AIDSTeaching tool Dr.T.V.Rao MD                 2
UnderstandingHIV Infection
Beginning of HIV/AIDS The first published article related to  AIDS was in 1981. The principal  author’s name was Michael ...
Discovery of HIV infection. In 1982, the term Acquired Immune Deficiency  Syndrome is used for the first time. The name  ...
Learn about: HIV                 Viral load The immune          Why some people  system               with HIV are wel...
History of HIV The HIV virus first came to light  during the early 1980’s. A number of healthy gay men in New  York bega...
Dr. Luc Montagnier wins theNobel Prize in Medicine in 2008             Dr.T.V.Rao MD        8
What is Human Immune          Deficiency Virus Genus Reoviridae Lentivirus, which literally means  slow virus - it takes...
What is Human Immune Deficiency             Virus These contain RNA, the genetic  material of HIV The outer layer of the...
HIV is a Virus.      H: Human       I:Immunodeficiency       V: Virus
Our immune system is attacked       in HIV infection
HIV Origins Research teams in the U.S.A & France  made independent research discoveries of  the virus. French researcher...
Origin of AIDS; Controversial,        similar to SIV
Dr.T.V.Rao MD   15
Family : Retroviridae          Subfamily : Lentivirus RNA virus, 120nm in  diameter Envelope gp160; gp120 &  gp41 Icosa...
Retroviral Genes gag (group-specific antigen): makes the  cone shape viral capsid. pol (polymerase): codes for viral enz...
Genes Coding Structural Proteins             gag                      1 The gag gene –                       core and she...
Envelop glycoproteins              env The env determines the synthesizes  of envelop glycoproteins gp160  cleaved into t...
Polymerase reverse transcriptase                pol The pol gene codes  for the polymerase  reverse transcriptase  and ot...
   Genome and Proteins of HIV              Dr.T.V.Rao MD   21
Other genes Tat  The Tran activator gene influences the function of genes  some distance away. It controls transactivatio...
Genes differ HIV I for HIV II vpu The virus protein U gene is required for  efficient viral replication and release. It ...
Types of HIV    Dr.T.V.Rao MD   24
Dr.T.V.Rao MD   25
Subtype C is Major type in India Subtype C is  predominant in  Southern and East  Africa, India and  Nepal. It has caused...
Resistance The virus are inactivated in 10 minutes at 600c and in  seconds at 1000c At room temperature survive for seve...
HIV Replication   Attachment   Penetration   Uncoating   Reverse Transcription   Integration   Replication   Assemb...
Life Cycle of HIV1. Attachment: Virus binds to surface  molecule (CD4) of T helper cells and  macrophages.   Coreceptors:...
HIV Life Cycle: Attachment Requires  CD4 Receptor plus a Coreceptor              Dr.T.V.Rao MD           30
The HIV receptor Gp160 is composed of gp41 and gp120 and forms  the receptor for binding to the host cell (CD4  positive...
CD 4 Cells are Vital for Immunity The        virus gets attached
CD4 cells CD4 cell are  destroyed after  HIV uses them to  make more HIV. The body’s  immune system  works hard  making ...
Lifecycle of HIV   HIV particles enter the body in a fluid as it can not    survive without a support medium.   The vir...
Life Cycle of HIV3. ReverseTranscription: Viral RNA is converted into DNA by unique enzyme reverse transcriptase.         ...
Blood and Body fluids contain High  concentration of Viral particles Blood Semen/Vaginal  fluids (as high  as blood) Br...
HIV can be transmitted from one person to another by:
Dr.T.V.Rao MD   38
Low concentrations of HIV  It is highly unlikely you will be  infected if you come into contact  with: Sweat Tears Urin...
High Risk Populations:1. Males, homosexuals & bisexuals2. IV drug users3. Improperly screened transfusion    recipients4. ...
How is HIV Spread? ANY type of sexual activity (highest risk) Sharing used drug needles Pregnancy-from mother to child...
How is HIV not spread? Shaking hands Hugging Swimming pools Toilet seats Insect bites Donating blood              Dr...
HIV in Body FluidsBlood            Semen18,000                    Vaginal            11,000                           Flui...
Transmission Vaginal Intercourse Anal Intercourse (10x higher infection rate than  vaginal intercourse because of tissue...
Window Period This is the period of  time after becoming  infected when an HIV  test is negative 90 percent of cases  te...
Infection spread throughout the               Body Within the inflammatory cells of the infection (T  cells) Site of rep...
Low CD4 cells
Effects of HIV on the immune           system3 areas:1. Destruction of CD4+ T cells population2. Immune effects due to HIV...
.Host’s immune responses Both humoral and cell-mediated immune  responses partially control the viral  production but in ...
Pathogenesis of HIV / AIDS     Infected T-CellHIV                HIV Infected   New HIV        T-Cell       T-Cell        ...
 Immune responses fail to eradicate all viruses.     Viral load is maintained at low level      Continuous decline of C...
