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Introduction 1

Introduction 1. HIV/AIDS. Welcome to the HIV/AIDS module You will be learning about the Human Immunodeficiency Virus (HIV) that causes the Acquired Immunodeficiency Syndrome (AIDS) . Kaposi’s sarcoma. For more information about the authors and reviewers of this module, click here.

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Introduction 1

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  1. Introduction 1 HIV/AIDS Welcome to the HIV/AIDS module You will be learning about the Human Immunodeficiency Virus (HIV) that causesthe Acquired Immunodeficiency Syndrome (AIDS) Kaposi’s sarcoma For more information about the authors and reviewers of this module, click here

  2. How to use this module • This self-directed learning (SDL) module has been designed for medical and other health care students • We suggest that you start with the learning outcomes and try to keep these in mind as you go through the module slide by slide and at your own pace. • Print-out the answer sheet.Write your answers to the questions on the mark sheet as best you can before looking at the answers. • Repeat the module until you have achieved a mark of > 10/13 (>80%). • You should research any issues that you are unsure about. Look in your textbooks, access the on-line resources indicated at the end of the module and discuss with your peers and teachers. • Finally, enjoy your learning! We hope that this module will complement your learning about Global Burden of Disease from other sources.

  3. Introduction 2 Learning Outcomes By the end of the module, you will be expected to be able to: • state the routes of HIV transmission • name the risk factors for HIV transmission • describe how HIV causes disease following infection • list the specific clinical features of HIV infection • discuss disease staging and AIDS-defining illnesses • discuss how clinical features and serology are used in diagnosis • describe how HIV is treated • describe important features of prevention programmes at the community level

  4. Epidemiology 1 What is HIV? • HIV is the causative agent of AIDS • It is an RNA virus - its genetic information is stored on a single strand of RNA instead of the double-stranded DNA found in most organisms • The RNA includes 3 genes that are essential for retroviral replication: gag, env, pol • It belongs to the retrovirus family - distinguished by the presence of an enzyme called reverse transcriptase which converts RNA into DNA. HIV reverse transcriptase is error-prone and, therefore, introduces a high mutation rate in the viral genome • There are two types of HIV: HIV-1 and HIV-2 • Both HIV-1 and HIV-2 are associated with similar opportunistic infections and AIDS • HIV-1 is much more common worldwide • HIV-2 is found predominantly in West Africa, Angola, and Mozambique

  5. Evolution of HIV epidemic 1981: CDC issues warning on a rare pneumonia in LA 2001: China’s acknowledgement Early 90s: Central & Latin America Early/mid 1990s: Asia End-1980s: Sub Saharan Africa Source: UNAIDS, 2001

  6. Epidemiology In 2008: • An estimated 33.4 million people were living with HIV • 2.7 million people acquired HIV In 2008: AIDS killed 2.0 million people. The number of people living with HIV continues to rise in every region, with the steepest increases occurring in East and Central Asia and in Eastern Europe reflecting the combined effects of continued high rates of new HIV infections and the beneficial impacts of ART • Sub-Saharan Africa remains by far the worst affected region in the world, with 22.4 million people living with HIV in 2008 • About two-thirds (67%) of all people living with HIV are in sub-Saharan Africa • More than three quarters (76%) of all women living with HIV live in sub-Saharan Africa AIDS orphans in Zambia Source: AIDS epidemic update, 2009; Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization

  7. Global epidemiology of HIV/AIDS

  8. Molecular epidemiology • HIV-1 strains can be classified into 3 groups: M (major), N (non-M) and O (outlier) • Groups N and O are limited to Cameroon and neighbouring countries • Group M is further divided into 9 subtypes (A,B,C,D,F,G,H,J and K) and several circulating recombinant forms • Subtype C is the most predominant globally and in Southern Africa • Subtype A is common in Central, West and East Africa • Subtype B in USA and Western Europe • All HIV-1 groups and subtypes have been reported in central Africa

  9. Morphology of HIV • It is icosahedral in shape • Outer envelope studded with spikes formed by envelope (gp120) and transmembrane (gp41) glycoproteins • Central core contains consist of • viral proteins (e.g. p24) • HIV RNA genome • enzymes

