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The most important way to stop HIV/AIDS is education. People can get HIV from sex and from blood. Children can also get HIV from their mothers (when they grow inside pregnant mothers and when they drink breast milk.) Sex is one way to get HIV. If people use condoms when they have sex, there is a much smaller chance of catching HIV.

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  2. 2. • AIDS is caused by human immunodeficiency virus• Genetically the virus has two types• HIV-1 (World wide)• HIV-2 which is less aggressive slow and restricted mainly to western Africa.
  3. 3. How it got transferred to humans• The HIV-1 actually got transfered from African green monkeys
  4. 4. How it got transferred to humans• HIV-2 got transferred from Sooty managbey monkeys or Chimpanzees
  5. 5. Natural transfer theory• Commonly held theory is that HIV got transferred through hunting and handling of chimpanzees and through slaughtering and eating “bush meat” of these (monkeys).The epidemic required urbanization and increased population mobility
  6. 6. Human error theory• Oral polio vaccine or some other injectable vaccines used enmass in West Africa during the late 1950s may have been contaminated with HIV since these vaccines were prepared by using these monkeys or their tissues in process of their preparation.
  7. 7. How HIV can be transmitted• Unprotected sexual contact – be it vaginal, oral, or anal Mucosa - with an infected partner• Contact of abraded skin or mucosa with body secretions such as blood, CSF or semen;
  8. 8. Actually making sex with Bugs
  9. 9. How HIV can be transmitted• Sharing unsterilized needles or syringes with an HIV positive person, for example, when using drugs or in a healthcare setting.• During pregnancy or birth and through breastfeeding from an HIV positive mother to her baby.• Blood transfusions with infected blood• Accidental occupational exposure
  10. 10. Populations particularly at risk• Has a sexually transmitted infections(STIs)• Has anal sex with her/his partner(s)• Exchanges sex for money or drugs• Has many sex partners• Non-circumcised
  11. 11. Populations particularly at risk• Leads life separated from spouse due to professional obligations (e.g., truck drivers, laborers, migrants)• Homosexuals/ bisexuals• Certain sexual practices increases the disease• Like sexual Contact with• Male-to-male• Female-to-female
  12. 12. How HIV can NOT be transmitted• Through air or by coughing and sneezing• Through food or water• Through sweat and tears
  13. 13. How HIV can NOT be transmitted• By sharing cups, plates, and utensils with an infected person• By touching, hugging and kissing an infected person• By sharing clothes or shaking hands with an infected person• By sharing toilets and bathrooms with an infected person• By living with an infected person• By mosquitoes, fleas, or other insects
  14. 14. How HIV can NOT be transmitted• While the virus has occasionally been found in saliva, tears, urine and bronchial secretions, transmission after contact with these secretions has not been reported.• No laboratory or epidemiological evidence suggests that biting insects have transmitted HIV infection.
  15. 15. CONCENTRATION OF VIRUS• Blood, Menstrual Blood – Very High• Vaginal Fluids, Semen, Pre ejaculate Fluid – High• Bone Marrow – High• Saliva – No• Sweat, Tears, urine - No 26
  16. 16. HIV in Body FluidsBlood Semen18,000 Vaginal 11,000 Fluid Amniotic 7,000 Fluid 4,000 Saliva 1Average number of HIV particles in 1 ml of these body fluids
  17. 17. HIV STRUCTURE• HIV belongs to a special class of viruses called retroviruses. Within this class, HIV is placed in the subgroup of lentiviruses.• Other lentiviruses include SIV, FIV, Visna and CAEV, which cause diseases in monkeys, cats, sheep and goats.• All viruses except retroviruses contain DNA
  18. 18. HIV STRUCTURE• So Retroviruses are the exception because their genes are composed of RNA (Ribonucleic Acid).• However RNA has a very similar structure to DNA with small differences
  19. 19. HIV STRUCTURE• HIV has just nine genes (compared to more than 500 genes in a bacterium• Three of the HIV genes, called gag, pol and env, contain information needed to make structural proteins for new virus particles.
