HIV transmission. Pathogenesis.

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1 HIV transmission. Pathogenesis. September 27-28, 2012 TUBIDU International training (WP 7), Riga Dr.Inga Upmace, NGO,,Baltic HIV Association

2 Discovery of HIV virus First reported in 1981 Discovered in by Luc Antoine Montagnier, France, and Robert Gallo, USA who published similar findings in the same issue of Science and later confirmed the discovery of the virus and presented evidence that it caused AIDS. ASV) Today it is agreed that Montagnier's group first isolated HIV In 2008, the Nobel Prize in Physiology or Medicine was awarded to Montagnier and Françoise Barré-Sinoussi for the discovery of HIV Inga Upmace, TUBIDU International Training, Riga, September 27-28,

3 Infectious agent - Human immunodefiency virus: Retrovirus 2 tipes - HIV1 and HIV2 with similar epidemiological and pathological characteristics; virus size ~ 100 nm; has a genetic polimorphism, not resistant in the external environment, HIV is made up of Genetic material, Chemicals and a coating the Genetic material RNA; the Chemicals enzymes, which help the virus enter and use other cells to make copies of itself. lipid-containing Outer coverings, which mounted surface antigens gp41, gp120; Inga Upmace, TUBIDU International Training, Riga, September 27-28,

4 Infectious agent - Human immunodefiency virus (2): mainly infects white blood cells - T-lymphocyte cells (T-cells) Virus genom contains structural genes + regulator genes; The inside of outer envelop contains proteins p17; Virus core nucleic acid and it s envelope (nucleokapsid) contains the protein p24, (antigen, what is important for early detection of HIV); Inga Upmace, TUBIDU International Training, Riga, September 27-28,

5 HIV,,life cycle (replication) I. Stage 1. Adsorption: HIV glycoprotein (gp120) + host cell s CD4 receptor, 2. Breaking in to the target cell 3. undressing (,,striptise ) 4. virus-rns sinthesis to DNS (reverse transcription), 5. Entering into nucleus 6. integration into cell s genome 7.b dormant HIV pro-virus formation II. Stage 7.a -b HIV proteins un RNS copies synthesis, fitting, 8. HIV particles gemmation 9. liberation and 10. maturation Inga Upmace, TUBIDU International Training, Riga, September 27-28,

6 Summarizing: HIV enters T lymphocyte or other,,target cell HIV uses cell s own DNA and enzymes to copy its RNA Enzymes divide RNA to make new HIV Reproduct a new HIV then emerges out of the T lymphocyte

7 HIV,,target cells (contain CD- 4 receptors) : Lymphocytes (T-cells or T-helpers); Macrofags; Monocits; CNS glial cells; Epithelial cells (vascular, rectal);

8 HIV infection definition: Illness, what s caused by HIV, if virus entered lymphocytes, macrophags and nervous system cells, as a result of creating a slowly progressive immune and nervous system demage, in the form of secondary infections, tumors, encephalitis, and other pathologies may lead to exitus letalis.

9 Fluids containing HIV virus: blood; serum; semen; vaginal discharge; amniotic fluid; breast milk; various organs (heart, lungs, joints, brain) mantle fluids any liquid with a bloody

10 3 modes of transmission: Sexual Contact Any type of unprotected intercourse with someone who is infected with HIV can transmit the virus. This includes oral, vaginal and anal sex. Exposure to blood or tissues Blood transfusion was a more common way to contract HIV in the 1970s and '80s. Sharing needles with someone infected by HIV will put the infected blood directly into contact with the new vein. Actual transmission mode for IDUs. Mother to Child A pregnant mother who has HIV can transmit the virus to the fetus or baby. The infant can become infected in utero, during delivery or through feeding on infected breast milk.

11 Organism responce to HIV infection Acute HIV sindrom (30%) Latent period Simptomatic period CD4 AIDS (B) Windows period Contamination Inga Upmace, TUBIDU International Training, Riga, September 27-28,

12 Clinical manifestations : Acute retrovirus or HIV sindrom High level of: p24 Ag; RNS copies in blood and plazma HIV Ab (serological tests) mostly negative Asimptomatical (latent) period Seroconversion (HIV-Ab) 6-12 weeks after contamination

13 Clinical manifestations (2): Acute symptomatic early period CD4 T-Ly cells / mm 3 ; AIDS associated complex: weakness, sweating, loss of appetite, diarrhea, weight loss, oral candidiasis, herpes zoster, frequent bacterial infections

14 Clinical manifestations (3): Acute symptomatic late period (AIDS) CD4 T Ly < 200 /mm 3; Oportunists: Pneumocystis Carinii pneimonia; Candida esophagitis, tuberculosis; AIDS dementia, CMV, other Malignant neoplasms: Kaposi's sarcoma, cervical cancer, etc.

15 HIV Contamination risk: by blood transfusions 99,9% through a needle puncture 0.33% transmucosally 0.09% through the intact skin 0%

16 The risk of infection increases, if: a deep injury; the syringe or object - visible blood; the needle is in a blood vessel; a lot of blood, a large contact area; infected material s high HIV viral load.

17 Thank you for your attention!

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