  10. Cell invasion and viral replication • HIV possess 3 enzymes that are essential for viral replication: • Following infection, viral envelope glycoprotein gp120 binds to receptors on the host CD4 cell, a sub-set of white blood cells • Fusion of the viral envelope with the cell membrane is mediated by gp41 • Viral core and its components are released into the host cell cytoplasm • Viral RNA is converted into DNA by the reverse transcriptase • HIV DNA enters the nucleus of the CD4+ cell and is incorporated into the host cell DNA by the viral enzyme integrase • HIV DNA then instructs the cell to make many copies of the original virus • Viral protease cleaves precursor protein gp160 into gp120 and gp41 so that new viruses can be assembled • New virus particles leave the cell, ready to infect other CD4+ cells As well as CD4+ cells, HIV also establishes infection in the CNS, lymphoid tissue and testes (“virus reservoirs”)

  11. End of Section 1 Well done! You have come to the end of the first section. We suggest that you answer Question 1 to assess your learning so far. Please remember to write your answers on the mark sheet before looking at the correct answers!

  12. Question 1: Regarding HIVWrite “T” or “F” on the answer sheet. When you have completed all 4 questions, click on the box and mark your answers Click to for the correct answer • Reverse transcriptase reliably converts the viral RNA into DNA in the host cell cytoplasm • HIV infection rates are increasing most rapidly in sub-Saharan Africa • HIV 1 subtype C is the most prevalent viral subtype • As well as CD4+ cells, primary infection of the brain occurs a b c d

  13. Transmission routes: Sexual contact: sexual intercourse (vaginal, oral or anal) Direct contact with HIV-infected body fluids such as semen, cervical and vaginal secretions Maternal-to-child transmission (MTCT): from mothers who are HIV-positive to their infants during pregnancy, labour, delivery, and breast-feeding Blood-to-blood transmission: transfusion or direct contact with HIV-infected blood HIV infection occurs in people of all ages, races and nationalities, the rich and the poor. Now that you know how HIV is transmitted, list 5 groups of people who are particularly at risk of acquiring infection. Answers on the next slide. How is HIV transmitted?

  14. Major groups at risk of HIV infection 3 Answers: Risk factors (1) • Sexually active men and women. The most common route of HIV transmission is unprotected, heterosexual intercourse. Women, especially young girls, are more likely than men to become infected due to a complex interplay between biological, socio-economic and cultural factors. Women taking oral contraceptives, which may alter the physical properties of the cervical mucosa, are at greater risk of infection. • People with multiple sexual partners • Being a prostitute or having unprotected sex with a prostitute • People who engage in unprotected anal intercourse • The infants of infected mothers • IV drug abusers: injection using contaminated needles or syringes Other important risk factors are: • Lack of circumcision: uncircumcised men probably get more prepuceal trauma during intercourse • Use of unsterilized instruments - e.g. in body piercing • HIV infection also results from sexual abuse of infants and children

  15. 60 to 75 infants will not be HIV-infected 100 infants born to HIV-infected women who breastfeed, without any interventions 25 to 40 infants will be HIV-infected About 15 infants infected during labour and delivery 5–15 infants infected during breast-feeding 5–10 infants infected during pregnancy Outcomes of infants born to women infected with HIV

  16. HIV cannot be transmitted by: • Coughing or sneezing • Being bitten by an insect • Touching or hugging • Holding a baby • Going to a public bath/pool • Using a public toilet • Shaking hands • Using telephones • Working or going to school with a person who is HIV-infected • Drinking water or preparing or eating food • Sharing cups, glasses, plates, or other utensils

