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Aids

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Publicado en: Salud y medicina, Tecnología
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Aids

  1. 1. AIDS Megha J Nair 6th Batch
  2. 2. INTRODUCTION Acquired Immunodeficiency Syndrome First indication in 1981 with reports from New York and Los Angeles-sudden outbreak of two rare diseases-kaposi’s sarcoma and Pnuemocystis carinii
  3. 3. HUMAN IMMUNODEFICIENCY VIRUS Causative agent of AIDS Spherical enveloped virus about 90-120 nm in size Genome is diploid composed of two identical single stranded positive RNA copies Along with viral RNA – reverse transcriptase enzyme-characteristic feature of retrovirus When virus infects cell-reverse trancriptase transcribe the single stranded RNA to double stranded RNA nand then to double stranded DNA(PROVIRUS)-integrates into human genome!
  4. 4.  During viral replication , when the virus buds out of the host cell surface membrane-acquires a lipoprotein envelop-consists of lipid derived from the host cell membrane and glycoproteins which are virus coded Major virus coded envelop protein –projecting knob like spikes and anchoring transmembrane pedicles Spikes-major surface component of virus which binds to CD4 receptors on host cells…transmembrane proteins help in cell fusion
  5. 5. PATHOGENESIS Transmitted mainly through sexual contact or through blood transfusion Transmitted when the virus enters the blood or the tissues and come in contact with suitable host cells Receptor for virus –CD4 antigen-thus infect any cells bearing CD4 antigen on surface-primarily the CD4+ helper T cell Others include B lymphocytes,monocytes and macrophages such as specialised macrophages of lungs langerhan cells in dermis.
  6. 6.  After fusion of virus with the cell-HIV genome uncoated and internalised into the cell Action of reverse transcriptase enzyme-double stranded DNA integrated into the human genome with the help of integrase-causes latent infection Long and variable incubation period is due to latency Primary pathogenic mechanism-due to damage caused to the CD4 T lymphocytes T4 cells decrease in number,CMI reduces T4:T8 ratio reverses Helper T cell function-essential for B cell function-polyclonal activation of Bcells - hypergammaglobulinemia
  7. 7. CLINICAL MANIFESTATIONS Not primarily to viral cytopathology but due to failure of immune responses AIDS – only the last stage in the wide spectrum of clinical features
  8. 8. STAGES OF EVOLUTION Acute HIV infection Asymptomatic or latent infection Persistent generalised lymphadenopathy AIDS related complex AIDS
  9. 9. ACUTE HIV INFECTION Within 3-6 weeks of infection Low grade fever,malaise,head ache,lymphadenopathy,sometimes with rashes arthropathy resembling glandular fever.Spontaneous resolution within weeks Tests for HIV antibodies negative in early stage and get positive during its course- seroconversion illness.
  10. 10. ASYMPTOMATIC AND LATENT INFECTION Symptomless infection Positive HIV antibodies test Passes through various stages-CD4 lymphocytopaenia,minor oppurtunistic infection,persistent generalised lymphadenopathy,ARC and full blown AIDS Viral multiplication goes on-immune response mounnted by host-only helps in limiting viral load Tcell-500 from 1000/microlitre-acute infection and when 200 or less , clinical AIDS
  11. 11. PGL Enlarged lymph nodes Atleast 1 cm or more In two or more non contiguous extrainguinal sites-that persists for more than 3 months in the absence of any current illness or medication
  12. 12. PGL
  13. 13. ARC Patients with considerable immunodeficiency suffering from various constitutional symptoms or minor oppurtunistic infections Fatigue , unexplained fever , persistent diarrhoe , marked weight lose-symptoms-also gen. lymphadenopathy and splenomegaly Oppurtunistic inf.-oral candidiasis,herpes zoster,hairy cell luekoplakia,salmanellosis or tb
  14. 14. ORAL THRUSH
  15. 15. AIDS• End stage disease-irreversible breakdown of immune system-progressive oppurtunistic infection and malignancies.• Dry cough , dyspnea , fever , recurrent pneumonia• GIT-thrush , herpetic steatites , gingivitis , hairy luekoplakia or kaposi’s sarcoma.A characteristic intestinal pathogen is cryptosporidium
  16. 16. HAIRY LEUKOPLAKIA
  17. 17.  CNS-toxoplasmosis and cryptococcosis,lymphomas of CNS also seen.also can cross blood brain barrier and cause encephalopathy leading to loss of higher function-then dementia Malignancies-kaposi’s sarcoma(nonmetastasing mucosal or cutaneous tuour of endothelial orgin)Hodgkin and Non Hodgkin lymphomas Babies born to infected mothers-also positive-
  18. 18. KAPOSI’S LESIONS
  19. 19. DIAGNOSIS IMMUNOLOGICAL TESTS: Total luecocyte and lymphocyte count Tcell subset assay-ratio inversion.Absolute CD4 cell count less than 200/cubic mm Platelet cout will show thrombocytopaenia Raised IgG and IgA levels Diminished CMI by skin tests Lymph node biopsy
  20. 20.  Specific tests: Antigen detection:major core antigen- p24-earliest marker-p24 antigen capture assay Viral isolation:cocultivation of patient’s lymphocyte with uninfected lymphocyte in the presence of interluekin 2.viral replicatio detected by demo of reverse transcriptase activity as well as antigen PCR:golden standard for diagnosis of all stages of HIV infection
  21. 21.  Antibody detection: ELISA Test Western blot test-HIV proteins seperated by their electrophoretic mobility by poly acrylamide gel electrophoresis are blotted on to the strips of nitrocellulose paper.strips are reacted with test sera and then with enzyme conjugated anti human globulin
  22. 22. TREATMENTTreatment and prophylaxis of infections and tumoursGeneral managementImmunorestortive measures(administration of interluekin 2,thymic factors etc)Specific anti-HIV drugs(anti retroviral drugs)

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