Presentation on HIV-AIDS - Copy.pptx

HIV/AIDS
Human Immunodeficiency Virus
&
Acquired Immunodeficiency Syndrome
PRESENTED BY: JOSIAH REBECCAADENIKE
Serial Number: 30
Department: Internal Medicine
Presented to: Dr. Mrs. Eborieme-Oikeh and Dr. Osarenkhoe

OUTLINE OF PRESENTATION
1. INTRODUCTION
2. EPIDEMIOLOGYAND RISK FACTORS
3. ANATOMYAND PHYSIOLOGY OF THE IMMUNE SYSTEM
4. HIV ANATOMYAND PATHOGENESIS
5. CLINICAL MANIFESTATIONS
6. HIV DIAGNOSIS, INVESTIGATION AND TESTING
7. MANAGEMENT
8. PREVENTION AND RISK REDUCTION
9. HIV/AIDS IN SPECIAL POPULATIONS
10. PSYCHOSOCIALAND MENTAL HEALTH EFFECTS
11. PROGNOSIS
12. CONCLUSION
13. REFERENCES

1. INTRODUCTION:
1.1. Definition and background of HIV/AIDS
1.2. Historical context and global impact
1.3. Differences between HIV and AIDS

1.1. DEFINITION AND BACKGROUND OF HIV/AIDS

1.1. DEFINITION AND BACKGROUND OF HIV/AIDS
▪ HIV stands for human immunodeficiency virus. AIDS stands for acquired immunodeficiency syndrome.
▪ HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T
cells, which play a role in defending the body against infections
▪ An RNA virus that is replicated in a host cell via the enzyme reverse transcriptase to produce DNA from its RNA genome.
▪ The DNA is then incorporated into the host’s genome by an integrase enzyme. The virus thereafter replicates as part of the
host cell’s DNA.
▪ That is, its brings its genetic information(material) in the form of RNA and not DNA
▪ Normally, DNA holds the genetic information and forms RNA which forms protein either structural or functional
▪ Without effective treatment, HIV progressively weakens the immune system, making individuals susceptible to
various opportunistic infections and cancers. The ultimate stage of HIV infection is known as AIDS - Acquired
Immunodeficiency Syndrome
▪ Acquired immunodeficiency syndrome (AIDS) is a chronic, potentially life-threatening condition caused by the human
immunodeficiency virus (HIV).
▪ By damaging the immune system, HIV interferes with the body's ability to fight the organisms that cause disease

1.2. HISTORICAL CONTEXT AND GLOBAL IMPACT
▪ The disease first came to light in the early 1980s, initially identified among homosexual men in the
United States. Since then, it has spread across the globe, leaving behind a trail of devastation. The initial
response to the pandemic was slow, marred by misinformation and stigmatization.
▪ The rate of HIV-related deaths in the United States rose steadily through the 1980s and peaked in 1995.
Since then, the HIV death rate has fallen fourfold.
▪ This trend is likely due to several factors, including improved prophylaxis and treatment of
opportunistic infections, growing experience among the health professions in caring for HIV-infected
individuals, improved access to health care, and a decrease in new infections. However, the most
influential factor clearly has been the increased use of potent antiretroviral drugs, generally administered
in a combination of three or four agents
▪ HIV/AIDS has become a formidable global health crisis, affecting millions of people, with sub-Saharan
Africa bearing the brunt of the burden. Countless lives have been lost, leaving families shattered and
communities torn apart. But beyond the human toll, HIV/AIDS has also had far-reaching social and
economic consequences. It has affected productivity, education, and the workforce, particularly in
resource-limited regions.