Immune defects due to HIV infection B cells – impaired humoral response B-cell hyper reactivity Polyclonal hypergammagl...
Immune defects due to HIV         infection Lymph nodes HIV kills cells in the lymph nodes Early HIV infection: destruc...
CDC Classification of HIV Category 1: > 500 cells/mm3 (or  CD4% > 28%) Category 2: 200-499 cells/mm3 (or CD4%  14% - 28...
Progression of HIV infection After initial infection with  HIV, there is usually an                                      ...
Stage 1 - Primary Short, flu-like illness -  occurs one to six weeks  after infection no symptoms at all Infected perso...
Stage 2 - Asymptomatic Lasts for an average of ten years This stage is free from symptoms There may be swollen glands ...
Stage 3 - Symptomatic The symptoms are mild The immune system deteriorates Emergence of opportunistic  infections and c...
Stage 4 - HIV  AIDS The immune  system  weakens The illnesses  become more  severe leading  to an AIDS  diagnosis      ...
Progression to AIDS During the latency period, lymph nodes and the spleen are  sites of continuous HIV replication and ce...
Progression to AIDS Final stage of HIV infection - AIDS Occurs when the destruction of peripheral lymphoid tissue  is co...
Opportunistic Infections
Mother-to-Baby Before Birth During Birth Postpartum  After the birth                 Dr.T.V.Rao MD   63
Measuring CD4 cells
Adult CD4 counts
WHO clinical case definition for     AIDS in South-East Asia WHO clinical case definition for AIDS in  South-East Asia  C...
THE NATIONAL HIV TESTING POLICY No individual should be made to undergo a  mandatory testing for HIV No mandatory HIV te...
Counseling   Dr.T.V.Rao MD   68
Pre-test Counseling explain to              individuals Transmission Prevention Risk Factors Voluntary &  Confidential...
Post-test Counseling Clarifies test  results Need for  additional testing Promotion of  safe behavior Release of  resu...
Diagnosis ofHIV and AIDS
Three types of tests                  - ELISA and(i) Screening tests simple/rapid tests.(ii) Confirmatory or supplemental ...
Diagnosis of HIV Initial test for HIV is an indirect ELISA test Economic, rapid, performed easily, high  sensitivity and...
HIV Testing                                           EIA/ELISA                                              Test         ...
Diagnosis of HIV Positive or indeterminate ELISA tests for anti-  HIV antibodies are confirmed by immunoblotting  (Wester...
Indirect ELISA test       Dr.T.V.Rao MD   76
Absence of Antibodies to do notconfirm absence of HIV infection Absence of antibody, as in ‘window period’  does not excl...
Antibodies signal infection Antibodies are special proteins in the  blood made by the immune system to fight  a specific ...
Western blot Test Confirms HIV infection Proteins are separated by electrophoresis  and transferred to a nitrocellulose ...
Western Blotting A discrete protein band represents the  specific antigen that the antibody recognizes The bands from a ...
HIV Western blot      Dr.T.V.Rao MD   81
Viral load test The amount of HIV in an infected patient’s  blood can be measured. It is called the  viral load. The vir...
Understanding  viral load LOW viral load  is less than  10,000 copies. HIGH viral load  is more than  10,000 copies.
Rapid Tests ADVANTAGES: quicker to perform   do not require batching   do    not     require    specialised    equipme...
The „Window period‟              Aware of itFollows acute infection with HIV, before HIV antibodies can be detected in the...
Paediatric HIV TestingInfants born to HIV infected mothers will have antibodies to HIV in their serum as a result of:  ma...
Treatment of HIV Eradication of HIV infection not possible with currently  available drugs Viral replication can not be ...
Measuring CD4 cells
Normal CD4 Counts in Children               Normal CD4 counts in                children vary widely by                ag...
Early stages of HIV Infection         ©2002 Boehringer Ingelheim GmbH             ©2002 Boehringer Ingelheim GmbH         ...
Viral load and CD4 cells Eventually, the immune system  is unable to make enough CD4  cells to replace the ones killed  b...
WHO HIV clinical stages
AIDSA Acquired—not  inheritedI Immuno—attacks  the immune systemD Deficiency—  destroys CD4 cellsS Syndrome—a group  of sy...
HIV is NOT transmitted by:
Section 2    Understanding Antiretroviral Therapy
What is antiretroviral therapy?
“Classes”ofARV therapy    NRTIs    NNRTIs    PIs    Fls
Learn about: Highly active antiretroviral therapy  (HAART) How HAART works Adherence Resistance Side effects Why HAA...
Treatment of HIV Eradication of HIV infection not possible with currently  available drugs Viral replication can not be ...
Antiretroviral Drugs Significant declines in AIDS related morbidity and mortality are   seen as a result of HAART Severa...
AIDS (Pregnancy & AIDS) Zidovudine(AZT) – recommended for px of  maternal fetal HIV transmission & administered  after 14...
