Hiv/AIDS

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  • Simian virüs HIV1in prokürsörüdür. Retrovirüsler viral RNA’nın reverz transkriptazını kullanarak lineer çift zincirli DNA’ya döner ve konak genomuna integre olur. Pariste bir hastanın LN’da izole edildi.
    HIV-2 birçok maymun türünü enfekte edebilir.
  • Once HIV comes into contact with a T-cell, it must attach itself to the cell so that it can fuse with the cell and inject its genetic material (a blueprint for making more HIV) into it. Attachment is a specific binding between proteins on the surface of the virus and proteins that serve as receptors on the surface of the T-cell. Normally, these receptors help the cell communicate with other cells. Two receptors in particular, CD4 and a beta-chemokine receptor (either CCR5 or CXCR4), are used by HIV to latch onto the cell. On the surface of the viral envelope, two sets of proteins (also known as antireceptors) called gp120 and gp41 attach to CD4 and CCR5/CXCR4.
    Drugs called attachment or entry inhibitors are currently being studied in clinical trials. These drugs block the interaction between the cellular receptors and the antireceptor on the virus by binding to or altering the receptor sites. Scientists have found that people who naturally lack these cellular receptors because of a genetic mutation, or those who have them blocked by natural chemokines (chemical messengers), may not get infected as readily with HIV or may progress more slowly to AIDS. Scientists are also examining vaccines that may help the body block these receptors.
    After attachment is completed, viral penetration occurs. Penetration allows the nucleocapsid -- the genetic core -- of the virus to be injected directly into the cell's cytoplasm. gp120 actually contains three sugar-coated proteins (glycoproteins) and, once gp120 attaches itself to CD4, these three proteins spread apart. This allows the gp41 protein, which is normally hidden by the gp120 proteins, to become exposed and bind to the chemokine receptor. Once this has occurred, the viral envelope and the cell membrane are brought into direct contact and essentially melt into each other.
    Drugs called fusion inhibitors prevent the binding of gp41 and the chemokine receptor. T-20 (enfuvirtide, Fuzeon), an experimental fusion inhibitor that is nearing FDA approval, binds to a portion of gp41, preventing it from binding to the chemokine receptor.
    Once HIV has penetrated the cell membrane, it is ready to release its genetic information (RNA) into the cell. The viral RNA is protected in the nucleocapsid. The nucleocapsid needs to be partially dissolved so that the virus's RNA can be converted into DNA, a necessary step if HIV's genetic material is to be incorporated into the T-cell's genetic core.
    The process by which HIV's RNA is converted to DNA is called reverse transcription. This transcription process happens in almost every human cell, but in the opposite direction -- from DNA to RNA. DNA from the cell nucleus is transcribed into messenger RNA, which then directs the cell's various metabolic functions needed to do its job in the body. HIV uses an enzyme called reverse transcriptase to accomplish this transcription. The single-stranded viral RNA is transcribed into a double strand of DNA, which contains the instructions HIV needs to hijack a T-cell's genetic machinery in order to reproduce itself. Reverse transcriptase uses nucleotides -- building blocks of DNA -- from the cell cytoplasm to make this process possible.
    Drugs called reverse transcriptase inhibitors block HIV's reverse transcriptase from using these nucleotides. Nucleoside and nucleotide analog reverse transcriptase inhibitors (NRTIs) -- such as Zerit, Epivir, and Viread -- contain faulty imitations of the nucleotides found in a T-cell's cytoplasm. Instead of incorporating a nucleotide into the growing chain of DNA, the imitation building blocks in NRTIs are inserted, which prevents the double strand of DNA from becoming fully formed. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) -- such as Viramune and Sustiva -- block reverse transcription by attaching to the enzyme in a way that prevents it from functioning.
  • If HIV succeeds in translating its instructions from RNA to DNA, HIV must then insert its DNA (also called the preintegration complex) into the cell's DNA. This process is called integration. In most human cells, there is a structure called the cell nucleus, where the cell's DNA is stored. In order for integration to occur, the newly translated DNA must be transported across the nuclear membrane into the nucleus.
