Human inmunodefinciency virus


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Human inmunodefinciency virus

  1. 1. 4 José Aurelio Beltrán V. José Manuel Yépiz Carrillo José Luis Martínez Pérez Paul Enrique López UNIVERSIDAD DE SONORA Licenciatura en Medicina
  2. 2. Human immunodeficiency virus (HIV) is a blood-borne virus typically transmitted via sexual intercourse, shared intravenous drug , and mother-to-child transmission (MTCT), which can occur during the birth process or during breastfeeding. HIV disease is caused by infection with HIV-1 or HIV- 2, which are retroviruses in the Retroviridae family, Lentivirus genus.
  3. 3. 1981 Centers for Disease Control and Prevention (CDC) Unexplained appearance Pneumocystis Carinii, 1983 virus was isolated from patients with lymph nodes. 1984 It was found that the virus was the responsible agent of AIDS. 1985 development of a test that allowed realizing the scope and evolution of the epidemic infection.
  4. 4. Studies in the U.S. have identified five high-risk groups, distribution by cases: • Homosexuality or bisexuality 50% of reported cases. • IV Drug without history of homosexuality 20% • Hemophiliacs, before 1985, 0.5% • Blood transfusion, hemophiliacs, 1% • Heterosexual contact, 10%
  5. 5. "Extensive studies indicate that HIV infection cannot be transmitted by personal contact. The spread by insect bites is impossible "
  6. 6. HIV disease is caused by infection with HIV-1 or HIV-2, both of which cause very similar conditions. They differ in transmission and progression risks. Human Retrovirus Family not transforming Lentivirus subfamily. Two genetically distinct forms: - HIV-1 (USA, Europe, Central Africa) - HIV-2 (West Africa, India)
  7. 7. MorphologyStructures: • It’s a spherical particle of 0.1 microns • The viral core (or capsid): is usually conical or bullet-shaped and is made from the protein p24. • The viral envelope (or membrane): it's a lipid envelope derived from host cell membrane that surrounding the core. • The matrix: It´s just below the viral envelope, which is made from the protein p17 that cover the capsid directly. Human Immunodeficiency Virus.
  8. 8. MorphologyComponents: Inside the core • p24: major capsid protein. (viral antigen easier to detect) • p7/p9: nucleocapsid protein. • RNA genome, two copies. • Viral enzymes (protease, reverse transcriptase and integrase) On the membrane • Around 72 membrane complexes composed of… • gp120 and gp41: glycoproteins that protrude viral coat. That help HIV to enter the cell. Human Immunodeficiency Virus.
  9. 9. Viral Genetic gag. - Proteins of the capsid, RNA and matrix. pol. - reverse transcriptase, protease and Integrase. env. - surface membrane and transmembrane proteins. Structural genes: contain information needed to make structural proteins for new virus particles. HIV has just nine genes (compared to more than 500 genes in a bacterium, and around 20,000-25,000 in a human HIV is a retrovirus of the lentivirus subgroup.
  10. 10. Viral Genetic Accessory genes: General functions: 1) Code for proteins that control the ability of HIV to infect a cell 2) Produce new copies of virus 3) Cause disease How do they do? Synthesis and assembly product transactivators Efect: increase 1000 times viral gene transcription
  11. 11. Viral Genetic Vif.- Encodes a protein associated to virus infectivity Tat.- Transactivator gene of proteins Rev.- Regulator gene of the proteic exprecion viral Nef.- Negative regulator (not proved ) Vpr.- Accelerator of cycle gene transcription and protein synthesis Vpu.- Increases speeds of release virions (HIV-1 only) Accessory genes:
  12. 12. Viral Genetic At either end of each strand of RNA is a sequence called the long terminal repeat, which helps to control HIV replication. Grouped into regions of the envelope glycoproteins, that is, in the env gene Subgroups M, O and N. Subtypes of Subgroup M are named as A - K. Genomic variability
  13. 13. membrane proteins. Core and matrix structure proteins.