  17. CD4 count When HIV multiplies, it infects and kills CD4 T cells Because of their key role in protecting against infection, the CD4 count reflects the functional state of the immune system normal count in a healthy adult = 600 - 1,200 cells/mm3 CD4 count of <200 cells/mm3 in an adult increases greatly the risk of opportunistic and serious infection Viral load Viral load is the amount of HIV in the blood It can be measured by the HIV ribonucleic acid polymerase chain reaction blood test (HIV-RNA PCR) Viral load is very high shortly after primary HIV infection It falls steeply when the body develops antibodies and rises again after a number of years as the CD4 count drops High viral load leads to higher transmission risk High viral load is a sign of more severe disease as people develop AIDS Viral load is also used to assess the response to antiretroviral (ARV) treatment Two measures of the progression of HIV infection

  18. Tests for HIV detect either antibodies or antigens associated with HIV in whole blood, saliva, or urine A person whose blood test results show HIV infection is said to be “seropositive” or “HIV-positive” A person whose blood test results do not show HIV infection is said to be “seronegative” or “HIV-negative” Seroconversion People infected with HIV usually develop antibodies 4 to 6 weeks after being infected, but it may take as long as 3 months for antibodies to develop Some people may experience a glandular fever-like illness (fever, rash, joint pains, and enlarged lymph nodes) at the time of seroconversion The period of time between when a person is infected with HIV and when the antibody test result is positive is called the "window period.“ Despite being seronegative, the person may be infectious during the window period Testing for HIV

  19. Assessing the stage of disease • There are several classification or staging systems in use • The US Centers for Disease Control and Prevention (CDC) categorizes HIV infection in adults on the basis of: • Associated clinical conditions (3 categories) • CD4+ T lymphocyte count (3 ranges) • This results in a matrix of nine mutually exclusive categories (next slide) • Using this system • Any HIV-infected individual with a CD4+ T cell count of <200/ml has AIDS (regardless of the presence of symptoms or opportunistic diseases), and • Any HIV-infected individual with an AIDS indicator (category C) condition has AIDS

  20. Clinical Categories CD4+ T cell count A Asymptomatic, acute (primary) HIV or PGL B Symptomatic, Not A or C conditions C AIDS indicator conditions >500/mL A1 B1 C1 200-499/mL A2 B2 C2 <200/mL A3 B3 C3 Persons in categories A3, B3, C1, C2, and C3 have AIDS under the 1993 surveillance CDC case definition CDC 1993 revised classification system for adolescents and adults

  21. Modified from: CDC. 1994 Revised classification system for human immunodeficiency virus infection in children less than 13 years of age Note: Sometimes absolute CD 4 cell count adjusted for age and CD 4 percentage may not fall in the same immune category. Thus, of the 2 parameters, whichever is in the lower category is taken into consideration before starting ART.

  22. AIDS-indicator conditions (1) Opportunistic infections • Candidiasis (oesophagus, bronchi, trachea, and lungs) • Coccidioidomycosis (disseminated or extrapulmonary) • Cryptococcosis, extrapulmonary • Cryptosporidiosis, chronic intestinal (>I month duration) • Cytomegalovirus disease (other than liver, spleen, or nodes) • Herpes simplex: chronic ulcer(s) (>1-month duration) or bronchitis, pneumonitis, or oesophagitis • Histoplasmosis, disseminated or extrapulmonary • Isosporiasis, chronic intestinal (> 1-month) Mycobacterium avium complex or Mycobacterium kansasii, disseminated or extrapulmonary • Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary) • Pneumocystis jiroveci pneumonia • Pneumonia, recurrent • Progressive multifocal leucoencephalopathy • Salmonella septicaemia, recurrent • Toxoplasmosis of brain An HIV positive infant with severe oral candidiasis

  23. Neoplasia Kaposi’s sarcoma Lymphoma (Burkitt’s, immunoblastic, primary in brain) Invasive cervical cancer General Wasting syndrome, HIV-related Encephalopathy, HIV-related AIDS-indicator conditions (2) Kaposi’s sarcoma

  24. WHO identifes 4 clinical stages based on the performance level of the person and the associated illnesses: Clinical stage I Asymptomatic Generalised lymphadenopathy Performance Scale 1: asymptomatic, normal activity Clinical Stage II Weight loss <10% of body weight Minor mucocutaneous manifestations (seborrhoeic dermatitis, prurigo, fungal nail infections, recurrent oral ulcerations, angular cheilitis) Herpes zoster within the last 5 years Recurrent upper respiratory tract infections (e.g., bacterial sinusitis) And/or Performance Scale 2: symptomatic, normal activity WHO staging system for HIV infection and disease in adults (1) Source: http://www.who.int/docstore/hiv/scaling/anex1.html

