Clinical manifestation of AIDS
• Treatment of AIDS
28
HIV laboratory of antibody
1. Benefit :
- to protect blood supply in blood bank
- to describe big problem/crucial HIV/AIDS in society.
- to know HIV in early stage
2. Test:
- ELISA - screening
- Immunoblot or Western blot
- PCR
3. Interpretation :
if (+): - have antibody for HIV
- infected HIV
- can transmission HIV
confirmation with western blot
if (-): - uninfected HIV
- infected, window period : 0 – 6 month
repeated in 3 - 6 month 29
 Topics
Acquired Immunodeficiency Syndrome

• Introduction
• Pathogenesis AIDS
• Laboratory examination
• Clinical manifestation AIDS
• Treatment of AIDS
30
Infection period HIV

HIV host incubation 5-10 y AIDS

window periode
3-6 month
HIV (-) Step by step
infectious
became severe
Healthy person and cause death

31
Clinical manifestation HIV/AIDS
5 stage of HIV diseases
* Early stage of HIV infection
* Stage without symptom
* Early symptomatic stage
* Advanced symptomatic AIDS stage
* Severe Stage

Early stage of HIV infection

* Suffer complain in many d/w after infected
* Flulike symptom
* Fever
disappear
* Fatigue
* Muscle pain
* cough/sorethroath 32
* Lymphonode enlargement
 Stage without symptom
* No symptom
* Looks normal/healthy
* HIV (+)
* Can occur 5-7 years
* Virus attack immune system

Early symptomatic stage.

* Clinically if occur 2 or more symptom within 3 mo
* Abnormal blood examination
* fever > 38 C, sweating at night (continously)
* Decreased/loss body weight more than 10 %, in 3 mo
* Body weakness that bother daily activity
* Multiple lymphonode enlargement (neck, inguinal, axilla)
* Diarrhea for longtime with unknown cause
* Cough & dyspneu > 1 mo
* Itchy skin, erythematous- blue plaque
* sorethroath
* Bleeding with unknown cause
33
AIDS stage (Advanced symp)
* Immune system damage
* Opportunistic infection
* Tuberculosis
* Candidiasis Death
* Toxoplasmosis
* Pneumocystis
* Sarcoma kaposi
* Limphoma

34
Early stage

Primary Infection
Exantem HIV/ retrovirus

35
Latency stage
(Early symptomatic stage)

Reiter`s syndrome:
Balanitis circinata

Can be fluctuative

36
Late stadium
(Opportunistic Infection)

Oral lesion often raise as initial HIV infection

Sometime forgettable

Oral lesion painless, discrete lesion

Sometimes only one opportunistic symptom of HIV

that has been found
Oral manifestation HIV infection :
1. Fungal infection
2. Bacteria infection
3. Virus infection
4. Malignancy 37
Fungal infection

•Most of fungal infection is candidiasis

•Oral candidiasis in young patient and health
 HIV

Four type oral candidiasis :

1. Pseudomembranous = thrush  most of case in cv. oris
2. Hyperplastic
Similar with pseudomembranous but thigh bind in tissue
3. Erythematous
Erithematous patch lesion in mucosa
In tongue shows atrophy, smooth without texture
4. Angular cheilitis
Show fissura at the angular mouth

38
 pseudomembrane type

Pseudomembrane candidiasis
with geographic border

39
 Hypertropic candidiasis
at hard palate

Hypertrophic type

40
Penicillosis

41
VIRUS INFECTION
HSV Herpes labialis

Immunocompetent HIV patient 42

Genital Herpes

Immunocompetent HIV patient

43
 Herpetic Whitlow
gangrenous

Genital herpes ANAL GH

(HIV patient)
44
Zoster in HIV patient
C
• Zoster dissemination multidermatom
contralateral (C dan L)

multidermatom
contralateral (ulserative chronic)
L
• Recurrent
• Persistency
• ulceration >