  20. 20. HIV STRUCTURE• The other six genes, known as tat, rev, nef, vif, vpr and vpu, code for proteins that control the ability of HIV to infect a cell, produce new copies of virus, or cause disease.
  21. 21. HIV STRUCTURE• An HIV particle is around 100-150 billionths of a metre in diameter. Thats about the same as:• 0.1 microns• 4 millionths of an inch• one twentieth of the length of an E. coli bacterium• one seventieth of the diameter of a human CD4+ white blood cell.
  22. 22. HIV STRUCTURE• HIV particles surround themselves with a coat of fatty material known as the viral envelope .• This envelope gives out lots of little spikes around 72 in number.
  23. 23. HIV STRUCTURE• These spikes are made of knobs and handles made of proteins gp120 and gp41 respectively.
  24. 24. HIV STRUCTURE• Just below the viral envelope is a layer called the matrix, which is made from the protein p17(Matrix proteins)
  25. 25. HIV STRUCTURE• Below the matrix is another layer of proteins P24 forming viral core (or capsid) and is usually bullet- shaped.
  26. 26. HIV STRUCTURE• Inside the core are three enzymes required for HIV replication called• Reverse transcriptase• Integrase• And protease
  27. 27. HIV STRUCTURE• Also held within the core is HIVs genetic material, which consists of two identical copies of single stranded RNA.
  28. 28. The virus, entering through which ever route, acts primarily on the following cells:• * Lymphoreticular system:• o CD4+ T-Helper cells• o CD4+ Macrophages• o CD4+ Monocytes• o B-lymphocytes• *
  29. 29. The virus, entering through which ever route, acts primarily on the following cells:• Certain endothelial cells• * Central nervous system:• o Microglia of the nervous system• o Astrocytes• o Oligodendrocytes• o Neurones - indirectly by the action of cytokines and the gp-120
  30. 30. Pathogenesis• HIV binds to CD4 molecule, CD4 molecule is found on the T helper-cell Macrophages etc.Binding of CD4 is not sufficient for entry• Therefore gp120 protein also binds to co- receptor• CCR5 Co-receptor - is used by macrophages• CXCR4 Co-receptor - is used by lymphocytes
  31. 31. Pathogenesis• Binding of virus to cell surface results in fusion of viral envelope with cell membrane of T-helper cell and thus Viral core is released into cell cytoplasm• After uniting with T-helper cells the T-Helper cells through• Th1 - activate Tc (CD8) lymphocytes, promoting cell- mediated immunity• Th2 - activate B lymphocytes, promoting antibody mediated immunity
  32. 32. Pathogenesis• CD8 Cytotoxic T lymphocyte (CTL) is Critical for containment of HIV.Derived from T8 cells, recognize viral antigens and directly destroy infected cells
  33. 33. Pathogenesis• Antibodies formed bind to surface of virus to prevent attachment to target cells• Fc portion of antibody also binds to NK cells and Stimulates NK cell to destroy infected cell
  34. 34. Pathogenesis• Numerous organ systems are infected by HIV:• Brain: macrophages and glial cells• Lymph nodes and thymus: lymphocytes and dendritic cells• Blood, semen, vaginal fluids: macrophages• Bone marrow: lymphocytes• Skin: langerhans cells• Colon, duodenum, rectum: chromaffin cells• Lung: alveolar macrophages
  35. 35. Pathogenesis• About (10 billion) virions are produced daily• Average life-span of an HIV virion in plasma is ~6 hours• Average life-span of an HIV-infected CD4 lymphocytes is ~1.6 days• HIV hides in cells like CNS etc and can lie dormant within a cell for many years, especially in resting (memory) CD4 cells, unlike other retroviruses etc
  36. 36. Pathogenesis• All elements of immune system are affected. Advanced stages of HIV are associated with destruction and disruption of lymphoid tissue(T- helper cells etc) that result in• Impaired ability to mount immune response• Impaired ability to maintain memory responses• Loss of containment of HIV replication• ultimately results in severe immunosuppression susceptibility to opportunistic infections
  37. 37. HIV Life Cycle• Step 1: Attachment of virus at the CD4 receptor and chemokine co-receptors CXCR4 or CCR5
  38. 38. HIV Life Cycle• Step 2: viral fusion and uncoating
  39. 39. HIV Life Cycle• Steps 3-5: Reverse transcriptase makes a single DNA copy of the viral RNA and then makes another to form a double stranded viral DNA
  40. 40. HIV Life Cycle• Step 6: migration to nucleus
  41. 41. HIV Life Cycle• Steps 7-8: Integration of the viral DNA into cellular DNA by the enzyme integrase
  42. 42. HIV Life Cycle• Steps 9-11: Transcription and RNA processing
  43. 43. HIV Life Cycle• Steps 12-13: Protein synthesis
  44. 44. HIV Life Cycle• Step 14: protease cleaves polypeptides into functional HIV proteins and the virion assembles• Step 15: virion budding• Step 16: Virion maturation
  45. 45. HIV Life Cycle
  46. 46. Window period• The window period begins at the time of infection and can last 4 to 8 weeks.• During this period, a person is infected, infectious and viremic, with a high viral load and a negative HIV antibody test.• The point when the HIV antibody test becomes positive is called the point of seroconversion.