Antiretroviral Drugs Nucleoside Reverse Transcriptase  inhibitors   AZT (Zidovudine) Non-Nucleoside Transcriptase  inhi...
Goals of ARV therapy           Lower the amount            of HIV in the blood           Save CD4 cells            and a...
HAART
When to start ARVsGuidelines vary from one country to another
Missed dosesIf dosesare missed,medicinesmay ceaseto beeffective.
Adherence Doctors, nurses,  counsellors,  family and  friends  provide  support for  taking medicines.
Monitoring treatment
Side effects Most side effects  are mild and  temporary, but  others are more  serious. If side effects  occur—talk to y...
Treatment failure Missed doses Viral resistance Medicines not taken due to side  effects Other medicines interfere Ad...
Prevention and control of HIV   Education   Prevention of blood born HIV transmission   Anti Retro Viral treatment   C...
For antiretroviral therapy      (ART) to succeed… Keep all clinic appointments so clinicians can  check your health In b...
For ART to succeed… If vomiting occurs fewer than 30 minutes  after taking a dose, repeat the dose. If the  repeat dose i...
HIV Occupational Exposure Review facility policy and report the incident Medical follow-up is necessary to determine  th...
HIV Non-Occupational          Exposure        PREVENTION --- FIRST   No data exists on the efficacy of antiretroviral    ...
Play safe Use the  common sense   Be faithful to  one partner,  Use Condom. Antiretroviral  drugs Caesarean    Dr.T.V.R...
Abstinence It is the only 100 %  effective method of  not acquiring  HIV/AIDS. Refraining from  sexual contact:  oral, a...
Monogamous relationship A mutually monogamous (only one sex partner)  relationship with a person who is not infected  wit...
Sex Education – Best option to Prevent                AIDS      Move from Past to Future                Dr.T.V.Rao MD     ...
World AIDS Day, World AIDS Day, observed December 1  each year, is dedicated to raising  awareness of the AIDS pandemic c...
Do not Discriminate AIDS        Patients         Dr.T.V.Rao MD     121
 Programme Created byDr.T.V.Rao MD for Medical and   Paramedical Students in      Developing World              Email   ...
AIDS Teaching Module
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AIDS Teaching Module

  1. 1. AIDSTeaching tool Dr.T.V.Rao MD 2
  2. 2. UnderstandingHIV Infection
  3. 3. Beginning of HIV/AIDS The first published article related to AIDS was in 1981. The principal author’s name was Michael Gottlieb and it appeared in the Morbidity and Mortality Weekly Report for June 5th. This article reported that there was a random increase in pneumocystis carinii pneumonia (PCP), a rare lung infection. Dr.T.V.Rao MD 4
  4. 4. Discovery of HIV infection. In 1982, the term Acquired Immune Deficiency Syndrome is used for the first time. The name was designated by the CDC. In 1983, French scientists at the Institute Pasteur found a new virus that they called lymphadenopathy-associated virus or LAV. About a year later, Dr. Robert Gallo, of the National Cancer institute discovered HLTV-III. The first discovery was made in France at the Institute Pasteur, but shared credit is given to Dr. Robert Gallo, the discoverer of AIDS and his French counterparts for discovering HIV on April Dr.T.V.Rao MD 5 23, 1984.
  5. 5. Learn about: HIV  Viral load The immune  Why some people system with HIV are well and others are CD4 cells very sick Checking how the  How you get HIV immune system is working
  6. 6. History of HIV The HIV virus first came to light during the early 1980’s. A number of healthy gay men in New York began to develop rare opportunistic infections & cancers, that were resistant to treatment. One such viral opportunistic infection is cytomegalovirus that causes blindness & inflammation of the colon Dr.T.V.Rao MD 7
  7. 7. Dr. Luc Montagnier wins theNobel Prize in Medicine in 2008 Dr.T.V.Rao MD 8
  8. 8. What is Human Immune Deficiency Virus Genus Reoviridae Lentivirus, which literally means slow virus - it takes such a long time to develop adverse effects in the body. This virus attacks the immune system There are two strains – HIV 1 & HIV 2 Dr.T.V.Rao MD 9
  9. 9. What is Human Immune Deficiency Virus These contain RNA, the genetic material of HIV The outer layer of the HIV virus cell is covered in coat proteins, which can bind to certain WBCs. This allows the virus to enter the cell, where it alters the DNA. The virus infects and destroys the CD4 lymphocytes which are critical to the body‟s immune response. Dr.T.V.Rao MD 10
  10. 10. HIV is a Virus. H: Human I:Immunodeficiency V: Virus
  11. 11. Our immune system is attacked in HIV infection
  12. 12. HIV Origins Research teams in the U.S.A & France made independent research discoveries of the virus. French researchers discovered a virus linked to AIDS in 1983, they called it Lymphadenopathy-Associated Virus (LAV) In 1984, American researchers isolated a virus that caused AIDS, calling it Human T-lymph tropic Virus type III (HTLV- III ) These two viruses were later found to be the same virus - HIV Dr.T.V.Rao MD 13