HISTORICAL
CONTEXT AND
GLOBAL IMPACT

1.3. DIFFERENCES BETWEEN HIV AND AIDS
Aspect
HIV (Human Immunodeficiency
Virus) AIDS (Acquired Immunodeficiency Syndrome)
Definition
HIV is a virus that attacks the
immune system.
AIDS is the final stage of HIV infection,
characterized by severe immune suppression and
opportunistic infections.
Transmission
Primarily transmitted through
unprotected sexual intercourse,
sharing of contaminated needles,
mother-to-child during childbirth
or breastfeeding, and, rarely,
through blood transfusions.
Not transmitted; it is a stage of HIV infection
resulting from uncontrolled viral replication and
immune system damage.
Stages
Acute HIV infection, Chronic
asymptomatic HIV infection,
Symptomatic HIV infection.
Final and most advanced stage of HIV infection.
CD4+ T-Cells
Targets and destroys CD4+ T-cells,
which are vital in fighting
infections and maintaining
immune function.
CD4+ T-cell count falls below a critical level
(usually below 200 cells/mm³).

Aspect
Virus) AIDS (Acquired Immunodeficiency Syndrome)
Symptoms
Flu-like symptoms (Acute HIV
infection), mild or no symptoms
(Chronic asymptomatic HIV
infection), symptomatic infections
due to immune weakening.
Severe immune deficiency, leading to opportunistic
infections and certain cancers.
Diagnosis
Detected through specific blood
tests for antibodies or viral genetic
material (RNA/DNA).
Diagnosed based on specific criteria established by
WHO or CDC, depending on the country.
Progression
Can progress to AIDS if left
untreated, but effective
antiretroviral therapy (ART) can
prevent progression.
Results from untreated HIV infection and indicates
significant immune system damage.

Aspect
Virus)
AIDS (Acquired Immunodeficiency
Syndrome)
Opportunistic Infections
Generally not present in early stages,
but may occur in symptomatic HIV
infection.
Occur due to severe immune suppression,
making the body susceptible to various
infections.
Management
Managed with antiretroviral therapy
(ART) to suppress viral replication and
preserve immune function.
Management focuses on treating opportunistic
infections, providing supportive care, and
preventing complications.
Life Expectancy
With proper treatment and care, people
living with HIV can lead long and
healthy lives.
Life expectancy may be significantly reduced
if untreated, but with early diagnosis and
proper care, it can improve.

2. EPIDEMIOLOGY AND RISK FACTORS:
2.1. Worldwide prevalence and incidence rates
2.2. High-risk populations and vulnerable groups
2.3. Mode of Transmission
2.4. Factors increasing risk of transmission

2.1. WORLDWIDE PREVALENCE AND INCIDENCE RATES
▪ As of the most recent data available, HIV/AIDS remains a major global health issue. According to the Joint United
Nations Programme on HIV/AIDS (UNAIDS), an estimated 38 million people were living with HIV worldwide.
▪ 70% are in Africa
▪ 20% are in Asia
▪ 10% are in rest of the world
▪ Sub-Saharan Africa continues to be disproportionately affected by the HIV/AIDS pandemic, accounting for the majority of
new infections and deaths related to AIDS. Within this region, certain countries bear a particularly heavy burden of the
disease. Eastern and Southern Africa have higher prevalence rates compared to other regions.
▪ In the United States, the estimated rate of HIV infections diagnosed during 2016 varied significantly by race/ethnicity,
with certain communities experiencing higher rates per 100,000 populations.
▪ It's essential to note that HIV-2, a less aggressive variant of the virus, mainly occurs in West Africa, contributing to the
overall burden of HIV/AIDS in that region.
▪ And approximately 2 million people are dying every year of HIV/AIDs
▪ Every year 2.5 million people are diagnosed with HIV/AIDs
▪ Nigeria Ranks third among the countries with highest burden of HIV/AIDS

WORLDWIDE
PREVALENCE AND
INCIDENCE RATES
Estimated rate of HIV infections
(including children) diagnosed during
2016 in the United States, by
race/ethnicity (per 100,000 population).
(From CDC.)