  47. 47. Window Period• Some times 90 percent of cases test positive within three months of exposure• 10 percent of cases test positive within three to six months of exposure
  48. 48. Four Stages of HIV
  49. 49. Stage 1 - Primary• Short, flu-like illness - occurs one to six weeks after infection• Or there may be no symptoms at all• Infected person though looking normal can infect other people
  50. 50. 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 very low levels• HIV antibodies are detectable in the blood
  51. 51. Stage 3 - Symptomatic• The symptoms are mild• The immune system deteriorates• emergence of opportunistic infections and cancers
  52. 52. Stage 4 - HIV  AIDS• The immune system weakens• The illnesses become more severe leading to an AIDS diagnosis
  53. 53. AIDS-DEFINING DISEASES• Oesophageal candidiasis• Cryptococcal meningitis• Chronic cryptosporidial diarrhoea• CMV retinitis or colitis• Chronic mucocutaneous herpes simplex• Disseminated Mycobacterium avium intracellulare• Pulmonary or extrapulmonary tuberculosis• Pneumocystis carinii (jirovecii) pneumonia
  54. 54. AIDS-DEFINING DISEASES• Progressive multifocal leucoencephalopathy• Recurrent non-typhi Salmonella septicaemia• Cerebral toxoplasmosis• Extrapulmonary coccidioidomycosis• Invasive cervical cancer• Extrapulmonary histoplasmosis• Kaposis sarcoma• Non-Hodgkin lymphoma• Primary cerebral lymphoma• HIV-associated wasting• HIV-associated dementia
  55. 55. Oral Candidiasis (thrush)
  56. 56. Opportunistic Oral Yeast Infection by Candida albicans in an AIDS Patient
  57. 57. Chronic Herpes Simplex infection with lesions on tongue and lips..
  58. 58. Oral Hairy Leukoplakia• Being that HIV reduces immunologic activity, the intraoral environment is a prime target for chronic secondary infections and inflammatory processes, including OHL, which is due to the Epstein-Barr virus under immunosuppressed conditions
  59. 59. Kaposi’s sarcoma (KS)• Kaposi’s sarcoma (shown) is a rare cancer of the blood vessels that is associated with HIV. It manifests as bluish-red oval-shaped patches that may eventually become thickened. Lesions may appear singly or in clusters.
  60. 60. Extensive tumor lesions of Kaposis sarcoma in AIDS patient.
  61. 61. Pneumocystis pneumonia• X-ray of Pneumocystis jirovecii caused pneumonia. There is increased white (opacity) in the lower lungs on both sides, characteristic of Pneumocystis pneumonia
  62. 62. Pneumocystis pneumonia• Pneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still abbreviated as PCP, which now stands for Pneumocystis pneumonia) is relatively rare in healthy, immunocompetent people, but common among HIV- infected individuals. It is caused by Pneumocystis jirovecii.