    Although the exact mechanism that HIV uses to transport its genetic cargo into the cell nucleus is still unclear, viral protein R (VPR), which is carried by HIV, may facilitate the movement of the preintegration complex to the nucleus. Once the viral RNA has successfully bridged the nuclear membrane and been escorted to the nucleus, HIV uses an enzyme called integrase to insert HIV's double-stranded DNA into the cell's existing DNA.
    Drugs that inhibit the HIV preintegration complex from traveling to the nucleus -- integrase inhibitors -- are currently in early clinical trials.
    After successful integration of the viral DNA, the host cell is now latently infected with HIV. This viral DNA is referred to as provirus. The HIV provirus now awaits activation. When the immune cell becomes activated, this latent provirus awakens and instructs the cellular machinery to produce the necessary components of HIV, like plastic pieces of a model airplane. From the viral DNA, two strands of RNA are constructed and transported out of the nucleus. One strand is translated into subunits of HIV such as protease, reverse transcriptase, integrase, and structural proteins. The other strand becomes the genetic material for the new viruses. Compounds that inhibit or alter viral RNA have been identified as potential antiviral agents.
    Once the various viral subunits have been produced and processed, they must be separated for the final assembly into new virus. This separation, or cleavage, is accomplished by the viral protease enzyme.
    Drugs called protease inhibitors -- such as Kaletra, Crixivan, and Viracept -- bind to the protease enzyme and prevent it from separating, or cleaving, the subunits.
    If cleavage is successfully completed, the HIV subunits combine to make up the content of the new virons. In the next step of the viral life cycle, the structural subunits of HIV mesh with the cell's membrane and begin to deform a section of the membrane. This allows the nucleocapsid to take shape and viral RNA is wound tightly to fit inside the nucleocapsid. Researchers are looking at drugs called zinc finger inhibitors, which interfere with the packaging of the viral RNA into the nucleocapsid.
    The final step of the viral life cycle is called budding. In this process, the genetic material enclosed in the nucleocapsid merges with the deformed cell membrane to form the new viral envelope. With its genetic material tucked away in its nucleocapsid and a new outer coat made from the host cell's membrane, the newly formed HIV pinches off and enters into circulation, ready to start the whole process again.
    During HIV's life cycle, the T-cell, known as the host cell, is altered and perhaps damaged, causing the death of the cell. Scientists are not sure exactly how the cell dies but have come up with a number of scenarios. First, after the cell becomes infected with a virus or other pathogen, internal signals may tell it to commit suicide. This is known as apoptosis or programmed cell death -- a self-destruct program intended to kill the cell with the hopes of killing the virus as well. A second possible mechanism for the death of the cell is that, as thousands of HIV particles bud or escape from the cell, they severely damage the cell's membrane, resulting in the loss of the cell. Another possible cause for the cell's death is that other cells of the immune system, known as killer cells, recognize that the cell is infected and inject it with chemicals that destroy it.
    Montaj
  • In February 1999 a group of researchers from the University of Alabama2 announced that they had found a type of SIVcpz that was almost identical to HIV-1. This particular strain was identified in a frozen sample taken from a captive member of the sub-group of chimpanzees known as Pan troglodytes troglodytes (P. t. troglodytes), which were once common in west-central Africa.
  • Hunter; The most commonly accepted theory is that of the 'hunter'. In this scenario, SIVcpz was transferred to humans as a result of chimps being killed and eaten or their blood getting into cuts or wounds on the hunter. 
  • HIV can be transmitted from mother to infant during pregnancy, childbirth,
    or breastfeeding.
  • Viral yük düşük olduğundan PCR – olabilir.
  • PEP almak, HCV koenfeksiyonu, agamaglobulinemi
    Antikor yanıtının gecikmesine sebep olabilir
  • Once HIV comes into contact with a T-cell, it must attach itself to the cell so that it can fuse with the cell and inject its genetic material (a blueprint for making more HIV) into it. Attachment is a specific binding between proteins on the surface of the virus and proteins that serve as receptors on the surface of the T-cell. Normally, these receptors help the cell communicate with other cells. Two receptors in particular, CD4 and a beta-chemokine receptor (either CCR5 or CXCR4), are used by HIV to latch onto the cell. On the surface of the viral envelope, two sets of proteins (also known as antireceptors) called gp120 and gp41 attach to CD4 and CCR5/CXCR4.