  14. 14. Pathogeny of HIV infection Severe loss of CD4 + T lymphocytes (helpers), macrophages and dendritic cells. • Main Targets: Immune System and CNS.
  15. 15. Pathogeny of HIV infection • HIV enters the body through mucosal tissues and blood. • Infection is established in lymphoid tissues where it can remain dormant for an extended period.
  16. 16. Cycle of the HIV HIV can only replicate by invading the host cells , mainly CD4 T lymphocytes begins with the union of the membrane surface protein gp120 with the CD4 receptor of T helper lymphocytes (also present in macrophages and dendritic cells ) . There is a conformational change in gp120 , allowing it to bind to receptors CXCR4 and CCR5 on the cell under attack. Finally, gp41 contributes to the union of the membranes. Cycle of the HIV
  17. 17. Viral RNA is released into the host cell The reverse transcriptase catalyzing transcript of viral RNA to DNA Viral DNA enters the nucleus and is bound to the cell chromosomes by integrase preferentially in areas of major genetic expression. Cell's DNA polymerase initiates transcription of proviral DNA integrated into the DNA of the cell , yielding a mRNA Following transcription , the HIV mRNA is translated into proteins which are modified by glycosylation, myristylation, phosphorylation and cleavage . The viral particle is formed by the assembly of proteins , enzymes and HIV genomic RNA in the membrane of the cell which formed the outer casing of immature viron . Protease ( coded by the virus before ) catalyzes the cleavage of gag-pol precursor to yield the mature virion Cycle of the HIV
  18. 18. Cytotoxic T lymphocytes.- HIV antigens induce exprecion of cytokines such as IFN-y and lysis of infected cells Proliferative cellular response.- Viral antigens induce the proliferation of CD8 cytotoxic lymphocytes and NK After the first viral outbreak in primary infection, it's produces a solid immune response that determines the slow development that characterize to HIV infection. Immune response to HIVCellular
  19. 19. Neutralizing antibodies.- Are produced against structural proteins gag gene (bases of diagnosis), preventing binding of HIV to CD4 cells Antibody dependent cellular cytotoxicity.- When a phagocyte in contact with an infected cell or HIV, opsonized; released cytokines that collaborate in defense against infection Humoral Immune response to HIV
  20. 20. immune response to HIV
  21. 21. Clinical manifestations • The clinical consequences of HIV infection encompass a spectrum ranging from an acute syndrome associated with primary infection to a prolonged asymptomatic state to advanced disease. It is best to regard HIV disease as beginning at the time of primary infection and progressing through various stages.
  22. 22. The Acute HIV Syndrome • It is estimated that 50–70% of individuals with HIV infection experience an acute clinical syndrome 3–6 weeks after primary infection Opportunistic infections have been reported during this stage of infection, reflecting the immunodeficiency that results from reduced numbers of CD4+ T cells and likely also from the dysfunction of CD4+ T cells
  23. 23. Clinical findings in Acute HIV Syndrome Generals Especifics -Fever -Meningitis -Pharyngitis -Encefalitis -Lymphadenopaty - Peripheral neuropathy - Headache /retroorbital pain - Myelopathy - Arthralgias / myalgias - Erythematous maculopapular rash -Anorexia - Mucocutaneous ulceration - Nausea/ vomiting / diarrhea
  24. 24. The Asymptomatic Stage (Latency) • Although the length of time from initial infection to the development of clinical disease varies greatly, the median time for untreated patients is 10 years. • The rate of disease progression is directly correlated with HIV RNA levels • Patients with high levels of HIV RNA in plasma progress to symptomatic disease faster than do patients with low levels of HIV RNA • During the asymptomatic period of HIV infection, the average rate of CD4+ T cell decline is 50/µL per year. When the CD4+ T cell count falls to <200/µL, the resulting state of immunodeficiency is severe enough to place the patient at high risk for opportunistic infection and neoplasms and, hence, for clinically apparent disease.