  63. 63. Non-Hodgkin’s Lymphoma & ascites in AIDS patient
  64. 64. African AIDS patient with slim disease
  65. 65. Blood Detection Tests• Enzyme-Linked Immunosorbent Assay/Enzyme Immunoassay (ELISA/EIA)• Radio Immunoprecipitation Assay/Indirect Fluorescent Antibody Assay (RIP/IFA)• Polymerase Chain Reaction (PCR)• Western Blot Confirmatory test
  66. 66. Immunologic Manifestations• Antibodies are produced to all major antigens. – First antibodies detected produced against gag proteins p24 and p55. – Followed by antibody to p51, p120 and gp41 – As disease progresses antibody levels decrease.
  67. 67. ELISA Testing• First serological test developed to detect HIV infection. – Easy to perform. – Easily adapted to batch testing. – Highly sensitive and specific.• Antibodies detected in ELISA include those directed against: p24, gp120, gp160 and gp41, detected first in infection and appear in most individuals
  68. 68. Western Blot• Most popular confirmatory test. – Utilizes a lysate prepared from HIV virus. – The lysate is electrophoresed to separate out the HIV proteins (antigens). – The paper is cut into strips and reacted with test sera. – After incubation and washing anti-antibody tagged with radioisotope or enzyme is added. – Specific bands form where antibody has reacted with different antigens. – Most critical reagent of test is purest quality HIV antigen. – The following antigens must be present: p17, p24, p31, gp41, p51, p55, p66, gp120 and gp160.
  69. 69. Western Blot• Antibodies to p24 and p55 appear earliest but decrease or become undetectable.• Antibodies to gp31, gp41, gp 120, and gp160 appear later but are present throughout all stages of the disease.
  70. 70. Western Blot• Interpretation of results. – No bands, negative. – In order to be interpreted as positive a minimum of 3 bands directed against the following antigens must be present: p24, p31, gp41 or gp120/160.• CDC criteria require 2 bands of the following: p24, gp41 or gp120/160.
  71. 71. Western Blot • Expensive – $ 80 - 100 • technically more difficult • visual interpretation • lack standardisation – - performance – - interpretation – - indeterminate reactions – resolution of ?? • ‘Gold Standard’ for confirmation
  72. 72. Virus isolation• Virus isolation can be used to definitively diagnose HIV.• Best sample is peripheral blood, but can use CSF, saliva, cervical secretions, semen, tears or material from organ biopsy.• Cell growth in culture is stimulated, amplifies number of cells releasing virus.• Cultures incubated one month, infection confirmed by detecting reverse transcriptase or p24 antigen in supernatant.
  73. 73. Urine Testing• Urine Western Blot – As sensitive as testing blood – Safe way to screen for HIV – Can cause false positives in certain people at high risk for HIV
  74. 74. Oral TestingOrasure – The only FDA approved HIV antibody. – As accurate as blood testing – Draws blood-derived fluids from the gum tissue. – NOT A SALIVA TEST!
  75. 75. Indirect immunofluorescence• Can be used to detect both virus and antibody to it.• Antibody detected by testing patient serum against antigen applied to a slide, incubated, washed and a fluorescent antibody added.• Virus is detected by fixing patient cells to slide, incubating with antibody.
  76. 76. Polymerase Chain Reaction (PCR)• Looks for HIV DNA in the WBCs of a person.• PCR amplifies tiny quantities of the HIV DNA present, each cycle of PCR results in doubling of the DNA sequences present.• The DNA is detected by using radioactive or biotinylated probes.• Once DNA is amplified it is placed on nitrocellulose paper and allowed to react with a radiolabeled probe, a single stranded DNA fragment unique to HIV, which will hybridize with the patient’s HIV DNA if present.• Radioactivity is determined.
  77. 77. Virus isolation• Virus isolation can be used to definitively diagnose HIV.• Best sample is peripheral blood, but can use CSF, saliva, cervical secretions, semen, tears or material from organ biopsy.• Cell growth in culture is stimulated, amplifies number of cells releasing virus.• Cultures incubated one month, infection confirmed by detecting reverse transcriptase or p24 antigen in supernatant.