    Drugs called attachment or entry inhibitors are currently being studied in clinical trials. These drugs block the interaction between the cellular receptors and the antireceptor on the virus by binding to or altering the receptor sites. Scientists have found that people who naturally lack these cellular receptors because of a genetic mutation, or those who have them blocked by natural chemokines (chemical messengers), may not get infected as readily with HIV or may progress more slowly to AIDS. Scientists are also examining vaccines that may help the body block these receptors.
    After attachment is completed, viral penetration occurs. Penetration allows the nucleocapsid -- the genetic core -- of the virus to be injected directly into the cell's cytoplasm. gp120 actually contains three sugar-coated proteins (glycoproteins) and, once gp120 attaches itself to CD4, these three proteins spread apart. This allows the gp41 protein, which is normally hidden by the gp120 proteins, to become exposed and bind to the chemokine receptor. Once this has occurred, the viral envelope and the cell membrane are brought into direct contact and essentially melt into each other.
    Drugs called fusion inhibitors prevent the binding of gp41 and the chemokine receptor. T-20 (enfuvirtide, Fuzeon), an experimental fusion inhibitor that is nearing FDA approval, binds to a portion of gp41, preventing it from binding to the chemokine receptor.
    Once HIV has penetrated the cell membrane, it is ready to release its genetic information (RNA) into the cell. The viral RNA is protected in the nucleocapsid. The nucleocapsid needs to be partially dissolved so that the virus's RNA can be converted into DNA, a necessary step if HIV's genetic material is to be incorporated into the T-cell's genetic core.
    The process by which HIV's RNA is converted to DNA is called reverse transcription. This transcription process happens in almost every human cell, but in the opposite direction -- from DNA to RNA. DNA from the cell nucleus is transcribed into messenger RNA, which then directs the cell's various metabolic functions needed to do its job in the body. HIV uses an enzyme called reverse transcriptase to accomplish this transcription. The single-stranded viral RNA is transcribed into a double strand of DNA, which contains the instructions HIV needs to hijack a T-cell's genetic machinery in order to reproduce itself. Reverse transcriptase uses nucleotides -- building blocks of DNA -- from the cell cytoplasm to make this process possible.
    Drugs called reverse transcriptase inhibitors block HIV's reverse transcriptase from using these nucleotides. Nucleoside and nucleotide analog reverse transcriptase inhibitors (NRTIs) -- such as Zerit, Epivir, and Viread -- contain faulty imitations of the nucleotides found in a T-cell's cytoplasm. Instead of incorporating a nucleotide into the growing chain of DNA, the imitation building blocks in NRTIs are inserted, which prevents the double strand of DNA from becoming fully formed. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) -- such as Viramune and Sustiva -- block reverse transcription by attaching to the enzyme in a way that prevents it from functioning.
  • If HIV succeeds in translating its instructions from RNA to DNA, HIV must then insert its DNA (also called the preintegration complex) into the cell's DNA. This process is called integration. In most human cells, there is a structure called the cell nucleus, where the cell's DNA is stored. In order for integration to occur, the newly translated DNA must be transported across the nuclear membrane into the nucleus.
    Although the exact mechanism that HIV uses to transport its genetic cargo into the cell nucleus is still unclear, viral protein R (VPR), which is carried by HIV, may facilitate the movement of the preintegration complex to the nucleus. Once the viral RNA has successfully bridged the nuclear membrane and been escorted to the nucleus, HIV uses an enzyme called integrase to insert HIV's double-stranded DNA into the cell's existing DNA.
    Drugs that inhibit the HIV preintegration complex from traveling to the nucleus -- integrase inhibitors -- are currently in early clinical trials.