  25. Clinical stage III Weight loss >10% of body weight Unexplained chronic diarrhoea lasting for more than 1 month Unexplained prolonged fever (intermittent or constant) lasting for more than 1 month Oral candidiasis (thrush) Oral hairy leukoplakia Pulmonary tuberculosis Severe bacterial infections (e.g., pneumonia, pyomyositis) And/or Performance Scale 3: bedridden less than 50% of the day during the past month Clinical Stage IV HIV wasting syndrome Pneumocystis jiroveci pneumonia Toxoplasmosis of the brain Cryptosporidiosis with diarrhoea lasting more than 1 month Cryptococcosis, extrapulmonary Cytomegalovirus (CMV) disease of an organ other than liver, spleen or lymph node (e.g., retinitis) Herpes simplex virus (HSV) infection, mucocutaneous (lasting for more than 1 month), or visceral Progressive multifocal leukoencephalopathy (PML) Any disseminated endemic mycosis Candidiasis of the oesophagus, trachea, bronchi Atypical mycobacteriosis, disseminated or pulmonary Non-typhoid salmonella septicaemia Extrapulmonary tuberculosis Lymphoma Kaposi's sarcoma (KS) HIV encephalopathy And/or Performance Scale 4: bedridden more than 50% of the day during the past month WHO staging system for HIV infection and disease in adults (2) Source: http://www.who.int/docstore/hiv/scaling/anex1.html

  26. Clinical stage I Asymptomatic Generalised lymphadenopathy Clinical stage II Chronic diarrhoea lasting more than 30 days in the absence of known etiology Severe persistent or recurrent candidiasis outside the neonatal period Weight loss or failure to thrive in the absence of known etiology Persistent fever lasting longer than 30 days in the absence of known etiology Recurrent severe bacterial infections other than septicaemia or meningitis (e.g., osteomyelitis, bacterial (non-TB) pneumonia, abscesses) Clinical Stage III AIDS-defining opportunistic infections Severe failure to thrive (wasting) in the absence of known etiology Progressive encephalopathy Malignancy Recurrent septicaemia or meningitis WHO staging system for HIV infection and disease in children Testing for HIV may be indicated in malnourished children in whom a specific cause can not be identified Source: http://www.who.int/hiv/pub/guidelines/clinicalstaging.pdf

  27. Early, acute Middle chronic Final crisis The 3 phases of HIV infection The course of HIV infection can be best understood in terms of interplay between HIV and the immune system. Three phases can be recognized: Characteristic viral load (HIV RNA) and CD4 count over time

  28. 1. The early, acute phase Initial response of an immunocompetent adult to HIV infection High level of virus production and viraemia widespread viral seeding of the lymphoid tissues Approximately 100 billion new viral particles are produced every day 1-2 billion CD4+ T-cells die each day Clinically, this stage is characterized by infectious mononucleosis-like features of sore throat, myalgias, fever, weight loss, and fatigue all of which are self-limiting 2. The middle, chronic phase Relative containment of the virus and clinical latency Virus replication continues for several years, predominantly in the lymphoid tissues Immune system largely intact Clinically, patients are either asymptomatic or develop persistent generalized lymphadenopathy (PGL). Many patients have herpes zoster, oral thrush or thrombocytopaenia Phases 1, 2 and 3 • 3. The final, crisis phase • breakdown of host defense • CD4 count usually < 200 cells/mm3 • sudden and rapid viraemia • clinical disease • Clinically, the patient presents with marked weight loss, chronic diarrhoea, and fever lasting more than 1 month • Opportunistic infections (OI) occur • The clinical picture of AIDS will depend on the type of OI or cancer