  25. 25. Symptomatic Disease • Symptoms of HIV disease can appear at any time during the course of HIV infection • Generally, the spectrum of illnesses that one observes changes as the CD4+ T cell count declines • The more severe and life-threatening complications of HIV infection occur in patients with CD4+ T cell counts <200/µL • Diagnosis of AIDS is made in anyone with HIV infection and a CD4+ T cell count <200/µL  Indicate defect in cell- mediated immunity
  26. 26. Diseases of respiratoy sistem Acute bronchitis and sinusitis Pulmonary disease (Pneumonia and TB) Fungal infections (coccidioides immitis and aspergillus) Neoplastic diseases (lymphoma)
  27. 27. Diseases of cardiovascular system - Myocardial infarction -Myocarditis - Pericarditis Patients with HIV infection have higher levels of triglycerides, lower levels of high-density lipoprotein cholesterol
  28. 28. Diseases of oropharinx and gastrointestinal system -Aphtous ulcers - Candida infections - Leukoplakia - Perirectal ulcers
  29. 29. Diseases of kidney and genitourinary tract - Genitourinary tract infections - Syphilis - Vulvovaginal candidiasis
  30. 30. Diseases of hematopoietic system -Lymphadenopaty -Anemia -Leukopenia - Trombocytopenia Can be the direct result of HIV, manifestations of secondary infections and neoplasms, or side effects of therapy
  31. 31. Dermatologic diseases - Folliculitis - Reactivation herpes zoster -Psoriasis -Seborrheic dermatitis
  32. 32. Neurologic diseases - Toxoplasmosis - Cryptococcosis -Trypanosomiasis - Peripheral neuropathies - Myopathy
  33. 33. Neoplastic diseases - Kaposi’s sarcoma -Lymphomas - Burkitt’s lymphoma
  34. 34. Kaposi sarcoma and VIH • It is the most common malignancy in patients with SIDA. • At the beginning of the epidemic, 30% of gay or bisexual men were infected, today declined. • Mushrooms. From fusiform smooth muscle cells. • Profusion of vascular spaces. • chronic inflammatory cell infiltrates. • affects homosexual men with AIDS 20 times more often than male patients with hemophilia and SIDA having a similar degree of immunosuppression.
  35. 35. DIAGNOSIS
  36. 36. Screening test: the presence of antibodies to HIV in serum or plasma , as evidenced by one of the following methods : • - linked immunosorbent assay ( ELISA ) • - passive agglutination . Additional Tests: presence of HIV antibodies in serum or plasma. • - blot ( Western blot test ) • - Immunofluorescence • - Radioimmunoprecipitation ( RIPA ) Additional tests to determine the presence of virus or any component • - virus culture ; • - determination of viral antigen ; • - chain reaction of the polymerase, to determine the viral RNA or proviral DNA . Detection Procedure
  37. 37. Diagnosis of infection • Detection in serum : Anti - HIV antibody ELISA test . With a sensitivity of 99.5 %. Detection of antibodies and p24 antigen are those with greater sensitivity. • Confirmation: Western Blot: timely assessment of the specific reactivity of antibodies to different viral proteins. When we do the study? • When the person claims the study. • Exposure to HIV infection • unexplained Immunosuppression • Pregnancy • Son of a mother with HIV + • Blood Donor
  38. 38. Person having two test results positive antibody screening and supplemental testing positive, including asymptomatic patients who refuse risk factors. For present two screening test results positive, but further evidence is indeterminate, should be considered as potentially infected and so be informed , recommending repeat laboratory diagnosis three months later. Person positive zero
  39. 39. Treatment a) Find a combination of highly active antiretroviral drugs that are capable of removing virtually HIV-1 replication. b) allow the immune system is reconstituted. Reverse transcriptase inhibitors : Zidovudine , Abacavir Non-Nucleoside Inhibitors of Reverse Transcriptase : Efavirenz , Nevirapine Protease Inhibitors : Saquinavir, Indinavir
  40. 40. thanks for your attention