    After successful integration of the viral DNA, the host cell is now latently infected with HIV. This viral DNA is referred to as provirus. The HIV provirus now awaits activation. When the immune cell becomes activated, this latent provirus awakens and instructs the cellular machinery to produce the necessary components of HIV, like plastic pieces of a model airplane. From the viral DNA, two strands of RNA are constructed and transported out of the nucleus. One strand is translated into subunits of HIV such as protease, reverse transcriptase, integrase, and structural proteins. The other strand becomes the genetic material for the new viruses. Compounds that inhibit or alter viral RNA have been identified as potential antiviral agents.
    Once the various viral subunits have been produced and processed, they must be separated for the final assembly into new virus. This separation, or cleavage, is accomplished by the viral protease enzyme.
    Drugs called protease inhibitors -- such as Kaletra, Crixivan, and Viracept -- bind to the protease enzyme and prevent it from separating, or cleaving, the subunits.
    If cleavage is successfully completed, the HIV subunits combine to make up the content of the new virons. In the next step of the viral life cycle, the structural subunits of HIV mesh with the cell's membrane and begin to deform a section of the membrane. This allows the nucleocapsid to take shape and viral RNA is wound tightly to fit inside the nucleocapsid. Researchers are looking at drugs called zinc finger inhibitors, which interfere with the packaging of the viral RNA into the nucleocapsid.
    The final step of the viral life cycle is called budding. In this process, the genetic material enclosed in the nucleocapsid merges with the deformed cell membrane to form the new viral envelope. With its genetic material tucked away in its nucleocapsid and a new outer coat made from the host cell's membrane, the newly formed HIV pinches off and enters into circulation, ready to start the whole process again.
    During HIV's life cycle, the T-cell, known as the host cell, is altered and perhaps damaged, causing the death of the cell. Scientists are not sure exactly how the cell dies but have come up with a number of scenarios. First, after the cell becomes infected with a virus or other pathogen, internal signals may tell it to commit suicide. This is known as apoptosis or programmed cell death -- a self-destruct program intended to kill the cell with the hopes of killing the virus as well. A second possible mechanism for the death of the cell is that, as thousands of HIV particles bud or escape from the cell, they severely damage the cell's membrane, resulting in the loss of the cell. Another possible cause for the cell's death is that other cells of the immune system, known as killer cells, recognize that the cell is infected and inject it with chemicals that destroy it.
  • Hiv/AIDS

    1. 1. HIV/AIDS Dr.Hayati Demiraslan Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Anabilim Dalı 11/02/14 1
    2. 2. SUNUM PLANI          Nedir Yapısı Tarihçe Epidemiyoloji Bulaşma yolları Tanı Klinik Tedavi Korunma 11/02/14 2