  29. Acute retroviral syndome The majority of people do not show any signs of illness when they acquire HIV infection. However, some people do show the following symptoms and signs of Acute Retroviral Syndrome: • Fever • Diarrhea • Headache • Nausea/vomiting • Adenopathy • Pharyngitis (non exudative) • Rash (morbiliform, maculopapular) • Neurological (Guillain – Barre Syndrome, encephalitis, aseptic meningitis)

  30. Clinical phase 2 - Mother and child This HIV-positive mother was asymptomatic apart from shingles. The child was also seropositive and had just recovered from pneumonia (below)

  31. Tuberculous adenitis in a confirmed HIV-infected patient (with discharging abscesses on the right and suprasternal area) Opportunistic infections

  32. HIV-associated malignancy The same patient after a course of cytotoxics Kaposi’s sarcoma

  33. End of Section 2 Well done! This is the end of the second section. We suggest that you proceed to answer question 2 to assess your learning further. Do remember to write your answers on the mark sheet before looking at the right answer!

  34. Question 2: The following are recognised manifestations of Acute retroviral syndrome:Write “T” or “F” on the answer sheet. When you have completed all 5 questions, click on the box and mark your answers. Click to for the correct answer • Fever • Pharyngitis • Erythema Nodosum • Adenopathy • Constipation a b c d e

  35. Confirmation of HIV infection can be done by isolation of the virus detection of viral antigen detection of viral antibody Detection of viral antigen and virus isolation are expensive and technically demanding. Therefore, testing for antibodies to HIV in serum or plasma is the mainstay of laboratory diagnosis. In patients with suspected or confirmed HIV, a wide range of additional clinical and laboratory investigations is often indicated to detect opportunistic infections and neoplasia. Screening tests ELISA Latex agglutination Confirmatory tests Western Blot Indirect immunofluorescence antibody assay Radioimmunoprecipitation assay Supplemental tests HIV-1 culture PCR ELISA for P24 antigen Diagnosis (1)

  36. Where diagnostic facilities are limited, AIDS can be diagnosed using the WHO Clinical Case Definition in adults : AIDS defined by the existence of AT LEAST 2 major signs associated with AT LEAST 1 minor sign in the absence of known causes of immunosuppression Major signs Weight loss >10% body weight Chronic diarrhoea (lasting >1 month) Fever intermittent or constant (lasting >1 month) Minor signs Persistent cough (>1 month) Generalized pruritic dermatitis Recurrent herpes zoster Oropharyngeal candidiasis Chronic progressive and disseminated herpes virus infection Generalized lymphadenopathy Diagnosis (2)

  37. Diagnosing HIV infection and AIDS in children < 18 months • seropositive (test again after 18 months) or born to positive mother with positive HIV culture, DNA PCR Or Meets clinical criteria for AIDS And/or CD4 percentage < 20% >18 months • positive antibody tests Or Meets clinical criteria for AIDS. NB • Testing is performed in the immediate newborn period, at 1-2 months and 3-6 months of age. False negative are sometimes observed in the newborn period but the sensitivity of the test after 1 month is about 99%. If the child is being breastfed the test should be performed 3 months after cessation of breastfeeding). • The diagnosis of HIV amongst children begins with the diagnosis in the mother • In infected women, the maternal HIV antibody is passively transmitted across the • placenta to the fetus during pregnancy. • A single positive HIV-I DNA PCR test result should be interpreted with caution. Any infant with a positive result should be retested immediately.

  38. Clinical management • Management in practice • Caring for people with HIV infection is often difficult for a number of reasons: • HIV infection is incurable • the infection is associated with stigmatization and discrimination • infected individuals need to be counselled to ensure they do not transmit the disease to others • diagnosing HIV-related diseases may be problematic, as they often present with atypical clinical manifestations and may occur simultaneously, even in the same organs • unavailability of treatment for some HIV-related diseases • patients often develop serious adverse effects to drugs • the number of healthcare workers with experience in counselling and managing people with HIV is limited, particularly in Africa Goals of treatment • Clinical • Prolong survival • Prevent disease progression • Minimize drug toxicity • Virological • Maximal and durable suppression of viral load for as long as possible to below detectable levels (currently defined as <50 copies/ml) • Immunological • Preserve immune function (CD4 cell count in normal range) • Public health • Reduce HIV transmission • Preserve future treatment options