2.2. HIGH-RISK POPULATIONS AND VULNERABLE GROUPS
▪ Unsafe Sex: Engaging in unprotected sexual intercourse remains one of the primary modes of HIV
transmission worldwide. Individuals who have multiple sexual partners or do not consistently use
condoms are at a higher risk of acquiring and spreading the virus.
▪ Men having Sex with Men (MSM):Men who have sex with men, often referred to as MSM, constitute a
significant risk group for HIV/AIDS.
▪ Injection Drug Users (IDUs):Injection drug use is another significant risk factor for HIV transmission.
Sharing needles and syringes among drug users can facilitate the spread of the virus
▪ Widespread Stigma: Stigma associated with HIV/AIDS remains a significant barrier to prevention and
care. Fear of discrimination often prevents individuals from getting tested, disclosing their HIV status,
or seeking treatment, leading to higher transmission rates.
▪ Sex Workers: Sex workers are at an elevated risk of HIV infection due to the nature of their work and
limited access to protective measures.

High-risk populations
and vulnerable
groups
Data for 2015. (From UNAIDS.)

2.3. MODE OF TRANSMISSION
HIV is transmitted:
▪By sexual contact.
▪By exposure to blood or blood products (e.g. drug users,
patients with haemophilia or occupationally in healthcare
workers).
▪Vertically from mother to child in utero, during birth or
by breastfeeding

2.4. FACTORS INCREASING RISK OF TRANSMISSION
▪ Common to all transmission categories:
▪ High Viral Load: Individuals with higher viral loads are more likely to transmit the virus to others as they have a
higher concentration of the virus in their body fluids.
▪ Sexual Transmission:
▪ Sexually Transmitted Infections (STIs): Presence of STIs, particularly those causing genital ulcers (e.g., herpes),
can increase the risk of HIV transmission during sexual activity due to increased susceptibility.
▪ Cervical Ectopy: In females, cervical ectopy (a condition where columnar cells from inside the cervix are
exposed on the outer surface) may increase vulnerability to HIV infection.
▪ Rectal or Vaginal Lacerations: Any cuts or tears in the rectal or vaginal mucosa can provide entry points for the
virus during sexual intercourse.
▪ Uncircumcised Male Partner: Studies have shown that uncircumcised men have a slightly higher risk of
acquiring HIV from infected partners.
▪ Receptive Anal Intercourse: This sexual practice carries a higher risk of HIV transmission compared to other
sexual activities.

2.4. FACTORS INCREASING RISK OF TRANSMISSION
▪ Occupational Transmission:
▪ Deep Injury: Healthcare workers and others may be at risk if they experience deep injuries with potential
exposure to HIV-infected blood.
▪ Visible Blood on Device: Presence of visible blood on a device increases the risk of occupational HIV
transmission.
▪ Needle in a Blood Vessel: If a needle or sharp object punctures a healthcare worker's skin and is within a blood
vessel, the risk of HIV transmission is heightened.
▪ Vertical Transmission:
▪ Prolonged Rupture of Membranes: In pregnant women with prolonged rupture of membranes (waters), the risk of
transmitting HIV to the newborn during childbirth is increased.
▪ Older Gestational Age: Delivering a baby at a more advanced gestational age may elevate the risk of vertical
HIV transmission.

3. ANATOMY AND PHYSIOLOGY OF THE
IMMUNE SYSTEM:
3.1. The immune system's components and
functions

▪ Protects the body by recognizing antigens on invading bacteria and viruses and reacting to them.
▪ Antigen
▪ Any substance that induces a state of sensitivity and immune responsiveness.
▪ They interact with antibodies and immune cells, initiating an immune response. (This process destroys the antigen, allowing the body to be free of
infections.)
▪ Types of antigens: Bacteria, viruses, fungi, parasites
▪ When the immune system is weakened or destroyed by a virus such as HIV, the body is left vulnerable to infections.
▪ The immune system consists of lymphoid organs and tissues, including the bone marrow, thymus gland, lymph nodes, spleen,
tonsils, adenoids, appendix, blood, and lymphatic vessels.
▪ All components of the immune system are vital in the production and development of lymphocytes, or white blood cells.
▪ B lymphocytes (or B cells) and T lymphocytes (or T cells) are produced from stem cells in the bone marrow.
▪ B cells – stay in the bone marrow to complete the maturation process
▪ T lymphocytes – travel to the thymus gland to complete their maturation. There T lymphocytes become immunocompetent,
multiply, and become more differentiated.
3.1. THE IMMUNE SYSTEM'S COMPONENTS AND
FUNCTIONS

