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AIDS
Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV) which impairs the immune system. HIV specifically targets CD4+ T cells (helper T cells). The virus can be transmitted through bodily fluids like blood, semen, vaginal fluids. The natural course of HIV infection progresses from primary infection with flu-like symptoms, to asymptomatic latency period that can last 10 years, to symptomatic stage as the immune system deteriorates, and finally AIDS when opportunistic infections take hold. While there is no cure for HIV/AIDS, antiretroviral treatment can control the virus and prevent transmission.
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AIDS
- 1. Acquired Immunodeficiency Syndrome G Vijay Narasimha Asst.Professor, Dept.of. Pharmacology Sri Padmavathi school of Pharmacy
- 2. Immunodeficiencies •Due to impairedfunction of one or more components of the immune or inflammatory responses. •Problem may be with: •B cells • T cells • phagocytes •or complement
- 3. Immunodeficiency's may be: •Congenital(primary) •Caused by a genetic or developmental abnormality of the immune system. Ex: Reticular dysgenesis- Failure to develop primitive reticular cells Ataxia telangiectasia- Defective T-cell maturation
- 4. •Acquired (secondary) –more common •Normal physiologic changes – aging •Severe malnutrition or selective deficiency Ex: Infections- AIDS, Protozoal infections, Tuberculosis Cancer Autoimmune diseases- RA, DM Transplant cases- Due to immunosuppressive therapy
- 5. Main cause isdisruption of lymphocyte function Stem cell defect : Prevent normal lymphocyte development and tota failure of immune system Lymphoid organ dysfunction: prevents maturation of B or T cells or final maturation of B cells = lack of specific class of immunoglobulin's
- 6.
- 7. WHAT IS HIV?? •“Human Immunodeficiency Virus” • A unique type of virus (a retrovirus) • Invades the helper T cells (CD4 cells) in the body of the host (defense mechanism of a person) • Threatening a global epidemic. • Preventable, managable but not curable.
- 8. OTHER NAMES FORHIV • Former names of the virus include: • Human T cell lymphotrophic virus (HTLV-III) • Lymphadenopathy associated virus (LAV) • AIDS associated retrovirus (ARV)
- 9. AIDS = AcquiredImmune Deficiency Syndrome Acquired - because it's a condition one must acquire or get infected with, not something transmitted through the genes Immune - because it affects the body's immune system, the part of the body which usually works to fight off germs such as bacteria and viruses Deficiency - because it makes the immune system deficient Syndrome - because someone with AIDS may experience a wide range of different diseases and opportunistic infections
- 10. History • Probably arosein central Africa before 1931 • Believed to be a monkey virus mutated to affect humans • Found Ab’s against HIV in serum samples taken in 1960’s • First cases reported 1980’s in male homosexuals
- 11. ESCALATING EPIDEMIC !!! Source:WHO/UNAIDS/UN The Millennium Development Goals Report, 2009, p.32 and WHO.
- 12. Specific Immune Response Pathogenesisand Natural Course of the 12
- 13.
- 15. “THE VIRAL GENOME” •Icosahedral(20 sided), enveloped virus of the lentivirus subfamily of retroviruses. •Retroviruses transcribe RNA to DNA. Two viral strands of RNA found in core surrounded by protein outer coat. Outer envelope contains a lipid matrix within which specific viral glycoproteins are imbedded. These knob-like structures responsible for binding to target cell.
- 16. Characteristics of HIV •Classification • Family of retroviruses (RNA -> DNA -> RNA) • Subfamily of lente (slow) viruses • Cytopathic to cells that replicate it • Infects many cells types and is latent in some cells • Infects and depletes CD4 lymphocytes • Causes cell-mediated immunosuppression Pathogenesis and Natural Course of the 16
- 17. HIV Strains • HIV-1Group M (main), the cause of the AIDS epidemic • HIV-2, a less virulent retrovirus causing an epidemic in West Africa Pathogenesis and Natural Course of the 17
- 18. Characteristics of HIV •HIV infect cells that express CD4 receptor molecules • CD-4 receptor molecules are expressed by T-helper cells and monocyte-macrophage cell lines • Successful entry of the virus to a target cell also requires cellular co- receptors Pathogenesis and Natural Course of the 18
- 19. Characteristics of HIV •A fusion co-receptor is designated CXCR4 for T-cell tropic stain and CCR4 for monocyte-macrophage tropic strains • The receptor and co-receptors of CD4 cells interact with HIV’s gp-120 and gp-41 proteins during entry into a cell Pathogenesis and Natural Course of the 19
- 20. HIV and CellularReceptors Pathogenesis and Natural Course of the 20 HIV ReceptorsHIV Receptors Levy JA, NEJM, 335(20); 1528-1530
- 21. CCR5 Receptors C-C chemokinereceptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines, by which T cells are attracted to specific tissue and organ targets. Many forms of HIV, the virus that causes AIDS, initially use CCR5 to enter and infect host cells. CCR5 is predominantly expressed on T cells, macrophages, dendritic cells and microglia. It is likely that CCR5 plays a role in inflammatory responses to infection, though its exact role in normal immune function is unclear.