  78. 78. Viral Load Tests• Viral load or viral burden is the quantity of HIV-RNA that is in the blood.• RNA is the genetic material of HIV that contains information to make more virus.
  79. 79. Viral Load Tests• Viral load tests measure the amount of HIV-RNA in one milliliter of blood.• Take 2 measurements 2-3 weeks apart to determine baseline.• Repeat every 3-6 months in conjunction with CD4 counts to monitor viral load ant T-cell count.• Repeat 4-6 weeks after starting or changing antiretroviral therapy to determine effect on viral load.
  80. 80. Testing of Neonates• Difficult due to presence of maternal IgG antibodies.• Use tests to detect IgM or IgA antibodies, IgM lacks sensitivity, IgA more promising.• Measurement of p24 antigen.• PCR testing may be helpful but still not detecting antigen soon enough: 38 days to 6 months to be positive.
  81. 81. INVESTIGATIONS UNDER DIFFERENT CONDITIONSTo all:CD4 count and Viral loadHepatitis B and C AbHIVResistant TestCervical Smear in womenHep A IgG AntibodyToxoplasma AbCytomegalovirus Ig G AbTreponema SerologyGenitourinary Medicine Screen
  82. 82. INVESTIGATIONS UNDER DIFFERENT CONDITIONSFor CD4 < 200/mm3• CXR• HCV-RNA• Cryptococcal Ag• Stool for Ova ,cyst and parasites.For CD4 < 100/mm3• CMV –PCR• Dilated Fundoscopy• Electroencephalogram(EEG)• Mycobacterial Blood Culture
  83. 83. Who Should be Treated• HIV ELISA positive, confirmed with Western blot• HIV RNA >55,000 copies/ml• CD4 <350 cells/mm3• Special considerations: – Pregnant women – Acute HIV infection – Exposed healthcare workers
  84. 84. Who Should be Treated• Viral load is an indication of the amount of virus in the bloodstream in HIV infection• The viral load can also serve as a means to identify when HAART should be started. HAART is commenced when the CD4 cell count is less than 350 cells/mm3, sometimes as low as 200 cells/mm3.
  85. 85. Who Should be Treated• Considering starting HAART based on the viral load, however, is not as simple and many doctors may advise patients on HAART with a viral anywhere between 10,000 to 30,000 copies/mL
  86. 86. Who Should be Treated• A viral load exceeding 10,000 copies is considered to be high. A viral load below 500 copies/mL is considered as low. However, a level below 500 copies/mL is a good indication that viral replication has drastically slow or ceased.
  87. 87. Who Should be Treated• An undetectable viral load is reported when the level drops to below 50 copies/ milliliter. This does not mean that the virus has been eradicated from the bloodstream or that the patient is “cured”.
  88. 88. Who Should be Treated• The viral RNA may just be below the threshold and cannot be detected. Eventually the viral load will rise again and regular monitoring even with an undetectable viral load is therefore essential. The aim of treatment is to maintain the viral load at undetectable levels as long as possible.
  89. 89. Who Should be Treated• When the CD4 count drops below 200 due to advanced HIV disease, a person is diagnosed with AIDS. A normal range for CD4 cells is between 500 and 1,500.• Usually, when a person with low CD4 cells starts HIV medicines, the CD4 cell count increases as the HIV virus is controlled.
  90. 90. Who Should be Treated• The same test that measures your CD4 count usually includes a CD8 cell count, too. CD8 cells (also known as CD8+ T cells) are another type of white blood cell that seek out and destroy cells infected with viruses, including HIV-infected cells.
  91. 91. Who Should be Treated• CD8 counts in normal person are between 375 and 1100• The ratio of CD4 cells to CD8 cells is often reported. This is calculated by dividing the CD4 value by the CD8 value. In healthy people, this ratio is between 0.9 and 1.9, meaning that there are about 1 to 2 CD4 cells for every CD8 cell. In people with HIV infection, this ratio drops dramatically, meaning that there are many times more CD8 cells than CD4 cells.