  13. 13. Origin of AIDS; Controversial, similar to SIV
  14. 14. Dr.T.V.Rao MD 15
  15. 15. Family : Retroviridae Subfamily : Lentivirus RNA virus, 120nm in diameter Envelope gp160; gp120 & gp41 Icosahedral symmetry Nucelocapsid  Outer matrix protein (p17)  Major capsid protein (p24)  Nuclear protein (p7) Diploid RNA with several copies of reverse transcriptase Dr.T.V.Rao MD 16
  16. 16. Retroviral Genes gag (group-specific antigen): makes the cone shape viral capsid. pol (polymerase): codes for viral enzymes reverse transcriptase, integrase, and viral protease. env (envelope): makes surface protein gp120 and trans membrane gp41, enabling HIV to fuse to CD4 cells. Dr.T.V.Rao MD 17
  17. 17. Genes Coding Structural Proteins gag  1 The gag gene – core and shell expressed as p55 – ( p18,- p17) cleaved as p15, p18,and p24 make up as viral core and shell  p24 seen during early stages reappearance in the late stages exacerbation of disease Dr.T.V.Rao MD 18
  18. 18. Envelop glycoproteins env The env determines the synthesizes of envelop glycoproteins gp160 cleaved into two envelop components gp120 which forms the surface spike and gp 41 which trans membrane protein. The gp120 antibodies are present till the death of the patient. Dr.T.V.Rao MD 19
  19. 19. Polymerase reverse transcriptase pol The pol gene codes for the polymerase reverse transcriptase and other viral enzymes Expressed as precursor protein which is cleaved into proteins p31, p51,and p66 Dr.T.V.Rao MD 20
  20. 20.  Genome and Proteins of HIV Dr.T.V.Rao MD 21
  21. 21. Other genes Tat The Tran activator gene influences the function of genes some distance away. It controls transactivation of all HIV proteins. rev The differential regulator of expression of virus protein genes. vif The virus infectivity factor gene is required for infectivity as cell-free virus. nef The negative regulator factor retards HIV replication. vpr The virus protein R gene has an undetermined function.. Dr.T.V.Rao MD 22
  22. 22. Genes differ HIV I for HIV II vpu The virus protein U gene is required for efficient viral replication and release. It is found only in HIV-1. vpx The virus protein X gene has an undetermined function. It is found only in HIV-2 and SIV. Dr.T.V.Rao MD 23
  23. 23. Types of HIV Dr.T.V.Rao MD 24
  24. 24. Dr.T.V.Rao MD 25
  25. 25. Subtype C is Major type in India Subtype C is predominant in Southern and East Africa, India and Nepal. It has caused the worlds worst HIV epidemics and is responsible for around half of all infections. Dr.T.V.Rao MD 26
  26. 26. Resistance The virus are inactivated in 10 minutes at 600c and in seconds at 1000c At room temperature survive for seven days HIV are inactivated in 10 minutes by treatment with 50% ethanol 35% Isopropanol. 0.5% Lysol and paraformaldehyde 0.3% hydrogen 10% house hold bleach Hypochlorite solution at 0.5% 2% Glutaraldehyde Dr.T.V.Rao MD 27
  27. 27. HIV Replication Attachment Penetration Uncoating Reverse Transcription Integration Replication Assembly Release Dr.T.V.Rao MD 28
  28. 28. Life Cycle of HIV1. Attachment: Virus binds to surface molecule (CD4) of T helper cells and macrophages.  Coreceptors: Required for HIV infection.  CXCR4 and CCR5 mutants are resistant to infection.2. Fusion: Viral envelope fuses with cell membrane, releasing contents into the cell. Dr.T.V.Rao MD 29
  29. 29. HIV Life Cycle: Attachment Requires CD4 Receptor plus a Coreceptor Dr.T.V.Rao MD 30
  30. 30. The HIV receptor Gp160 is composed of gp41 and gp120 and forms the receptor for binding to the host cell (CD4 positive cells). The gp41 portion is half embedded in the membrane envelope and interacts with gp120 portion on the exterior side of the membrane. Each receptor is composed of 3 subunits of gp41 and 3 subunits of gp120. Dr.T.V.Rao MD 31
  31. 31. CD 4 Cells are Vital for Immunity The virus gets attached
  32. 32. CD4 cells CD4 cell are destroyed after HIV uses them to make more HIV. The body’s immune system works hard making more CD4 cells. ©2002 Boehringer Ingelheim GmbH
  33. 33. Lifecycle of HIV HIV particles enter the body in a fluid as it can not survive without a support medium. The virus targets any cell expressing CD4, including T helper cells, macrophages, dendritic cells and monocytes. Dr.T.V.Rao MD 34
  34. 34. Life Cycle of HIV3. ReverseTranscription: Viral RNA is converted into DNA by unique enzyme reverse transcriptase. Reverse transcriptase RNA ---------------------> DNA Reverse transcriptase is the target of several HIV drugs: AZT, ddI, and ddC. Dr.T.V.Rao MD 35
  35. 35. Blood and Body fluids contain High concentration of Viral particles Blood Semen/Vaginal fluids (as high as blood) Breast milk Pus from sores Dr.T.V.Rao MD 36
  36. 36. HIV can be transmitted from one person to another by:
  37. 37. Dr.T.V.Rao MD 38