FUNCTIONS
▪ B Lymphocytes
▪ Main function is humoral (antibody) immunity.
▪ Each B cell can recognize specific antigen targets and can secrete specific antibodies.
▪ Antibodies
▪ function by coating antigens, which makes the antigens more vulnerable to phagocytosis (engulfing and
ingestion of invading organisms by leukocytes and/ or macrophages),
▪ Or by triggering the complement system, leading to an inflammatory response.
▪ Highly specialized serum protein molecules.
▪ Grouped into five classes, each having a specialized function: Immunoglobulin G (IgG), IgA, IgM, IgE, IgD.
▪ T Lymphocytes
▪ Two major functions: regulation of the immune system and killing of cells that bear specific target antigens.
▪ Each T cell has a surface marker, such as CD4+, CD8+, and CD3+, that distinguishes it from other cells.

FUNCTIONS
▪ Cytokines – can bind to target cells and activate the inflammatory process. They also promote cell
growth, activate phagocytes, and destroy target cells.
▪ Interleukins – are cytokines that serve as messengers between white blood cells.
▪ Phagocytes
▪ Include monocytes and macrophages, large white blood cells that engulf and digest cells carrying antigenic
particles.
▪ Found throughout the body, phagocytes rid the body of worn-out cells, initiate the immune response by
presenting antigens to lymphocytes, are important in immune response regulation and inflammation, and carry
receptors for cytokines.
▪ Dendritic cells – another type of phagocyte, also are antigen-presenting cells. They have long,
threadlike extensions that help trap lymphocytes and antigens and are found in the spleen and lymph
nodes.
▪ Neutrophils – are granulocytic phagocytes that are important in the inflammatory response.

4. HIV ANATOMY AND PATHOGENESIS
4.1. Structure
4.2. Life cycle and Pathogenesis
4.3. Pathophysiology and Progression to AIDS
4.4. Development of Complications

4.1. STRUCTURE
▪ Genus: Lentivirus, Family Retroviridae
▪ Lentiviruses (HIV 1 and 2)
▪ There are two types of HIV that cause AIDS: HIV type 1 (HIV-1) and HIV-2, They
have the same modes of transmission and are associated with the same opportunistic
infections, but HIV-1 can be found throughout the world, but HIV-2 is almost
exclusively limited to West Africa. HIV-1 is transmitted more easily than HIV-2, and
HIV-1 infection progresses more rapidly to AIDS.
▪ HIV consists of a cylindrical centre surrounded by a sphere-shaped lipid bilayer
envelope with diameter ranging 100nm with 3 layers.
▪ Outer
▪ Matrix
▪ Capsid

4.1. STRUCTURE
▪ Outer:
▪ Outer envelope consisting of glycoprotein
▪ It is derived from host cell membrane
▪ There are two glycoprotein
▪ The inner one GP 41 [transmembrane]
▪ It has a clinical importance because it is the protein that fuses with the host membrane and it is a point of inhibition for drug
treatment
▪ The outer one GP 120 [superficial]
▪ It helps the virus to attach with the target receptor
▪ It binds to CD4 positive cells e.g. T-Helper cells, Monocytes, Macrophages, Microglial, Langerhans cells, Follicular
dendritic cell
▪ Matrix:
▪ Which is made up of p17 protein
▪ It is for stabilizing GP 41