- 22. CXCR-4 Receptor C-X-C chemokinereceptor type 4 (CXCR-4) also known as fusin or CD184 (cluster of differentiation 184) is a protein that in humans is encoded by the CXCR4 gene. CXCR4 is one of several chemokine receptors that HIV can use to infect CD4+ T cells.
- 23. Role of ChemokineReceptors in HIV Entry Host Cell Membrane Fusion Via CXCR4
- 24. Pathogenesis and Natural Courseof the 24
- 25. Pathogenesis and Natural Courseof the 25
- 26. Pathogenesis and Natural Courseof the 26
- 28.
- 29. Pathogenesis and Natural Courseof the 29
- 31. Pathogenesis • Retrovirus –RNA plus reverse transcriptase, integrase and protease • Attachment: Binds to CD4 receptors (TH) and chemokine receptors gp 120 or gp 41 • Internalization – RNA enters the cell • Reverse transcriptase converts RNA →DNA • Integrase inserts viral DNA into Host DNA
- 32. • Viral DNAis transcribed into mRNA • mRNA is translated into protein – polyprotein • Cleavage of polyprotein into usable proteins •HIV assembled under cell membrane and budded from cell • Host cell is killed as viruses are released •Proteases convert immature to infectious HIV • BUT helper T cells are replaced and viruses are killed, but CD4 cells decrease over time.
- 33. Proviral DNA Unintegrated,integrated Activated CD4+ T cell Inactive CD4+ Tcell Budding of viral particles, syncytia formation Latent Phase
- 35. HIV Life Cycle:Latent versus Active Infection in Macrophages
- 38.
- 39.
- 40. Through Bodily Fluids •Blood products • Semen • Vaginal fluids
- 41. IntraVenous Drug Abuse •SharingNeedles • Without sterilization Increases the chances of contracting HIV • Unsterilized blades
- 42. Through Sex • UnprotectedIntercourse • Oral • Anal
- 43. Mother-to-Baby • Before Birth •During Birth
- 44.
- 45. NATURAL COURSE OFHIV/AIDS
- 46. Stage 1 -Primary • Short, flu-like illness - occurs one to six weeks after infection • Mild symptoms • Infected person can infect other people
- 47. Stage 2 -Asymptomatic • Lasts for an average of ten years • This stage is free from symptoms • There may be swollen glands • The level of HIV in the blood drops to low levels • HIV antibodies are detectable in the blood
- 48. Stage 3 -Symptomatic • The immune system deteriorates • Opportunistic infections and cancers start to appear.
- 49. Stage 4 -HIV AIDS • The immune system weakens too much as CD4 cells decrease in number.
- 50. Opportunistic Infections associatedwith AIDS •Bacterial •Tuberculosis (TB) •Strep pneumonia •Viral •Kaposi Sarcoma •Herpes •Influenza (flu)
- 51. Opportunistic Infections associatedwith AIDS •Parasitic •Pneumocystis carinii •Fungal •Candida •Cryptococcus
- 52. TB & HIVCO-INFECTION • TB is the most common opportunistic infection in HIV and the first cause of mortality in HIV infected patients (10-30%) • 10 million patients co-infected in the world. • Immunosuppression induced by HIV modifies the clinical presentation of TB : 1. Subnormal clinical and roentgen presentation 2. High rate of MDR/XDR 3. High rate of treatment failure and relapse (5% vs < 1% in HIV)
- 54.