    3. 3. HIV enfeksiyonu  Human immunodeficiency virus (HIV) tarafından sebep     olunan ilerledikçe immün sistemi yıkan bir hastalıktır Akut HIV enfeksiyonu (bir kaç haftada sonlanır) Asemptomatik HIV enfeksiyonu (10 yıl) Erken semptomatik HIV enfeksiyonu AIDS 11/02/14 3
    4. 4. Retroviruslar  Çift zincirli RNA virüsü Lentivirus HIV-1 HIV-2 Simian IDV Onkovirus Spumavirus HTLV-1 Doğada yaygın HTLV-II patojenite? Felin leukemia virus Bovin leukemia virus ENV ve GAG genlerine göre A-J’ye kadar 10 farklı türü vardır Retrovirüsler viral RNA’nın reverz transkriptazını kullanarak lineer çift zincirli DNA’ya döner ve konak genomuna integre olur. 11/02/14 4
    5. 5. 11/02/14 5
    6. 6. 11/02/14 6
    7. 7. İntegrasyon Montaj ve tomurcuklanma 11/02/14 7
    8. 8.  Şubat 1999’da Alabama’da  bir tür SIVcpz keşfettiler 11/02/14 Pan troglodytes troglodytes 8
    9. 9. Tarihçe  HIV, Simian Immunodeficiency virüsün torunudur.  SIV’in bazı türleri HIV-1 ve HIV-2 ile sıkı benzerlikler taşır. 11/02/14 9
    10. 10. HIV enfeksiyonu örnekleri  1959’da Kongo’dan erişkin erkekten alınan    serumda elde edildi. 1960’da Kongo’dan erişkin kadının lenf bezinden saptandı. 1969’da St. Louis’de ölen bir Amerikalı delikanlının (teeneger) doku örneğinde 1976’da ölen bir denizcinin doku örneklerinde HIV saptandı Zhu, T et. al (1998, 5th February) ' An African HIV-1 Sequence from 1959 and Implications for the Origin of the Epidemic ' Nature, 391 Worobey, M et. al (2008, 2nd October) ' Direct Evidence of Extensive Diversity of HIV-1 in Kinshasa by 1960 ' Nature, 455(7213) Kolata, G (1987, 28th October) ' Boy's 1969 death suggests AIDS invaded U.S. several times ' New York Times 11/02/14 10 Frøland, SS et. al (1988, 11th June) ' HIV-1 infection in Norwegian family before 1970 ' The Lancet 331(8598)
    11. 11. EPİDEMİYOLOJİ    İlk kez 1981 yılında ABD de tanımlanmıştır ‘Akkiz immünyetmezlik sendromu’ adı verilmiştir Etken virus 1983 yılında izole edilmiştir 11/02/14 11
    12. 12. Milyon 11/02/14 12
    13. 13. Türkiye’de HIV enfekte kişi sayısı HIV 11/02/14 AIDS 13
    14. 14. Thelper lenfositler  B ve T sitotoksik lenfositlerinin aktivitelerini şiddetlendirirler.  Çeşitli sitokinler salgılayarak − T hücresi, − monosit-makrofaj güçlenmelerini sağlarlar. Bu özellikleri ile Th lenfosit immün sitemin orkestra şefi durumundadır. 11/02/14 14
    15. 15. BULAŞ      Cinsel yolla bulaş Kan ve diğer dokularla bulaş Perinatal bulaş Sağlık bakımında HIV bulaşı Bulaşın diğer yolları 11/02/14 15
    16. 16. Vücut sıvılarında HIV Vücut sıvılarının 1ml’sinde ortalama HİV partikül sayısı Kan 18,000 Semen 11,000 11/02/14 Vajinal sıvı 7,000 Amniyotik sıvı 4,000 Tükürük 1 16
    17. 17. BULAŞ YOLLARI  Cinsel yolla bulaş − En önemli bulaş yoludur − Bulaş için HIV pozitif kişiyle yapılan tek bir cinsel temas yeterlidir − Korunmasız cinsel temasta; virusun enfekte erkekten kadına bulaş riski, enfekte kadından erkeğe bulaş riskinden fazladır 11/02/14 17
    18. 18. Cinsel yolla bulaş VAJİNAL ORAL 11/02/14 18
    19. 19. Cinsel yolla bulaş 1000 koitus başına olgu 11/02/14 Wawer, J Infect Dis 2005;191:1403 19