4.1. STRUCTURE
▪ Capsid (the core)
▪ Made up of p24 capsid protein
▪ It is made up of 2 HIV RNA and enzymes
▪ The 2 single stranded RNA is in association with P7 and P9
▪ The enzymes are reverse transcriptase, integrase and Protease
▪ Reverse transcriptase aka RNA depended DNA-polymerase normally RNA is formed from DNA
through an enzyme DNA depended RNA polymerase but in the case of HIV it is Reverse
transcriptase which forms DNA from RNA
▪ Integrase is the enzyme that integrates the viral DNA into the target cell DNA
▪ Protease works when the virus forms new proteins which are larger in size and it cuts them into
smaller pieces which are the active form
▪ The p24 is used as diagnosis

4.1. STRUCTURE
▪ The number given to these proteins are based on their molecular
weight i.e p17 and p24
▪ HIV uses nine genes to code for the necessary proteins and
enzymes.
▪ The three principal genes are gag, pol, and env.
▪ Gag – encodes core proteins.
▪ Pol – encodes the enzymes reverse transcriptase, protease, and integrase.
▪ Env – encodes the HIV structural components known as glycoproteins.

4.2. LIFE CYCLE AND PATHOGENESIS
▪ Attachment
▪ Binding
▪ Fusion
▪ Reverse Transcription
▪ Integration
▪ Transcription and Translation
▪ Replication and Assembly
▪ Budding
▪ Maturation

▪ The most commonly and most infected is the T-Cells but it doesn't affect all type of T-Cell, it would never affect naive T-Cells but
affects Memory T-Cell
▪ Hiv use the host cells CD4 receptors and the Co-receptor cells which are very important to it
▪ The co receptors are the chemokines receptor which are the CCR5 (present in macrophages and T cells) and the CXCR4 (present
on T-Cells)
▪ Natural acquired HIV virus initially affects macrophages and dendritic cells with coreceptor CCR5 since they have attraction (Tropism) for this
receptor
▪ But when they get developed and new strains are produced due to mutation in GP120 and then virus is then able to predominantly interact with
CXCR4 making it more dangerous for T-cells [That’s why Aids appear after 7 years]
▪ 1% of the population in Northern Europe descendant population will survive with HIV virus for a long period of time without treatment and
without it progressing to AIDS. They have homogenous mutation (i.e from both parent) causing the CCR5 gene to produce defective CCR5
receptor which the HIV virus cannot act on, so even though they have the virus, it cannot progress to AIDS
▪ About 10-15% of Northern European population are heterogeneous mutation (i.e from either of the parents) and they will have defective CCR5
and normal CCR5 causing the HIV virus to progress slowly and develop into AIDS slowly than normal
▪ These co-receptors are of clinical points for combacting HIV virus, the drug competitively binds to the CCR5 molecule so the GP120 cannot
interact e.g Maraviroc
▪ It is a drug that blocks CCR5 and prevents the GP120 to attach to CCR5

▪ GP120 will attach to the CD4 receptor present in the plasma membrane which will bring conformational change
which will separate GP 41 from GP 120, the GP 120 will then combine with the chemokine receptor
▪ The combination of GP120 + CD4 receptor and Chemokine receptor will now enable the GP 41 to penetrate the
plasma membrane....that is why if the chemokine receptor are mutated this penetration cannot happen and will be
HIV resistant
▪ After membrane penetration the two RNA enters into the host cell cytoplasm
▪ Under the influence of reverse transcriptase, the two RNA are converted to double stranded DNA
▪ The reason it converts to DNA is because it is only DNA DNA combination that can happen and not DNA, RNA
▪ These DNA then contact with host DNA and integrate with the Host DNA using the enzyme integrase
▪ And from these New HiV RNA will be synthesized which will be forming virions which will be present at the
surface of the membrane
▪ Under the influence of proteases (the 3rd enzyme), the long virons will be broken down into smaller active viral
proteins and the membrane will be ruptured and the virus will be released to infect new cells