- 55. Anonymous Testing • Noname is used • Unique identifying number • Results issued only to test recipient 23659874515 Anonymous
- 56. Blood Detection Tests HIVenzyme-linked immunosorbent assay (ELISA) Screening test for HIV Sensitivity > 99.9% Western blot Confirmatory test Speicificity > 99.9% (when combined with ELIZA) HIV rapid antibody test Screening test for HIV Simple to perform Absolute CD4 lymphocyte count Predictor of HIV progression Risk of opportunistic infections and AIDS when <200 HIV viral load tests Best test for diagnosis of acute HIV infection Correlates with disease progression and response to HAART
- 57. Urine Testing • UrineWestern Blot • As sensitive as testing blood • Safe way to screen for HIV • Can cause false positives in certain people at high risk for HIV
- 58. Oral Testing • Orasure •The only FDA approved HIV antibody. • As accurate as blood testing • Draws blood-derived fluids from the gum tissue. • NOT A SALIVA TEST!
- 59. PRIMARY PREVENTION: Five waysto protect yourself? • Abstinence • Monogamous Relationship • Protected Sex • Sterile needles • New shaving/cutting blades
- 60. Abstinence • It isthe most effective method of not acquiring HIV/AIDS. • Refraining from unprotected sex: oral, anal, or vaginal. • Refraining from intravenous drug use
- 61. Monogamous relationship •A mutuallymonogamous (only one sex partner) relationship with a person who is not infected with HIV •HIV testing before intercourse is necessary to prove your partner is not infected
- 62. Protected Sex • Usecondoms every time you have sex • Always use latex or polyurethane condom (not a natural skin condom) • Always use a latex barrier during oral sex
- 63. WHAT WE CANDO?? UNAIDS Outcome Framework 2009–2011: nine priority areas • We can reduce sexual transmission of HIV. • We can prevent mothers from dying and babies from becoming infected with HIV. • We can ensure that people living with HIV receive treatment. • We can prevent people living with HIV from dying of tuberculosis. • We can protect drug users from becoming infected with HIV. • We can remove punitive laws, policies, practices, stigma and discrimination that • block effective responses to AIDS. • We can stop violence against women and girls. • We can empower young people to protect themselves from HIV. • We can enhance social protection for people affected by HIV.
- 64.
Editor's Notes
- #10 Due to the fact that AIDS is so prevalent in the US, it’s important to understand how it works and its impact on nutrition status So what does AIDS stand for – it stands for the acquired immune deficiency syndrome It is acquired because . . .
- #13 CD-4 cells remain as memory cells after infection is controlled. CD-8 cells transform themselves into cytotoxic T-cells. B-cells change to IG-secreting plasma cells.
- #17 HIV belongs to a family of HIV retroviruses that possess the reverse transcriptase enzyme. This enzyme enables the RNA virus to transform itself to DNA provirus and integrate itself into the nucleus of the activated T-cell lymphocyte. The virus is cytopathic to the T-cells that replicate or produce new HIV virus. The death and depletion of these infected T-cells cause immunosuppression. HIV can infect other cell types and remain latent in these cells, thus providing a reservoir of HIV. Once HIV infects a cell, it is part of the cell for life.
- #19 Viruses need a receptor on a cell surface in order to attach themselves and get access to inside of a cell. In order for a cell to be infected by HIV, there must be CD4 receptor molecules present. These receptors occur on CD4 cells and on other cells in the monocyte-macrophage cell lines. Once HIV attaches, there also needs to be a cellular co-receptor to facilitate entry into the CD4 cell (or other cell).
- #20 Fusion co-receptor CXCR5 or CCR4 is needed for entry. In some people with naturally occurring genetic defects at this cellular level, HIV infection can be prevented or lessened. For most, however, this co-receptor allows HIV to enter the CD4 cell (or other cell). The gp-120 and gp-41 (glycoprotein layer that we saw on the diagram of the AIDS virus) are needed for entry into the CD4 cell (or other cell).
- #21 This diagram illustrates the HIV virus’s attachment and entry into a host cell. The gp-120 protein attaches itself to a CD4 receptor. Then the gp-41 is exteriorized for attachment to the host cell, and the process of fusion starts. These glycoproteins form the connection and bridge, facilitating the attachment and entry of HIV into the CD4 (or other) cell.