  92. 92. When to start drugs to prevent opportunistic infections• when CD4 levels are:• •Less than 200: Pneumocystis pneumonia (PCP)• •Less than 100: toxoplasmosis and cryptococcosis• •Less than 75: mycobacterium avium complex (MAC).
  93. 93. Combination Therapy• Combination therapy often called HAART is standard care for people with HIV.• Monotherapy created virus resistance to the individual drug. Some combination therapies increase the time it takes for the virus to become resistant.• Combinations of a PI or NNRTI with one or two NRTI’s is often recommended.• Combination therapy may reduce individual drug toxicity by lowering the dosage of each drug
  94. 94. Treatment HAART: Highly Affective Anti-Retro Viral Therapy: Anti-retro viral therapy is recommended if:► Patient is asymptomatic/ symptomatic + CD4 count of <350/µl / any AIDS defining condition / plasma HIV RNA greater than 100,000 copies/ml HAART combines two types of antiretroviral drugs: Triple cocktail ◦ 2NRTI’S + 1PI or ◦ 2NRTI’S + 1NNRTI
  95. 95. Treatment► Entry inhibitors/Fusion inhibitors: Maraviroc, Enfuvirtide• Integrase inhibitors: Raltegravir• Maturation Inhibitors under trails: Bevirimat & vivicon
  96. 96. Treatment For needle stick: Post exposure Prophylaxis ZDV+3TC 28 days, but in high risk (high viral RNA copies) a combination of ZDV+3TC+Indinavir Pregnancy: ZDV full dose, trimester 2 and 3+ 6 weeks to neonate reduces vertical transmission by 80% ZDV restricted to intrapartum period + NEVIRAPINE- 1 dose at onset of delivery+ AZT+3TC for 1 week after delivery Neonate: 1 dose of Nevirapine within 24-72 hrs after birth + ZDV for 1 week Symptomatic tx and antibiotics/antivirals/glucocorticoids/thalidomide /antifungals/metronidazole for bacterial, viral, autoimmune, fungal and parasitic infections.
  97. 97. HAART (highly active antiretroviral therapy)• Four approved classes of drugs in the HAART regimens – Nucleoside and nucleotide reverse transcriptase inhibitors – Non-nucleoside reverse transcriptase inhibitors – Protease inhibitors – Fusion inhibitors
  98. 98. Currently Available Drugs• Nucleoside analogue reverse transcriptase inhibitors – Zidovudine – Lamivudine – Stavudine – Didanosine – Zalcitabine – Abacavir• Nucleotide … – Tenofovir
  99. 99. Currently Available Drugs• Non-nucleoside reverse transcriptase inhibitors – Nevirapine – Delavridine – Efavirenz• Fusion Inhibitors – Enfuvirtide
  100. 100. Currently Available Drugs• Protease Inhibitors • Indinavir • Nelfinavir • Ritonavir • Saquinavir soft gel • Amprenavir • Lopinavir/ritonavir • Amprenavir/ritonavir
  101. 101. What is the Best Initial Treatment• What we know – Two is better than one – Three is better than two• What we are trying to find out – Is four better than three????
  102. 102. Choice of Initial Regimen2 NRTI 1 PI2 NRTI 1 NNRTI3 NRTI 3rd NRTI is abacavir2 NRTI 1 nucleotide RTI (Tenofovir)2 NRTI 2 PI (ritonavir as booster)
  103. 103. Choice of Regimen• NNRTIs • PIs • Nevirapine (2 tab) • Indinavir (6 or 12 cap) • Efavirenz (3 cap) • Nelfinavir (10 tab) • Ritonavir (don’t even go • Delavridine (6 or there) 12) • Saquinavir soft gel (18 cap) • Amprenavir (16 cap) • Lopinavir/ritonavir (6 cap)
  104. 104. Averting Failure — Promote Adherence• HAART has increased long-term survival of patients with HIV – Before HAART, median survival: 8 to 10 years – After HAART, median survival: may be 36 years• Drug “holidays” or treatment interruptions result in rapid viral rebound within 2 to 3 weeks of treatment discontinuation• Simplification of dosing regimens to twice or once daily may improve long-term adherence
  105. 105. Summary• When to start treatment • CD4<350 • VL> 55,000• Choice of initial regimen • 3 drugs• Appropriate prophylaxis • Primary: PCP, MAC • Secondary: PCP, MAC, Toxo, candidiasis, CMV, etc.