    20. 20. Cinsel yolla bulaş riski  Sünnet (%50-60)  Kondom kullanımı  Tek eşlilik 11/02/14      HIV RNA Genital ülser Kanama Birden çok cinsel eş CYBH (üretrit, gonore) 20
    21. 21.  Kan ve kan ürünleri ile bulaş − HIV yönünden tarama yapılmaya (1985) başlandığından beri bu yolla bulaş azalmıştır  Kan ve KÜ transfüzyonu  Organ transplantasyonu Kornea ve işlenmiş dokularla Bulaş riski yok Yıl Risk 1996 p24 antijeni 1/200.000-1/ 2.000.000 2002 11/02/14 Test Nukleik asit testleri (12 gün) 1/ 2.135.000 21
    22. 22.  Kan ve kan ürünleri ile bulaş − Hepatit B İg − İmmün serum globulin − Rh İg − Hepatit B aşısı 11/02/14 Bulaştırmaz 22
    23. 23. Damar içi madde kullanımı İlişkili faktörler − Enjektör ve diğer aletlerle bulaş  Damar içi madde kullananlar     İğne paylaşma sıklığı Paylaşılan kişi sayısı Enjeksiyon sayısı Bölgedeki HIV sıklığı Kokain enjeksiyonu daha riskli bulunmuş 11/02/14 23
    24. 24. Anneden bebeğe bulaş Perinatal risk %13-40 − Gebelik süresince  %30-50 doğumda + − Doğum sırasında (%40) − Postpartum dönemde emzirmekle  %14-29 11/02/14  Preterm doğum  Uzamış membran    rüptürü (>4 saat) Madde kullanımı Antenatal düşük CD4+ sayısı Düşük doğum ağırlığı 24
    25. 25. Bebekte tanı  0-6 ayda PCR ve virüs kültürü (%50 tanı   koyar) Anti-HIV ab 12-18 ay + HIV-spesifik IgA (duyarlılığı düşük) 11/02/14 25
    26. 26. Sağlık bakımında HIV bulaşı − Sağlık personeline bulaş  İğne,enjektör batması ile (risk %0.2-0.5)  Kanlı vücut sıvıları ile mukozal temasla (risk <%0.1) − Sağlık personelinden hastaya − 53 HIV’li çalışanın 2’sinin hastalarında + Dişçi ve ortopedist − Hastadan hastaya − Malzemelerin tekrar kullanılması − İlaçların çoklu kullanımı 11/02/14 26
    27. 27. Bulaşın diğer yolları  Tükrükle ve ısırıkla bulaş nadirdir (kan yoksa) − HIV inhibitör etkisi 11/02/14 27
    28. 28. HIV enfeksiyonu ve antikor cevabı ---Başlangıç dönemi------------------Ara veya Latent Dönem------------Grip benzeri semptomlar veya Semptomsuz Semptomsuz ---Hastalık Dönemi-- AIDS ---- Enfeksiyon Virus Antibody ---11/02/14 < 6 m ont h ~ Years ~ Years ~ Years 28 ~ Years
    29. 29. TANI FDA 2002 PCR 10-12 gün P24 antijeni (combo test) 28 gün 16 gün Anti HIV (3.kuşak ELISA) 3 ay (%97) 22 gün Yeniler *HIV-1 p17 IgM 7 gün PEP almak, HCV koenfeksiyonu, agamaglobulinemi Antikor yanıtının gecikmesine sebep olabilir *Hashida S, et al. Clin Diagn Lab Immunol.2000; 7:872 11/02/14 29
    30. 30. HIV-enfekte erişkinlerde CDC sınıflaması CD4 hücre sayısı kategorileri Klinik Kategori : PGL = persistan generalize lenfadenopati A B* C# Asemptomatik, Akut Semptomatik, A AIDS-indikatör HIV veya PGL veya C dışı durumlar (1) ≥500 /µL A1 B1 C1 (2) 200-499 /µL A2 B2 C2 (3) <200 /µL A3 B3 C3 11/02/14 30
    31. 31. Kategori B Semptomatik durumlar 1. Bacillary angiomatosis 2. Orofaringeal kandidioz (thrush) 3. Vulvovaginal kandidoz, persistan veya rezistan 4. Pelvik inflammatuvar hastalık (PID) 5. Servikal displazi (orta, ağır)/servikal karsinoma in situ 6. Oral hairy lökoplaki, 7. Herpes zoster (shingles),en az bir dermatomu tutan veya ≥2 epizod 8. Idiopatik trombositopenik purpura 9. Konstitusyonel semptomlar (ateş>38.5ºC) ishal >1 ay 10. Periferik nöropati 11/02/14 31