  38. 38. Low concentrations of HIV It is highly unlikely you will be infected if you come into contact with: Sweat Tears Urine Saliva (-highly possible if blood from mouth sores is present) Dr.T.V.Rao MD 39
  39. 39. High Risk Populations:1. Males, homosexuals & bisexuals2. IV drug users3. Improperly screened transfusion recipients4. Sexual partners of persons infected with HIV5. Infants of HIV –infected mothers Dr.T.V.Rao MD 40
  40. 40. How is HIV Spread? ANY type of sexual activity (highest risk) Sharing used drug needles Pregnancy-from mother to child Sharing razors- if blood is present Kissing- if even the smallest amount of blood is present. (-membranes of mouth are thin enough for HIV to enter straight into the body.) Tattoos/body piercing if equipment is not clean. Dr.T.V.Rao MD 41
  41. 41. How is HIV not spread? Shaking hands Hugging Swimming pools Toilet seats Insect bites Donating blood Dr.T.V.Rao MD 42
  42. 42. HIV in Body FluidsBlood Semen18,000 Vaginal 11,000 Fluid Amniotic 7,000 Fluid 4,000 Saliva 1Average number of HIV particles MD 1 ml of these body fluids Dr.T.V.Rao in 43
  43. 43. Transmission Vaginal Intercourse Anal Intercourse (10x higher infection rate than vaginal intercourse because of tissue tear is higher Oral Intercourse Blood Transfusion (risk greater than 90% if sample is already infected) Needles (tattoos, injections) Infected mother to the infant through: Pregnancy (placenta), Birth, and breastfeeding Dr.T.V.Rao MD 44
  44. 44. Window Period This is the period of time after becoming infected when an HIV test is negative 90 percent of cases test positive within three months of exposure 10 percent of cases test positive within three to six months of exposure Dr.T.V.Rao MD 45
  45. 45. Infection spread throughout the Body Within the inflammatory cells of the infection (T cells) Site of replication shifts to lymphoid tissues: Lymph nodes Spleen Liver Bone marrow Macrophages and Langerhans cells become reservoirs and sites of replication but do not die themselves. Dr.T.V.Rao MD 46
  46. 46. Low CD4 cells
  47. 47. Effects of HIV on the immune system3 areas:1. Destruction of CD4+ T cells population2. Immune effects due to HIV infection3. Progression of HIV infection to AIDS Dr.T.V.Rao MD 48
  48. 48. .Host’s immune responses Both humoral and cell-mediated immune responses partially control the viral production but in this process they destroy the infected CD4+T cells, leading to a gradual decline of CD4+ T cells HIV-specific CTLs kill infected CD4+ T cells Antibodies that recognize a variety of HIV antigens are produced - Antibody dependent cell-mediated cytotoxicity Apoptosis of infected cells Dr.T.V.Rao MD 49
  49. 49. Pathogenesis of HIV / AIDS Infected T-CellHIV HIV Infected New HIV T-Cell T-Cell VirusVirus Dr.T.V.Rao MD 50
  50. 50.  Immune responses fail to eradicate all viruses.  Viral load is maintained at low level  Continuous decline of CD4+ T cells Dr.T.V.Rao MD 51
  51. 51. Immune defects due to HIV infection B cells – impaired humoral response B-cell hyper reactivity Polyclonal hypergammaglobulinemia due to enhanced nonspecific IgG and IgA production. Impaired Ab-isotype switching and inability to respond to specific antigen. High incidence of B-cell lymphomas
  52. 52. Immune defects due to HIV infection Lymph nodes HIV kills cells in the lymph nodes Early HIV infection: destruction of dendritic cells Late stage: extensive damage, tissue necrosis, a loss of follicular dendritic cells and germinal centres. An inability to trap Ag or support activation of T+B cells
  53. 53. CDC Classification of HIV Category 1: > 500 cells/mm3 (or CD4% > 28%) Category 2: 200-499 cells/mm3 (or CD4% 14% - 28%) Category 3: < 200 cells/mm3 (or CD4% < 14%)(CD4+ T-lymphocyte counts per microliter of blood) Dr.T.V.Rao MD 54
  54. 54. Progression of HIV infection After initial infection with HIV, there is usually an Progression of HIV infection acute flu-like illness. Exposure to HIV This illness may include normal Acute HIV disease Fever Headache Clinical latency period Tiredness Slightly Immune competence reduced -declining CD4+ T cell amount Enlarged lymph nodes But after this most Abnormal AIDS individuals are clinically asymptomatic for years. This is called the clinical Opportunistic infections latency period. Severely impaired Time Dr.T.V.Rao MD 55
  55. 55. Stage 1 - Primary Short, flu-like illness - occurs one to six weeks after infection no symptoms at all Infected person can infect other people Dr.T.V.Rao MD 56
  56. 56. 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 Dr.T.V.Rao MD 57
  57. 57. Stage 3 - Symptomatic The symptoms are mild The immune system deteriorates Emergence of opportunistic infections and cancers Dr.T.V.Rao MD 58
  58. 58. Stage 4 - HIV  AIDS The immune system weakens The illnesses become more severe leading to an AIDS diagnosis Dr.T.V.Rao MD 59