4.3. PATHOPHYSIOLOGYAND PROGRESSION TO AIDS
▪ Early Stages of HIV Infection: After initial infection, there is an acute phase during which the virus
replicates rapidly and disseminates throughout the body. This phase is often associated with flu-like
symptoms, but they may go unnoticed in some individuals. During this stage, the viral load in the blood
is high, and there is a significant decrease in CD4+ T-cells.
▪ Clinical Latency: Following the acute phase, many individuals enter a prolonged period known as
clinical latency or chronic asymptomatic stage. During this phase, the virus continues to replicate at
lower levels, but there may be no noticeable symptoms. However, the immune system remains active,
trying to control the viral replication. This phase can last for several years, and people may not be aware
they are infected, but they can still transmit the virus to others.
▪ Progressive Immune Depletion: As the viral replication persists, the virus continues to attack and
destroy CD4+ T-cells, the primary target of HIV. The immune system tries to compensate for this loss
by producing new CD4+ T-cells, but the rate of destruction often outpaces the body's ability to replenish
them.

4.3. PATHOPHYSIOLOGYAND PROGRESSION TO AIDS
▪ Decreased Immune Function:Over time, the gradual decline in CD4+ T-cell levels
weakens the immune system's ability to fight infections. This leads to an increased
susceptibility to various opportunistic infections that a healthy immune system would
typically control. These infections can range from relatively mild conditions, like oral
thrush and skin infections, to more severe and life-threatening diseases, including
certain types of pneumonia and tuberculosis.
▪ Development of AIDS:When the CD4+ T-cell count falls below a critical threshold,
usually less than 200 cells per microliter of blood, the individual is considered to have
progressed to AIDS. At this point, the immune system is severely compromised, and
the risk of opportunistic infections and malignancies becomes significantly higher.
AIDS is a clinical diagnosis based on the presence of specific opportunistic infections
or certain AIDS-defining cancers, even in the absence of a known HIV positive status.

4.4. DEVELOPMENT OF COMPLICATIONS
▪ Opportunistic Infections: As HIV progresses and CD4+ T-cell levels decline, the immune system
becomes severely compromised, leading to a higher risk of opportunistic infections. These infections are
caused by microorganisms that are usually harmless in individuals with a healthy immune system but
can cause severe illness in people with advanced HIV. Some common opportunistic infections include:
▪ Pneumocystis jirovecii pneumonia (PCP): A severe fungal lung infection that can be life-threatening.
▪ Tuberculosis (TB): An airborne bacterial infection affecting the lungs and other organs.
▪ Candidiasis: An opportunistic fungal infection that can affect the mouth, throat, and other areas of the body.
▪ Cytomegalovirus (CMV) infection: A viral infection that can affect the eyes, gastrointestinal tract, and other
organs.
▪ Cryptococcal meningitis: A fungal infection that affects the brain and spinal cord.
▪ Toxoplasmosis: A parasitic infection that can cause neurological problems.

4.4. DEVELOPMENT OF COMPLICATIONS
▪ HIV-Associated Neurocognitive Disorders (HAND): HIV can also affect the central nervous system, leading to
a range of cognitive and neurological disorders collectively known as HAND. These disorders can manifest as
mild neurocognitive impairment, HIV-associated dementia, or other cognitive and motor deficits. The exact
mechanisms of how HIV affects the brain are still being studied, but chronic inflammation, direct viral effects,
and toxic viral proteins are believed to play a role.
▪ HIV-Associated Nephropathy: HIV-related kidney disease, known as HIV-associated nephropathy, can result in
significant damage to the kidneys' filtering and may lead to proteinuria and progressive kidney dysfunction.
▪ HIV-Related Cardiovascular Diseases: People with HIV have a higher risk of developing cardiovascular
diseases such as heart attacks, stroke, and hypertension. The exact mechanisms leading to these cardiovascular
complications are multifactorial and may include chronic inflammation, antiretroviral drug effects, and lifestyle
factors.
▪ Non-AIDS Defining Malignancies: Long-term untreated HIV infection is associated with an increased risk of
certain malignancies, even without reaching the stage of AIDS. These non-AIDS defining malignancies include
cancers like lung cancer, liver cancer, anal cancer, and certain types of skin cancers. The risk is attributed to
chronic inflammation, immunosuppression, and potential effects of certain viral co-infections, such as human
papillomavirus (HPV) and hepatitis B and C viruses.

