IMMUNODEFICIENCY

10703038 10704025 10705001 10705002 10705122 10705057 10705019 16207715 10705008 10705046 10705013 10705113 10705049

10705004 10705072 10705045 10704062

10705028 10705100 10705104 10705120 10705026 10705064 10705071 10705041 10705007 10705053 10705068 10705069 10704109

IMMUNODEFICIENCY

Immune disorder Immune system fails to develop normally or the immune response is blocked in some way.

Results from:
- embryological developments problem/ lymphoid organs and tissues - infection with virus depress immune function - treatment/exposure to immunosuppressive agents

IMMUNODEFICIENCY

Deficiency of innate immune mechanism

Complement system deficiencies

Primary immunodeficiency
B-cell deficiency T-cell deficiency Combined immunodeficiency

Secondary immunodeficiency Acquired immunodeficiency syndrome (AIDS)

IMMUNODEFICIENCY

Primary immunodeficiency
These occur in the human, although somewhat rarely, as a result of a defect in almost any stage of differentiation in the whole immune system.

Secondary immunodeficiency
Immunodeficiency may arise as a secondary consequence of malnutrition, lymphoproliferative disorders, agents such as X-rays and cytotoxic drugs, and viral infections.

PRIMARY IMMUNODEFICIENCY
B-cell deficiency

IgA deficiency & Common Variable Immunodeficiency (CVID) Most common primary immunodeficiencies, represent the extreme ends of a spectrum of immunoglobulin deficiencies. Transient hypo--globulinemia Immunoglobulin deficiency occurs naturally in human infants maternal IgG level . serious problem in very premature babies recurrent respiratory infections, is associated with low IgG levels which often return somewhat abruptly to normal by 4 years of age.

PRIMARY IMMUNODEFICIENCY
T-cell deficiency
No T-cells or poor T-cell function: - vulnerable to opportunistic infections - impacts negatively on humoral immunity - dysfunctional T-cells permit the emergence of allergies, lymphoid malignancies & autoimmune syndromes.

Due to: inefficient negative selection in the thymus or the failure to generate appropriate regulatory cells.

PRIMARY IMMUNODEFICIENCY
Combined Immunodeficiency

Severe combined immunodeficiency disease (SCID) involving B-, T- and NK cells. represents the most severe form of primary immunodeficiency defects in cellular and humoral immunity. + severe and recurrent opportunistic infections death.

SECONDARY IMMUNODEFICIENCY

Immune responsiveness can be depressed nonspecifically by many factors. CMI in particular may be impaired in a state of malnutrition. Iron deficiency is particularly important in this respect, as are zinc and selenium deficiencies.

Case In lepromatous leprosy and malarial infection, constraint on immune responsiveness imposed by distortion of the normal lymphoid traffic pathways dysfunction of macrophage Imbalance between Thl and Th2 cells: result of infection depress the subset most appropriate for immune protection.

RECOGNITION OF IMMUNODEFICIENCY
o

Defects in immunoglobulins
quantitative. 2g/L lower limit of normal.

The humoral immune response

screening the serum for natural antibodies (A and B isohemagglutinins, bactericidins against E. coli) attempting to induce active immunization with diphtheria, tetanus, pertussis and killed poliomyelitis-but no live vaccines. CD19, 20 and 22 markers enumerate B-cells by immunofluorescence.

RECOGNITION OF IMMUNODEFICIENCY
o

Patients with T-cell deficiency

hypo- or unreactive in skin tests to such antigens Active skin sensitization with dinitrochlorobenzene.

Complement, bactericidal and other functions of polymorphs

In vitro tests. Reduction of nitroblue tetrazolium (NBT) / stimulation of superoxide production measure of the oxidative enzymes associated with active phagocytosis.

ACQUIRED IMMUNODEFICIENCY SYNDROME

AIDS

results from infection by the RNA retroviruses HN-1 and HN-2. HIV infects T-helper cells through binding of its envelope gp120 to CD4 and either CCR5 or CXCR4 chemokine receptor cofactors. It also infects macrophages, microglia, T-cell-stimulating dendritic cells.

chemokines: A family of structurally-related cytokines which selectively induce chemotaxis and activation of leukocytes. They also play important roles in lymphoid organ development, cell compartmentalization within lymphoid tissues, Th1 /Th2. development, angiogenesis and wound healing.

Target

Gp120

HIV
Envelop Inti

HIVs Structure
Envelop nucleus

gp120 gp41

p17 p24 p7/p9

RNA HIV
Diploid single strand

Enzymes

RT Integrase Protease

Siklus Hidup HIV dalam Limfosit-T (CD4)

Virion Matang

ds DNA

Integrase
HIV DNA

Genomic RNA

3 RNA 2

4
Transkripsi 5

Proviral DNA

Protease

RT
mRNA Spliced mRNA Polyprotein Protein

AIDS

The RNA is converted by the reverse transcriptase to DNA incorporated into the host's genome dormant until the cell is activated by stimulators such as TNF.