In oral  bone necrosis

 tooth exfoliation 45
SARCOMA KAPOSI

46
 LIPOHYPERTROPHY* LIPOATROPHY**

HIV-ASSOCIATED

SYNDROME LIPODYSTROPHY

LIPOHYPERTROPHY* 47
“The Slim
Disease”

“The wasting
syndrome”
48
49
 Topics
Acquired Immunodeficiency Syndrome

• Introduction
• Pathogenesis AIDS
• Laboratory examination
• Clinical manifestation AIDS
• Treatment of AIDS
50
 Treatment purposes
Decreased viral load HIV maximally
Heal immune system
Improvement QoL
Decreased morbidity and mortality

Evaluation:RNA HIV level in plasma decreased

1 log 10 within 8 weeks and undetectable
within 4 - 6 month

51
• ARV treatment criteria not just CD4 level

• ARV not given in suspect patients  wisdom

ways, ability, long time treatment, drugs
resistent, side effect and the appropriate time
to start the therapy.

52
Treatment (A,B,C)

A 1. HIV
2. Opportunistic infection
3. Improving General condition
* IVFD
* Blood Transfusion
* Albumin
* Diet
4. etc 53
Treatment..con’t
•Be healthy
B •Bed rest
•Exercise
•Relaxation, meditation

Psychosocial
C •Prayer
•Job
•Enviromental acceptable

54
When the treatment start?

•Patient with acute HIV syndrome

•Patient with seroconversion in first 6 mo
•AIDS patient
•Patient without symptom:
# CD4 < 350
$ VL > 30,000 copies/mL (bDNA)
> 55,000 copies/mL (RT-PCR)

55
 Treatment Targets

peptide analogs of the carboxy terminal peptide of gp41 (T20)

 decline plasma HIV RNA levels

CXCR4 or CCR5

56
 Treatment Targets
Further cycles of infection Viral reverse
is prevented transcriptase inhibitor

CXCR4 or CCR5
57
Releasing virions Viral protease
are not infectious inhibitor

58
 Virus decay on
drug treatment

• Phase 1. Viral productions declines, virus level in plasma

decrease > 95%
• Phase 2. Activation of resting CD4 T cells and macrophages,
virus level declines to undetected level
• Phase 3. Provirus in memory T cells and other reservoirs
59
 ARV - WHO (2002)

NRTI NNRTI PI
Abacavir (ABC) Efavirenz (EFV Indinavir (DV)
Didanosin (ddi) atau EFZ) Ritonavir (RTV, r)
Lamivudin (3TC) Nevirapine Lopinavir +
Stavudin (d4T) (NVP) ritonavir (LPV/r)
Zidovudin (ZDV Nelfinavir (NFV)
atau AZT) Saquinavir (SQV)

60
Anti Retro Viral

61
ARV in Indonesia (Depkes 2003)

Group A Group B
Hb Normal: Neviral ®
Nevirapine AZT + ddI Duviral ®
(Neviral®) ddI + 3 TC
Nelfinavir d4T + ddI
AZT + 3 TC Low Hb : Neviral ®
Staviral®
(Duviral®) Hiviral ®

62
63
March 2003 September 2003
Before ART After ART

64
SO… WHAT ?
THE PROBLEM

ICE MOUNTAIN PHENOMENOME

• HIGH MOBILE SOCIETY
• CRISIS ECONOMY
• PROSTITUTION
• HIGH RISK GROUP
• KONDOM USE
• METROPOLITAN TREND
• MORAL CRISIS
• STATEMENT NO.. DRUG
• INCREASED IDU How
Much ? 65
How to prevention AIDS ?

ABC + D
A = Avoidance sexual intercourse
B = Both couple faithfull
C = Condom use. Can prevent transmission
HIV/AIDS effectively.
D = Don’t use contaminated needle.
(injection drug use , vitaminE , taTto or
body piercing)

66
THANKYOU FOR YOUR ATTENTION

67