  39. Drugs from different classes are used in combination to prevent emergence of resistance to single agents Critical questions are: When to initiate therapy? What is the optimal initial therapy? When to change therapy? What are the optimal subsequent therapies? Benefits of early therapy Control of viral replication easier Prevention of immune system compromise Lower risk of resistance with complete viral suppression Possible decreased risk of HIV transmission Avoid irreversible immune system depletion Risks of early therapy Drug-related reduction in quality of life Greater cumulative drug-related adverse events Earlier development of drug resistance Limitation of future antiretroviral treatment options Antiretroviral drug treatment

  40. Entry inhibitors Nucleus RNA Protease DNA Reverse transcriptase Reverse transcriptase inhibitors Antiviral Agents Nucleoside Reverse Transcriptase Inhibitors (e.g. Zidovudine, Lamivudine, Didanosine) Non-nucleoside Reverse Transcriptase Inhibitors (e.g. Nevirapine, Efavirenz, Delavirdine) Protease inhibitors (e.g. Indinavir, Nelfinavir, Ritonavir, Saquinavir, Amprenavir, Lopinavir) Entry inhibitors (e.g. Enfuvirtide) Coreceptor antagonists (e.g. Maraviroc) Protease inhibitors

  41. Guidelines for starting HAART All patients with WHO stage 3 and 4 irrespective of CD4+ cell count CD4+ count <350/mm3 irrespective of HIV RNA level CD4+ cell count between 200-350/mm3 and HIV RNA level >20,000 copies/mL CD4+ cell count >350/mm3 and HIV RNA level >55,000 copies/mL HIV+ child aged < 12 months HIV+ children over 1 year old who are symptomatic or immunosuppressed Monitoring HAART Measure plasma HIV RNA levels Immediately prior to initiation of Rx At 2-8 weeks after Rx Repeat every 3-4 months while being on therapy In case of a clinical event or a significant decline in CD4+ T cells CD4+ T cell count at the time of diagnosis and generally every 3-6 months thereafter Criteria for treatment failure Clinical Onset of new or recurrence of opportunistic infections Onset or recurrence of WHO stage III-defining condition Immunological Return of CD4 count to pretherapy level 30% fall CD4 count from peak level during therapy Failure to achieve CD4 cell count increase of 50-100 cells per year Virological Viral load not suppressed to undetectable levels after 4-6 months of ART A persistent increase in viral load following a period of adequate suppression Highly active antiretroviral therapy (HAART)

  42. Guidelines for starting HAART for HIV/TB co-infection All patients with active TB irrespective of HIV RNA level or CD4+ cell count TB treatment should be commenced first and ART commenced subsequently, as soon as possible and within the first 8 weeks of starting TB treatment. The recommended 1st line ART regimen in patients on TB treatment is AZT+3TC+EFV or TDF+(3TC or FTC)+ EFV. For those unable to tolerate or have contraindications to an EFV-based regimen, AZT+3TC+NVP or TDF+3TC or FTC+NVP or a triple NRTI regimen are recommended Guidelines for starting HAART for HIV/HBV co-infection In those who require treatment for HBV infection, ART should be initiated irrespective of CD4 cell count or WHO clinical stage. In those eligible for treatment, 1st line regimen should include TDF and 3TC or FTC In those failing treatment, 2nd and subsequent ART regimens should include TDF+3TC or FTC, both should be continued in the 2nd line regimen for anti-HBV activity & to reduce the risk of hepatic flares, irrespective of the 2nd line regimen ART for pregnant women Treat all pregnant women with CD4 count <350, irrespective of WHO clinical stage Treat all pregnant with WHO stage 3 and 4, irrespective of CD4 count One of the following regimens should be used for ART naïve pregnant women initiating ART AZT +3TC+EFVO (preferred) AZT +3TC+NVP (preferred) TDF+(3TC or FTC)+EFV TDF+(3TC or FTC)+NP It is recommended that an EFV-based 1st-line regimen should not be initiated during the first trimester of pregnancy Highly active antiretroviral therapy (HAART) in special circumstances

  43. What to start • It is recommended that one of the following regimens is used to initiate ART in ART-naïve individuals • AZT+3TC+EFV • AZT+3TC+NVP • TDF+(3TC or FTC)+EFV • TDF+(3TC or FTC)+NVP • Fixed dose combinations or co-packaged formulations are recommended wherever possible.