There is usually a long asymptomatic phase after the early acute viral infection has been curtailed by a CD8CTL immune response. Virus to the lymphoid follicles destroys the dendritic cell meshwork.

Long asymptomatic phase

AIDS

CD4 T-helpers, destroys cell mediated defenses life threatening infections through opportunist organisms such as Pneumocystis carinii and cytomegalovirus. Infection suppresor factors released by Ts inhibit an immune response before Th stimulating the formation of Tc/plasma cell in adequate number. Immune system VS virus extremely high rates of viral destruction and CD4 T-cell replacement.

AIDS

CD4 T-cell depletion: as a result of direct pathogenicity, syncytium formation, susceptibility to apoptosis and possibly other mechanisms. AIDS: diagnosed in an individual with opportunistic infections, by low CD4 but normal CD8 T-cells in blood, poor delayedtype skin tests, positive tests for viral antibodies and p24 antigen, lymph node biopsy and isolation of live virus or demonstration of HN genome by the PCR.

AIDS

Highly active antiretroviral drug therapy (HAART), combining inhibitors of reverse transcriptase and protease, can eliminate detectable virus early in disease, although latent virus remains. Vaccines are being targeted to Th1 responses but it is a very difficult virus to control.

HIV/AIDS

Apa itu HIV/AIDS??

Gp120

HIV
H I V : Human : Immunodeficiency : Virus

Envelop

Inti

Struktur HIV
Envelop Inti

gp120 gp41

p17 p24 p7/p9

RNA HIV
Diploid single strand

Enzim-enzim

RT Integrase Protease

Target

AIDS ?

Acquired Immuno Deficiency Syndrom

Didapat
Kekebalan

Penurunan
Kumpulan Gejala

Siklus Hidup HIV

Mekanisme CD4
Mekanisme pembunuhan sel T-CD4+ telah diteliti secara in vitro pada kelompok Lentivirus.
Langsung

(Direct) Tidak Langsung (Indirect) Mekanisme Lain

Replikasi virus HIV

Di bagian tubuh mana HIV berada?

HIV didapatkan di

darah
cairan sperma

cairan vagina
air susu ibu

Bagaimana Cara Penularannya?

Hubungan Seks

Transfusi darah

Hubungan perinatal (ibu ke janin)

Penggunaan jarum suntik yang pernah dipakai orang lain

Goldwater, Network

Holmes

Resiko penularan per paparan

Transfusi Ibu ke anak Seks anal (reseptif) Penasun bersama Tertusuk jarum
(petugas kesehatan)

~80 % 1:4 1:30 -1:125 1:150 1:313 1:700 1:2000 1:1000 -1:3000 <1:4000

Seks vaginal (reseptif) Seks vaginal (insertif) Terpercik ke sel lendir

HIV/AIDS tidak menular melalui

HIV TIDAK MENULAR MELALUI

KONTAK SOSIAL

Ciri-ciri Orang dengan HIV+

PERKEMBANGAN DARI HIV MENJADI AIDS:

Tertular Periode Jendela

HIV +

AIDS

3 - 6 BULAN

3 - 10 TAHUN

1 - 2 TAHUN

Hanya dua cara untuk tahu bila orang itu HIV positif
Orang

itu memberitahukan kepada kita. Melihat tes HIV Jumlah CD4 yang rendah dengan jumlah CD8 sel T yang normal. Ditemukan antibodi viral dan antigen P24.

Statistika tentang AIDS

Penderita HIV-AIDS berdasarkan Golongan Umur Di Kota Bandung Tahun 2007

GOLONGAN UMUR

20 - 29 th 67.06%

30 - 39 th 20.13% 15 - 19 th 4.55% 0 - 14 th 2.27% 50 th 1.01% 40 - 49 th 4.97%

Berdasarkan kelompok usia, maka kalangan remaja antara 20-29 tahun merupakan jumlah terbanyak yaitu 67.06 %

Penderita HIV-AIDS berdasarkan Profesi di Kota Bandung Tahun 2007

PEKERJAAN
TIDAK BEKERJA 16.01% WIRASWASTA 21.99%

SUPIR 0.25%

TIDAK DIKETAHUI 3.71% SWASTA 19.80%

PNS 2.11%

PEKERJA SEX 9.01% BURUH KASAR 0.25% LAIN-LAIN 0.67%

MAHASISWA 20.22%

IRT 5.98%

Penderita HIV-AIDS berdasarkan Faktor resiko di Kota Bandung Tahun 2006

FAKTOR RESIKO

IDU 67.31%

HOMOSEKSUAL 6.32% PERINATAL 2.02% TIDAK DIKETAHUI 1.26% HETEROSEKSUAL 23.08%

Bagaimana Cara Pengobatannya?

Highly Active Antiretroviral Drug Therapy (HAART) menggabungkan inhibitor reverse transkriptase dan protease Dapat mengeliminasi virus pada tahap awal penyakit namun virus laten bertahan

Terima Kasih !