  59. 59. Progression to AIDS During the latency period, lymph nodes and the spleen are sites of continuous HIV replication and cell destruction. The immune system remains competent at handling most infections with opportunistic microbes but the number of CD4+ T cells steadily declines.Symptoms often experienced months to years before the onset of AIDS. Lack of energy Weight loss Frequent fevers and sweats Persistent or frequent yeast infections Persistent skin rashes Dysfunction of CNS Dr.T.V.Rao MD 60
  60. 60. Progression to AIDS Final stage of HIV infection - AIDS Occurs when the destruction of peripheral lymphoid tissue is complete and the blood CD4+ T cell count drops below 200 cells/mm3. (Healthy adults usually have CD4+ T-cell counts of 1,000 or more). AIDS – acquired immunodeficiency syndrome – is marked by development of various opportunistic infections and malignancies. The level of virus in the blood and CD4+ T cell count can predict the risk of developing AIDS. Voral titers often accelerate as the patient progresses towards AIDS. Without treatment, at least 50% of people infected with HIV will develop AIDS within ten years. Dr.T.V.Rao MD 61
  61. 61. Opportunistic Infections
  62. 62. Mother-to-Baby Before Birth During Birth Postpartum  After the birth Dr.T.V.Rao MD 63
  63. 63. Measuring CD4 cells
  64. 64. Adult CD4 counts
  65. 65. WHO clinical case definition for AIDS in South-East Asia WHO clinical case definition for AIDS in South-East Asia Clinical AIDS in an adult is defined as an individual who has been identified as meeting the two criteria A and B below: A. Positive test for HIV infection by two tests based on preferably two different antigens. B. Any one of the following criteria: - Weight loss of 10% body weight or cachexia, not known to be due to a condition unrelated to HIV infection - Chronic diarrhoea of one months duration, intermittent or constant Dr.T.V.Rao MD 66
  66. 66. THE NATIONAL HIV TESTING POLICY No individual should be made to undergo a mandatory testing for HIV No mandatory HIV testing should be imposed as a precondition for - Employment - Providing health care services and facilities Any HIV testing must be accompanied by a pretest and posttest counseling services (through VCTC) Testing without consent – hindrance to the control of the epidemic Dr.T.V.Rao MD 67
  67. 67. Counseling Dr.T.V.Rao MD 68
  68. 68. Pre-test Counseling explain to individuals Transmission Prevention Risk Factors Voluntary & Confidential Report ability of Positive Test Dr.T.V.Rao MD 69 Results
  69. 69. Post-test Counseling Clarifies test results Need for additional testing Promotion of safe behavior Release of results Dr.T.V.Rao MD 70
  70. 70. Diagnosis ofHIV and AIDS
  71. 71. Three types of tests - ELISA and(i) Screening tests simple/rapid tests.(ii) Confirmatory or supplemental tests- Western Blot assay.(iii) Nucleic acid and antigen screening tests. Polymerase chain reaction (PCR), Ligase chain reaction (LCR), Nucleic acid based Sequence assays (NASBA) and some ELISA tests. Dr.T.V.Rao MD 72
  72. 72. Diagnosis of HIV Initial test for HIV is an indirect ELISA test Economic, rapid, performed easily, high sensitivity and specificity Detects anti-HIV antibodies in patient serum Antibodies are generally detectable within 3 months of infection Antibodies are typically directed at the envelope glycoproteins (gp120 and gp41) Dr.T.V.Rao MD 73
  73. 73. HIV Testing EIA/ELISA Test Negative PositiveNo HIV Exposure HIV Exposure Repeat Low Risk High Risk Positive Negative Repeat ELISA Run IFA Every 3 months Positive Confirmation for 1 year Repeat every 6 months for continued Indeterminate Negative Positive High risk behavior Repeat at Repeat at End Testing Negative 3 weeks 2-4 months HIV Dr.T.V.Rao MD 74 +
  74. 74. Diagnosis of HIV Positive or indeterminate ELISA tests for anti- HIV antibodies are confirmed by immunoblotting (Western Blotting) which identifies specific HIV virus proteins PCR can also be used Detects pro-viral DNA or viral RNA It is highly sensitive and specific but is more costly than ELISA Can be used to test infants born to HIV-infected mothers Dr.T.V.Rao MD 75
  75. 75. Indirect ELISA test Dr.T.V.Rao MD 76
  76. 76. Absence of Antibodies to do notconfirm absence of HIV infection Absence of antibody, as in ‘window period’ does not exclude the presence of the virus which can be detected by PCR amplification approx. ten days after infection ‘Window period’ – time between infection and detection of serological viral marker Direct ELISA for p24 antigen can also be used although the false negative rate is higher Dr.T.V.Rao MD 77
  77. 77. Antibodies signal infection Antibodies are special proteins in the blood made by the immune system to fight a specific infection. People with HIV usually develop HIV antibodies 4–6 weeks after being infected. In some cases, it may take as long as 3 months for antibodies to develop. To find out if a person has been infected with the virus, an HIV test is done that finds and measures antibodies in blood.