  106. 106. Nucleoside Analogues (NA’s) or NRTI’sAbbreviated Generic Name Trade Name DoseNameAZT Zidovudine Retrovir 200 mg TID 300 mg BIDddI Didanosine Videx 200 mg BID 400 mg QDddC Zalcitibine Hivid 0.75 mg TIDd4T Stavudine Zerit 20 mg BID 40 mg BID3TC Lamivudine Epivir 150 mg BIDAZT/3TC Combivir One BIDABC Abacavir Ziagen 300 mg BIDAZT/3TC/ABC Trizivir One BID
  107. 107. Nucleotide Analogues• Tenofovir• Dose: 300 mg once daily• Take with food for optimal absorption
  108. 108. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI’s)Generic Name Trade Name Usual Dose Nevirapine Viramune 200 mg QD x14 days, then 200 mg BID Delavirdine Rescriptor 400 mg TID Efavirenz SustivaTM 600 mg QD
  109. 109. Protease Inhibitors (PI’s)Generic Name Trade Name Usual Dose Saquinavir Invirase 400 mg BID with RTV Fortovase 1200 mg TID Indinavir Crixivan 800 mg q8h Ritonavir Norvir 600 mg BID 400 mg BID with SQV Nelfinavir Viracept 750 mg TID or 1250 mg BID TM Amprenavir Agenerase 1200 mg BID TM Lopinavir/ Kaletra 400 mg lopinavir/100 mg ritonavir Ritonavir BID= 3 caps BID
  110. 110. Some Alternative Therapies• Virus adsorption inhibitors – interfere with virus binding to cell surface by shielding the positively charged sites on the gp-120 glycoprotein – Polyanionic compounds• Viral co receptor antagonists – compete for binding at the CXCR4 (X4) and CCR5 (R5) coreceptors – bicyclams and ligands
  111. 111. HIV Occupational Exposure• Review facility policy and report the incident• Medical follow-up is necessary to determine the exposure risk and course of treatment• Baseline and follow-up HIV testing• Four week course of medication initiated one to two hours after exposure• AZT (200mg)-TID +lamivudine(3TC)(150mg)BID x 4days• Nelfinavir (750 mg) TID ,AZT/3TC• Exposure precautions practiced
  112. 112. Why Does Treatment Fail?• Intolerance• Infection with a resistant virus• Malabsorption• NON-ADHERENCE TOPS THE LIST – Rates of adherence have a direct correlation with success of HAART1 – Near perfect viral suppression in DOT trials2
  113. 113. Averting Failure — Promote Adherence• HAART has increased long-term survival of patients with HIV – Before HAART, median survival: 8 to 10 years – After HAART, median survival: may be 36 years• Drug “holidays” or treatment interruptions result in rapid viral rebound within 2 to 3 weeks of treatment discontinuation• Simplification of dosing regimens to twice or once daily may improve long-term adherence
  114. 114. Prevention and control of HIV• Education• Prevention of blood born HIV transmission• Anti Retro Viral treatment• Combination therapy• Post exposure prophylaxis• Specific prophylaxis• Primary health care
  115. 115. Four ways to protect yourself?• Abstinence• Monogamous Relationship• Protected Sex• Sterile needles
  116. 116. Protected Sex• Use condoms (female or male) every time you have sex (vaginal or anal)• Always use latex or polyurethane condom (not a natural skin condom)• Always use a latex barrier during oral sex
  117. 117. When Using A Condom Remember To:• Make sure the package is not expired• Make sure to check the package for damages• Do not open the package with your teeth for risk of tearing• Never use the condom more than once• Use water-based rather than oil-based condoms
  118. 118. THANK YOU• There is no end to education. It is not that you read a book, pass an examination, and finish with education. The whole of life, from the moment you are born to the moment you die, is a process of learning.
  119. 119. Any question ? or Doubt !EMAIL AT- (