- #24 This slide illustrates the way the HIV virus uses its gp-41 and gp-120 to attach to the receptors for these epitopes on the surface of the CD4 cell. Note in a figure A how the glycoproteins line up perfectly to the receptors. In figures B and C the attachment occurs. With the aid of the fusion domain and CCR5 and CXCR4, the entry to the CD4 cell starts in picture D. Entry into the CD4 cell is completed in picture E. This results in an infected CD4 cell that will be used to manufacture the HIV virus, resulting in the death of the CD4 cell itself.
- #25 This photomicrograph shows how the HIV viral particle attaches to the surface of the CD4 cell. Pictured on the right are the CD4 receptors vulnerable to attachment by the glycoproteins on the HIV viral surface. On the left you see the virus attaching to the receptors on the CD4 cell as “a perfect fit.” The chemokine co-receptors, CCR5 and CXR4, assist in the fusion or entry of the virus into the CD4 cell.
- #26 This photomicrograph illustrates the HIV virus after it has entered the CD4 cell. At this time, the virus is uncoated, and its viral RNA is exposed and converted to DNA. The process of reverse transciptase takes place within 4 to 6 hours of infection.
- #27 The final products of reverse transcriptase are double-stranded molecules. It is during this process that the backbone ARV drugs work the nucleosides, nucleotides and non nucleoside ARV. A new class of ARV called integrase inhibitors is under development and may be available in the future. Following entry the reverse transcription complex is formed. This pre-integration complex contains the newly made viral DNA and several HIV proteins: The matrix protein p17 Integrase Reverse transcriptase Viral protein R (vpr)
- #28 These double-stranded DNA are transported to the nucleus of the CD4 cell, where the HIV viral DNA is integrated into to DNA of the CD4 cell. The final product’s provirus remains a part of the CD4 genetic material until the death of the cell.
- #29 The primary transcripts of the provirus are made by the CD4 RNA and are spliced and made ready for assembly. Transcription starts and is completed with full-length transcripts that are spliced and translated.
- #30 Assembly occurs when the gag proteins put together viral proteins and CD4 cells into mature viral particles. The assembly takes place at the cell membranes, making possible the release of the viral particle. It is during these final steps of assembly and maturation that the potent ARV protease inhibitors are effective. Without the interruption of this final step, the newly released infectious virus will proceed to infect new CD4 cells.
- #40 Multiple infection : HIV Superinfection is a condition in which a person with established human immunodeficiency virus infection acquires a second strain of the virus.[1] The second strain may cause more rapid disease progression or carry resistance to medicines. As of 2005 there were 16 cases reported in the worldwide literature.[1] People who have HIV are at risk for superinfection if they continue to share needles (if they are injecting drug users) or do not use condoms with other HIV-positive sexual partners
- #64 Vulnerable and High-risk Groups: -Expand knowledge, access, and coverage of vulnerable populations—particularly in large cities—to a package of high impact services, through combined efforts of the government and NGOs. -Implement harm-reduction initiatives for IDUs and safe sex practices for CSWs. -Make effective and affordable STD services available for high-risk groups and the general population. General Awareness and Behavioral Change: -Undertake behavioral change communications with the following behavioral objectives: (i) use of condoms with non-regular sexual partners; (ii) use of STI treatment services when symptoms are present and knowledge of the link between STIs and HIV; (iii) use of sterile syringes for all injections; (iv) reduction in the number of injections received; (v) voluntary blood donation (particularly among the age group 18 to 30); (vi) use of blood for transfusion only if it has been screened for HIV; and (vii) display of tolerant and caring behaviors towards people living with HIV/AIDS and members of vulnerable populations. -Increase interventions among youth, police, soldiers, and migrant laborers. Blood and Blood Product Safety: -Ensure mandatory screening of blood and blood products in the public and private sectors for all major blood-borne infections. -Conduct education campaigns to promote voluntary blood donation -Develop Quality Assurance Systems for public and private blood banks to ensure that all blood is properly screened for HIV and Hepatitis B. Surveillance and Research: -Strengthen and expand the surveillance and monitoring system. -Implement a second-generation HIV surveillance that tracks sero-prevalence and changes in HIV-related behaviors, including the spread of STIs and HIV, sexual attitudes and behaviors, and healthcare-seeking behaviors related to STIs. Building Management Capacity -Continue to build management capacity within provincial programs and local NGOs to ensure evidence-based program implementation. -Identify gaps in existing programs and continue phased expansion of interventions.