    32. 32. # Kategori C AIDS-indikatör durumlar Rekürren bakteriyel pnçmoni (12 ayda ≥2 epizod) Bronş, trakea, akciğer kandidozu Özefageal kandidoz Servikal karsinoma, invaziv, dissemine veya extrapulmoner koksidiyomikoz extrapulmoner kriptokokkoz Kronik intestinal kriptosporidyaz (>1 ay) Cytomegalovirus hastalığı (KC, dalak ve LN dışı) HIV-ensefalopatisi Herpes simplex: kronik ülserler >1 ay, bronşit, pnömoni, özefajit Histoplasmoz, disseminated or extrapulmonary Izosporiyaz, kronick intestinal (>1 ay) Kaposi sarkomu Lenfoma, Burkitt, immunoblastik, primer santral sinir sistemi Mycobacterium avium complex (MAC) veya Mycobacterium kansasii, dissemine veya ekstrapulmoner Mycobacterium tuberculosis, pulmoner veya ekstrapulmoner Mycobacterium, diğer türler, dissemine veya ekstrapulmoner Pneumocystis jiroveci pnömonisi (PCP) Progressif multifokal lökoensefalopati (PML) Salmonella septisemi, rekürren Beyin toxoplasmozu Wasting sendromu (İstemeden kilo kaybı>%10) associated with either chronic diarrhea (hergün≥2 dışkılama ≥1 ay), kroniik yorgunluk, ateş ≥1 ay 11/02/14 32
    33. 33. HIV ENFEKSİYONUNDA KLİNİK KATEGORİLER (WHO)  KATEGORİ 1 − Asemptomatik HIV enfeksiyonu − Persistan generalize LAP (PGL)  KATEGORİ 2 − − − − − − − − 11/02/14 Açıklanamayan kilo kaybı (<%10) Tekrarlayan solunum yolu enfeksiyonları (sinüzit, otit, tonsillit) Herpes zoster Anguler cheilitis Recurrent oral ülserler Papüler kaşıntılı döküntüler Seboreik dermatit Fungal tırnakenfeksiyonları 33
    34. 34. KATEGORİ 3          Açıklanamayan ağır kilo kaybı (>%10) Açıklanamayan kronik ishal (1aydan uzun) Açıklanamayan ateş (>37.6 °C, intermittan, 1 aydan uzun) Persistan oral kandidiyazis Oral hairy lökoplaki Akciğer tüberkülozu Ağır bakteriyel enfeksiyonlar( pnömoni, ampiyem, kemik eklem enfeksiyonları, menenjit, bakteriyemi) Akut nekrotizan ülseratif stomatit, gingivit, periodontit Açılanamayan − anemi (<8 g/dL), − nötropeni (<500/ml), − kronik trombositopeni (<50.000/ml)
    35. 35. KLİNİK KATEGORİ 4            HIV yıkım sendromu Pneumocystis jirovecii Recurrent ağır bakteriyel pnömoni Kronik herpes simplex enfeksiyonu (orolabial, genital, anorektal, 1 aydan uzun veya herhangi visseral organı tutan) Özefagiyal kandidiyazis Ekstrapulmoner tüberküloz Kaposi sarkomu Sitomegalovirus enfeksiyonu (retinit veya diğer organ) Merkezi sinir sistemi toksoplasmozu HIV ensefalopatisi
    36. 36. KLİNİK KATEGORİ 4     Ekstrapulmoner kriptokokkoz Dissemine non-TB mikobakteriel enfeksiyonlar Progresif multifokal lökoensephalopati Kronik Kriptosporidiyaz (ishalle)  Kronik isosporiyaz  Yaygın mikozlar (histoplazma veya koksidiyomikoziz)  Rekürren non-tifoidal Salmonella bakteremisi  Lenfoma (serebral veya B-hücrerli non-Hodgkin's) veya diğer solid HIV  ilişkili tümörler Invaziv servikal karsinom Atipik dissemine leishmaniasis  Semptomatik HIV-ilişkili nöropati veya kardiyomiyopati
    37. 37. Oral kandidiyazis 11/02/14 37
    38. 38. Hairy lökoplaki 11/02/14 38
    39. 39. Kaposi sarkomu 11/02/14 39
    40. 40. Kaposi sarkomu 11/02/14 40
    41. 41. CD4 <50 kandida cilt enfeksiyonu
    42. 42. 11/02/14 Zona 42
    43. 43. Widespread non-lobar consolidation - bronchopneumonia from PCP in HIV patient
