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    IMMUNODEFICIENCY

    10703038 10704025 10705001 10705002 10705004 10705028 10705100 10705104 10705120

    10705122 10705057 10705019 16207715 10705072 10705026 10705064 10705071 1070504110705008 10705046 10705013 10705113 10705045 10705007 10705053 10705068 1070506910705049 10704062 10704109

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    IMMUNODEFICIENCY

    Immune disorder

    Immune system fails to develop normally orthe 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

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    IMMUNODEFICIENCY

    Deficiency ofinnate immune mechanism

    Complement system deficiencies

    Primary immunodeficiencyB-cell deficiency

    T-cell deficiency

    Combined immunodeficiency

    Secondary immunodeficiency

    Acquired immunodeficiency syndrome(AIDS)

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    IMMUNODEFICIENCY

    Primary immunodeficiency

    These occurin 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, lymphoproliferativedisorders, agents such as X-rays and cytotoxicdrugs, and viral infections.

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    PRIMARY IMMUNODEFICIENCYB-cell deficiency

    IgA deficiency & Common VariableImmunodeficiency (CVID)

    Most common primary immunodeficiencies,represent the extreme ends of a spectrum ofimmunoglobulin deficiencies.

    Transient hypo--globulinemia

    Immunoglobulin deficiency occurs naturally inhuman infants maternal IgG level . seriousproblem in very premature babies recurrentrespiratory infections, is associated with low IgGlevels which often return somewhat abruptly to

    normal by 4 years of age.

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    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.

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    PRIMARY IMMUNODEFICIENCY

    Combined Immunodeficiency

    Severe combined immunodeficiency disease (SCID)

    involving B-, T- and NK cells.

    represents the most severe form of primaryimmunodeficiency defects in cellular and humoralimmunity.

    + severe and recurrent opportunistic infections death.

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    SECONDARY IMMUNODEFICIENCY

    Immune responsiveness can be depressednonspecifically by many factors.

    CMI in particular may be impaired in a state ofmalnutrition. Iron deficiency is particularly important

    in this respect, as are zinc and seleniumdeficiencies.

    Case

    In lepromatous leprosy and malarial infection,

    constraint on immune responsiveness imposed bydistortion of the normal lymphoid traffic pathwaysdysfunction of macrophage

    Imbalance between Thl and Th2 cells: result ofinfection depress the subset most appropriate for

    immune protection.

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    RECOGNITION OFIMMUNODEFICIENCY

    o Defects in immunoglobulinsquantitative.

    2g/L lower limit of normal.

    o The humoral immune responsescreening the serum for natural antibodies (Aand B isohemagglutinins, bactericidins against E.coli) attempting to induce active immunizationwith diphtheria, tetanus, pertussis and killedpoliomyelitis-but no live vaccines. CD19, 20 and22 markers enumerate B-cells byimmunofluorescence.

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    RECOGNITION OFIMMUNODEFICIENCY

    o Patients with T-cell deficiency

    hypo- or unreactive in skin tests to such

    antigens Active skin sensitization withdinitrochlorobenzene.

    o Complement, bactericidal and otherfunctions of polymorphsIn vitro tests.Reduction of nitrobluetetrazolium (NBT) / stimulation of superoxideproduction measure of the oxidative enzymesassociated with active phagocytosis.

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    ACQUIRED IMMUNODEFICIENCYSYNDROME

    AIDS results from infection by the RNA

    retroviruses HN-1 and HN-2.

    HIVinfects T-helper cells throughbindingof its envelope gp120 to CD4 and eitherCCR5 or CXCR4 chemokine receptorcofactors. It also infectsmacrophages,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 compartmentalizationwithin lymphoid tissues, Th1 /Th2. development, angiogenesis and wound healing.

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    Target

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    Inti

    Gp120

    Envelop

    HIV

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    HIVs Structure

    gp120

    gp41

    Envelop nucleus

    p17

    p24

    p7/p9

    RT

    Integrase

    Protease

    RNA HIV

    Diploid single

    strand

    Enzymes

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    Siklus Hidup HIV dalam Limfosit-T (CD4)

    HIV

    RNA

    DNA

    ds DNA

    RT

    Integrase

    Transkripsi

    Proviral DNA

    Spliced mRNA

    mRNA

    Genomic RNA

    Polyprotein

    Protein

    Protease

    1

    2

    3 4

    5

    6

    7

    Virion Matang

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    AIDS

    TheRNAis convertedby thereversetranscriptase to DNA incorporated intothe host's genome dormant until the cell

    is activated by stimulators such as TNF.

    There is usually a long asymptomatic phaseafter the early acute viral infection has

    been curtailed by a CD8CTL immuneresponse. Virus to the lymphoid follicles destroys the dendritic cell meshwork.

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    Long asymptomatic phase

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    AIDS

    CD4 T-helpers, destroys cell mediateddefenses life threatening infections throughopportunist organisms such as Pneumocystiscariniiand cytomegalovirus.

    Infection suppresor factors released by Tsinhibit an immune response before Thstimulating the formation of Tc/plasma cell inadequate number.