  78. 78. Western blot Test Confirms HIV infection Proteins are separated by electrophoresis and transferred to a nitrocellulose membrane by the passage of an electric current The proteins are treated with antibodies Similar to ELISA technique, addition of secondary antibodies with an enzyme attached allows the use of colour to detect a particular protein Dr.T.V.Rao MD 79
  79. 79. Western Blotting A discrete protein band represents the specific antigen that the antibody recognizes The bands from a positive Western blot are from antibodies binding to specific proteins and glycoproteins from the HIV virus The CDC recommends that the blot should be positive for two of the p24, gp41 and gp120/160 markers (gp160 is the precursor form of gp41 and gp120, the envelope protein) Dr.T.V.Rao MD 80
  80. 80. HIV Western blot Dr.T.V.Rao MD 81
  81. 81. Viral load test The amount of HIV in an infected patient’s blood can be measured. It is called the viral load. The viral load test shows how much virus is present in the body.
  82. 82. Understanding viral load LOW viral load is less than 10,000 copies. HIGH viral load is more than 10,000 copies.
  83. 83. Rapid Tests ADVANTAGES: quicker to perform  do not require batching  do not require specialised equipment or trained personnel  results delivered on the same day Only ‘WHO recommended’ Rapid HIV antibody tests should be used to ensure quality. Dr.T.V.Rao MD 84
  84. 84. The „Window period‟ Aware of itFollows acute infection with HIV, before HIV antibodies can be detected in the patient’s blood stream. Patient is highly infectious, despite testing HIV antibody negative, HIV is replicating rapidly in all body compartments. Typically up to 12 weeks duration but may be shorter in more sensitive HIV antibody assays. Dr.T.V.Rao MD 85
  85. 85. Paediatric HIV TestingInfants born to HIV infected mothers will have antibodies to HIV in their serum as a result of:  maternal-fetal transfer during pregnancy  delivery  breast-feedingthey may not necessarily be infected ! Dr.T.V.Rao MD 86
  86. 86. Treatment of HIV Eradication of HIV infection not possible with currently available drugs Viral replication can not be completely suppressed Latently infected CD4+ T cells established at early stage Goals of antiretroviral therapy are to: - Suppress viral replication - Restore and/or preserve immune function - Improve quality of life - Reduce HIV-associated morbidity and mortality Combinations of antiretroviral drugs are used Referred to as HAART (highly active antiretroviral therapy) Suppress levels of plasma viraemia for long periods Plasma viraemia is a strong prognostic factor in HIV infection Dr.T.V.Rao MD 87
  87. 87. Measuring CD4 cells
  88. 88. Normal CD4 Counts in Children  Normal CD4 counts in children vary widely by age.  In children less than 5 years of age, instead of measuring the number of CD4 cells,CD4 percentage (%) is used to determine how much damage has been done to the immune system
  89. 89. Early stages of HIV Infection ©2002 Boehringer Ingelheim GmbH ©2002 Boehringer Ingelheim GmbH  HIV uses parts of the CD4 HIV enters the cell cell to make more virus (replicate). During this process the CD4 cell is destroyed.
  90. 90. Viral load and CD4 cells Eventually, the immune system is unable to make enough CD4 cells to replace the ones killed by HIV. The immune system gets weaker and disease symptoms may develop (symptomatic HIV infection). As the viral load goes up, the number of CD4 cells goes down.
  91. 91. WHO HIV clinical stages
  92. 92. AIDSA Acquired—not inheritedI Immuno—attacks the immune systemD Deficiency— destroys CD4 cellsS Syndrome—a group of symptoms or illnesses
  93. 93. HIV is NOT transmitted by:
  94. 94. Section 2 Understanding Antiretroviral Therapy
  95. 95. What is antiretroviral therapy?