    44. 44. bilateral pulmonary infiltrate (white triangles), caving formation“ (black arrows) present in the right apical region
    45. 45. Tedavi KLİNİK KATEGORİ CD4 HÜCRE SAYISI DHHS rehberi IAS rehberi (U.S) BASHH rehberi Semptomatik hasta Herhangi bir değer Önerilir Önerilir Önerilir Asemptomatik <350/mm3 hasta Önerilir Önerilir Önerilir Asemptomatik 350-500/mm3 hasta Önerilir Önerilir Önerilir Asemptomatik >500/mm3 hasta Düşünülmeliopsiyonel Düşünülmeli Belli durumlarda öner DHHS: Department of Health and Human Services (U.S) BASHH: British association for sexual health and HIV 11/02/14 45
    46. 46. CD4 sayısından bağımsız tedavi başlanmalı  Hastalığı hızlı ilerleme riski olanlar          − CD4 T hücrelerinin sayısında hızlı azalma (>100/mm3/yıl) Viral yük >100 000 kopya/ml >50 yaş Kronik hepatit B veya hepatit C varlığı* HIV ile ilişkili böbrek hastalığı Yüksek kardiyovasküler risk Fırsatçı hastalık varlığı Gebelik Malignite varlığı Serolojik açıdan uyumsuz eş 11/02/14 46
    47. 47. Gp41’in kemokin reseptörüne bağlanmasını inh füzyon inhibitörü T20 (enfuvirtide) Giriş inhibitörüi CCR5 antogonisti Maraviroc Ters transkriptaz inhibitörleri -Nukleozit-nükleotid -Non-nukleozit 11/02/14 47
    48. 48. integraz inhibitörü Raltegravir Proteaz inhibitörleri Proteaz enzimine bağlanır ayrılmayı önler 11/02/14 48
    49. 49. 11/02/14 49
    50. 50. KORUNMA  Cinsel yolla bulaşa karşı korunma − Genital ve oral mukoza membranlarının cinsel ilişki sırasında kan,semen,vajinal ve servikal sekresyonlarla temasının azaltılması − Kondom kullanımının teşvik edilmesi ve yaygınlaştırılması − Cinsel yolla bulaşan diğer hastalıkların tedavisi − Güvenli cinsel temasın yaygınlaştırılması (tek eşli cinsel yaşam veya uygun ve güvenli cinsel eş seçimi) 11/02/14 50
    51. 51. Cinsel yolla bulaşa karşı korunma •Erkek kondomunun koruyuculuğu %60-96 •Kadın kondomu kullanımı (%11-26 yetersiz) 11/02/14 51
    52. 52. Cinsel yolla bulaşa karşı korunma  Spermisit (nonoxinol 9) kullanımı HIV bulaşını artırır  Mikrobisit (polinaftalen sülfonat gel (PRO2000) HIV sıklığını kısmen azalttı 11/02/14 52
    53. 53.  Kan ve kan ürünleriyle bulaşa karşı korunma − Antikor testleri bulunduğundan beri bu yolla bulaş azalmıştır − Damar içi madde kullananlarda − Bu alışkanlığın önlenmesi ve tedavi edilmesi − Ortak enjektör kullanım risklerinin anlatılması − Steril enjektör kullanımının sağlanması − Eğitim 11/02/14 53
    54. 54.  Anneden bebeğe geçişe karşı korunma − HIV pozitif kadına doğum kontrol yöntemleri öğretilmelidir − Hamile kalan HIV pozitif kadına erken dönemde kürtaj yapılmalıdır − Bebeği doğurmakta ısrarlı ise gebeliğin son trimestırında anneye, doğumdan sonra da bebeğe antiretroviral tedavi başlanmalıdır − Elektif sezaryan uygulanırsa bebeğe HIV geçişi 4-5 kat azalır − Virusun anne sütü ile geçişi gösterildiğinden emzirme önerilmez 11/02/14 54
    55. 55. PrEp profilaksi  Truvada (emtricitabine/tenofovir disoproxil fumarate),  HIV enfeksiyonu riski yüksek ve HIV enfekte eşlerle seksüel aktivitede bulunan HIV (-) kişilerde bulaş riskini azaltır 11/02/14 55

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