    Immune system VS virus extremely highrates of viral destruction and CD4 T-cellreplacement.

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    AIDS

    CD4 T-cell depletion: as a result of directpathogenicity, syncytium formation,susceptibility to apoptosis and possiblyother mechanisms.

    AIDS: diagnosed in an individual withopportunistic infections, by low CD4 butnormal CD8 T-cells in blood, poor delayed-type skintests, positive tests for viralantibodies and p24 antigen, lymph nodebiopsy and isolation of live virus ordemonstration ofHNgenome by the PCR.

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    AIDS

    Highly active antiretroviral drug therapy(HAART), combining inhibitors of reversetranscriptase and protease, can eliminatedetectable virus early in disease, althoughlatent virus remains.

    Vaccines are being targeted to Th1responses but it is a very difficult virus to

    control.

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    HIV/AIDS

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    Apa ituHIV/AIDS??

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    Inti

    Gp120

    Envelop

    HIVH : HumanI : ImmunodeficiencyV :Virus

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    Struktur HIV

    gp120

    gp41

    Envelop Inti

    p17

    p24

    p7/p9

    RT

    Integrase

    Protease

    RNA HIV

    Diploid single

    strand

    Enzim-enzim

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    Target

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    AIDS ?

    Acquired

    ImmunoDeficiency

    Syndrom

    Didapat

    KekebalanPenurunan

    Kumpulan

    Gejala

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    Siklus Hidup HIV

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    Mekanisme CD4

    Mekanisme pembunuhan sel T-CD4+ telahditeliti secara in vitro pada kelompokLentivirus.

    Langsung (Direct)

    Tidak Langsung (Indirect)

    Mekanisme Lain

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    Replikasi virus HIV

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    Di bagian tubuh mana HIVberada?

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    cairan sperma

    darah

    HIV didapatkan di

    cairan vagina

    air susu ibu

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    Bagaimana Cara

    Penularannya?

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    HolmesGoldwater, Network

    Hubungan Seks Transfusi darah

    Hubungan perinatal (ibu ke janin)

    Penggunaan jarum suntik yang

    pernah dipakai orang lain

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    Resiko penularan per paparan

    Transfusi ~80 %Ibu ke anak 1:4

    Seks anal (reseptif) 1:30 -1:125

    Penasun bersama 1:150

    Tertusuk jarum 1:313(petugas kesehatan)

    Seks vaginal (reseptif) 1:700

    1:2000Seks vaginal (insertif) 1:1000 -1:3000

    Terpercik ke sel lendir

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    HIV/AIDS tidak menular

    melalui

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    KONTAK SOSIAL

    HIVTIDAK MENULAR MELALUI

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    Ciri-ciri Orang dengan HIV+

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    PERKEMBANGAN DARI HIV MENJADI AIDS:

    3 - 6 BULAN

    PeriodeJendela

    3 - 10 TAHUN 1 - 2 TAHUN

    Tertular

    HIV + AIDS

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    Hanya dua cara untuk tahu bilaorang itu HIV positif

    Orang itu memberitahukan kepada kita.

    Melihat tes HIV

    Jumlah CD4 yang rendah dengan jumlah CD8sel T yang normal.

    Ditemukan antibodi viral dan antigen P24.

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    Statistika tentang AIDS

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    Penderita HIV-AIDS berdasarkan GolonganUmur Di Kota Bandung Tahun 2007

    Berdasarkan kelompok usia, maka kalangan remaja antara 20-29 tahun

    merupakan jumlah terbanyak yaitu 67.06 %

    GOLONGAN UMUR

    30 - 39 th

    20.13%

    40 - 49 th

    4.97%

    15 - 19 th

    4.55%0 - 14 th

    2.27%

    50 th

    1.01%

    20 - 29 th

    67.06%

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    Penderita HIV-AIDS berdasarkan Profesidi Kota Bandung Tahun 2007

    PEKERJAAN

    TIDAKDIKETAHUI

    3.71%

    SWASTA

    19.80%

    BURUH

    KASAR

    0.25%

    LAIN-LAIN

    0.67%IRT

    5.98%

    MAHASISWA

    20.22%

    PEKERJA SEX

    9.01%

    PNS

    2.11%

    SUPIR

    0.25%

    TIDAK

    BEKERJA

    16.01%

    WIRASWASTA

    21.99%

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    Penderita HIV-AIDS berdasarkan Faktorresiko di Kota Bandung Tahun 2006

    FAKTOR RESIKO

    HOMOSEKSUAL

    6.32%

    HETEROSEKSUAL

    23.08%

    PERINATAL2.02%

    TIDAK DIKETAHUI

    1.26%

    IDU

    67.31%

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    Bagaimana CaraPengobatannya?

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    Highly Active Antiretroviral DrugTherapy (HAART) menggabungkaninhibitor reverse transkriptase dan

    protease

    Dapat mengeliminasi virus pada

    tahap awal penyakit namun viruslaten bertahan

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    Terima Kasih !