  96. 96. “Classes”ofARV therapy  NRTIs  NNRTIs  PIs  Fls
  97. 97. Learn about: Highly active antiretroviral therapy (HAART) How HAART works Adherence Resistance Side effects Why HAART sometimes doesn’t work well
  98. 98. Treatment of HIV Eradication of HIV infection not possible with currently available drugs Viral replication can not be completely suppressed Latently infected CD4+ T cells established at early stage Goals of antiretroviral therapy are to: - Suppress viral replication - Restore and/or preserve immune function - Improve quality of life - Reduce HIV-associated morbidity and mortality Combinations of antiretroviral drugs are used Referred to as HAART (highly active antiretroviral therapy) Suppress levels of plasma viraemia for long periods Plasma viraemia is a strong prognostic factor in HIV infection Dr.T.V.Rao MD 99
  99. 99. Antiretroviral Drugs Significant declines in AIDS related morbidity and mortality are seen as a result of HAART Several strategies for development of effective antiviral drugs Potential therapies based on knowledge of the way in which HIV gains access into the cells and its method of replication Targets for therapeutic anti-retroviral drugs:- Inhibiting reverse transcription- Inhibiting proteases- Inhibiting integrate – interferes with integration of viral DNA into host genome- Inhibiting fusion – prevents virus from fusing with host cell Dr.T.V.Rao MD 100
  100. 100. AIDS (Pregnancy & AIDS) Zidovudine(AZT) – recommended for px of maternal fetal HIV transmission & administered after 14 months AOG (PO meds); IVIT during labor;/ neonate post birth for 6 wks. Restrict breastfeeding –infant/neonate is seen by physician at birth, 1 wk. or 2 wks., a mos., 2 mos., & 4 mos. of life* Neonate- asymptomatic for 1st several yrs. Of life & monitored for early sign of immunodeficiency Dr.T.V.Rao MD 101
  101. 101. Antiretroviral Drugs Nucleoside Reverse Transcriptase inhibitors  AZT (Zidovudine) Non-Nucleoside Transcriptase inhibitors  Viramune (Nevirapine) Protease inhibitors  Norvir (Ritonavir) Dr.T.V.Rao MD 102
  102. 102. Goals of ARV therapy  Lower the amount of HIV in the blood  Save CD4 cells and allow the immune system to recover
  103. 103. HAART
  104. 104. When to start ARVsGuidelines vary from one country to another
  105. 105. Missed dosesIf dosesare missed,medicinesmay ceaseto beeffective.
  106. 106. Adherence Doctors, nurses, counsellors, family and friends provide support for taking medicines.
  107. 107. Monitoring treatment
  108. 108. Side effects Most side effects are mild and temporary, but others are more serious. If side effects occur—talk to your clinician.
  109. 109. Treatment failure Missed doses Viral resistance Medicines not taken due to side effects Other medicines interfere Advanced HIV disease
  110. 110. 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 Dr.T.V.Rao MD 111
  111. 111. For antiretroviral therapy (ART) to succeed… Keep all clinic appointments so clinicians can check your health In between appointments, report any changes in health right away. If a dose of an ARV medicine is missed, take the missed dose as soon as possible. But if it is close to the time when the next dose will be taken, don’t take the dose you missed, Two doses should never be taken at the same time.
  112. 112. For ART to succeed… If vomiting occurs fewer than 30 minutes after taking a dose, repeat the dose. If the repeat dose is vomited, contact the clinician. If side effects occur, discuss them with the clinician. Do not stop taking ARV medicines, and do not start any new medicine or home remedy without first discussing changes with the clinician.
  113. 113. 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 Dr.T.V.Rao MD 114
  114. 114. HIV Non-Occupational Exposure PREVENTION --- FIRST No data exists on the efficacy of antiretroviral medication after non-occupational exposures The health care provider and patient may decide to use antiretroviral therapy after weighing the risks and benefits Antiretroviral should not be used for those with low-risk transmissions or exposures occurring more than 72 hours after exposure Dr.T.V.Rao MD 115
  115. 115. Play safe Use the common sense Be faithful to one partner, Use Condom. Antiretroviral drugs Caesarean Dr.T.V.Rao MD 116 delivery
  116. 116. Abstinence It is the only 100 % effective method of not acquiring HIV/AIDS. Refraining from sexual contact: oral, anal, or vaginal. Refraining from intravenous drug Dr.T.V.Rao MD 117
  117. 117. Monogamous relationship A mutually monogamous (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 Dr.T.V.Rao MD 118
  118. 118. Sex Education – Best option to Prevent AIDS Move from Past to Future Dr.T.V.Rao MD 119
  119. 119. World AIDS Day, World AIDS Day, observed December 1 each year, is dedicated to raising awareness of the AIDS pandemic caused by the spread of HIV infection. It is common to hold memorials to honour persons who have died from HIV/AIDS on this day. Government and health officials also observe the event, often with speeches or forums on the AIDS topics. Dr.T.V.Rao MD 120
  120. 120. Do not Discriminate AIDS Patients Dr.T.V.Rao MD 121
  121. 121.  Programme Created byDr.T.V.Rao MD for Medical and Paramedical Students in Developing World  Email  doctortvrao@gmail.com
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