  44. Prevention Prevention and Control (1) • In the absence of a curative treatment or vaccine, prevention of HIV transmission is essential to controlling the epidemic • Effective education about HIV transmission and ways to prevent its spread has been considered a “social vaccine” • Successful prevention requires collaboration between the health care sector, civil society, many community-based groups and faith-based organizations. • Within the healthcare sector, clinicians, social workers, health education specialists, mental health specialists and patients must work together • In all settings, especially those that are resource-poor, selection of the most cost-effective interventions is imperative because allocation of resources to one intervention may prevent implementation of other interventions

  45. Prevention Prevention and Control (2) Since sexual contact accounts for most of HIV transmission globally, control measures directed against the spread of this infection must address squarely the issue of sexual promiscuity or excessive sexual activity Advice includes restriction to one partner only, if married. If unmarried, they should abstain or restrict themselves to the person they know best Condom use should be emphasized to those who cannot abstain People must be advised to screen themselves periodically if they expose themselves to more than one partner

  46. Prevention Prevention and Control (3) Some key elements of AIDS prevention • Provide early diagnosis and treatment of STIs • Make HIV testing and counselling widely available • Provide suitable counselling for women who are HIV-negative • Prevent unintended pregnancies among HIV positive women • Testing and counselling of pregnant women • ARV prophylaxis to mother –child pairs • Modification of infant feeding practices to reduce transmission via breastfeeding • Safe blood transfusion practices • Use of sterile instruments including like needles and syringes

  47. End of Section 3 You have come a long way! This is the last of the sections. We suggest that you proceed to answer question 3 to assess your learning. Do remember to write your answers on the mark sheet before looking at the right answer!

  48. Question 3: Following exposure to HIV: Write “T” or “F” on the answer sheet. When you have completed all 4 questions, click on the box and mark your answers. Click to for the correct answer • HIV infection is synonymous with AIDS • Having antibodies to HIV indicates protection • A glandular fever-like illness at seroconversion • Viral load is high shortly after primary HIV infection a b c d

  49. Sources of information / bibliography • Joint United Nations Programme on AIDS http://www.unaids.org/en/ • Multiple information database available from the CDC website: http://www.cdc.gov/ • Science 2000; 287: 607-614 • Science 2000; 288 (5472): 1789-1796 • UNAIDS/WHO. AIDS epidemic update, 2004. • Yusuph H, Garbati MA, Akeredolu P, Gashau W. HIV-1 and HIV-2 Seroprevalence and Risk Factors in Maiduguri, Nigeria. XV International AIDS Conference, Bangkok, Thailand July 11-16, 2004 (abstract E710I7776). End of module

  50. Authors and Permissions Dr. Yusuph Haruna, Senior Lecturer and Honorary Consultant Physician, Department of Medicine, University of Maiduguri Teaching Hospital, Nigeria. Dr. David Lewis, Learning Technologist and Prof. Steve Allen, Professor of Paediatrics and International Health, Swansea Medical School, Swansea, UK Dr. Mahibur Rahman, Senior House Officer, Singleton Hospital, Swansea, UK Permissions: Please note that many images included in this module are taken from readily-accessible websites. Verbal permission was granted from patients where appropriate. This module can be used for teaching purposes within our institutions but should not be used for any other purpose. We are very interested to receive feedback regarding any aspect of this module – especially if it helps us to improve it as a learning resource. Please e mail any comments to either s.j.allen@swansea.ac.uk. For further information about the Partnership in Global Health Education, visit: http://isp.swanih.org/ Back

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