5. CLINICAL MANIFESTATIONS
5.1. History Taking and Symptoms
5.2. Physical Examination and Signs
5.3. Systemic manifestations and Opportunist
Infections
5.4. WHO Staging of HIV/AIDS
5.5. CDC Classification of HIV/AIDS
5.6. AIDS

5.1. HISTORY TAKING AND SYMPTOMS
▪ Presenting Symptoms:
▪ Flu-like symptoms: Fever, fatigue, sore throat, and swollen lymph nodes.
▪ Skin rashes: Red, itchy rashes, and sores on the skin and mucous membranes.
▪ Weight loss: Unexplained and unintentional weight loss that can be significant over time.
▪ Night sweats: Excessive sweating, particularly at night, can be a distressing symptom.
▪ Gastrointestinal issues: Nausea, vomiting, diarrhea, and abdominal pain.
▪ Neurological symptoms: Headaches, confusion, and memory problems.
▪ Respiratory symptoms: Persistent cough, shortness of breath, and chest pain.
▪ Recurrent infections: Frequent and severe infections, including respiratory and urinary tract infections.

5.1. HISTORY TAKING AND SYMPTOMS
▪ Sexual History: Inquiring about the patient's sexual practices, number of sexual partners, and use of protection (condoms)
during intercourse..
▪ Injection Drug Use (IDU): Asking about a history of intravenous drug use is crucial, as sharing needles can significantly
increase the risk of HIV transmission.
▪ Blood Transfusions or Organ Transplants: Inquiring about any history of blood transfusions or organ transplants,
especially before the implementation of rigorous screening measures for HIV, can help assess potential HIV exposure.
▪ Past Medical History: Identifying any history of recurrent or unusual infections, such as opportunistic infections, can
raise suspicion for HIV/AIDS. Past conditions indicative of symptomatic HIV infection like zoster, thrush, vaginal
candidiasis, oral hairy leucoplakia, pneumocystis carinii pneumonia, cryptococcal meningitis e.t.c.
▪ Family History: Exploring the family medical history may provide insights into possible genetic predisposition or
familial infections.
▪ Symptom Onset and Progression: Gathering information about when the symptoms started, their duration, and any
changes or developments can help establish the stage of HIV infection.
▪ Recent Travel History: Inquiring about recent travel to regions with a higher prevalence of HIV can be essential in
evaluating potential exposure risks

Clinical
Manifestations of HIV

5.2. PHYSICAL EXAMINATION AND SIGNS
▪ Oral and mucosal findings: Oral thrush (white patches in the mouth), oral
ulcers, and other mucosal abnormalities.
▪ Skin changes: Skin lesions, rashes, or Kaposi's sarcoma
▪ Lymphadenopathy: Swollen lymph nodes in the neck, armpits, and groin.
▪ Hepatomegaly/Splenomegaly: Enlarged liver or spleen due to HIV-related
infections or conditions.
▪ Neurological signs: Abnormal reflexes, weakness, and loss of
coordination in advanced cases.
▪ Opportunistic infections: Specific signs related to infections that have
taken advantage of the weakened immune system.

Clinical
Oral Candidiasis

Clinical
Disseminated Histoplasmosis with
diffuse papular rash

Clinical
Oral Hairy Leucoplakia

Clinical
Cervical lymphadenopathy

Clinical
Cytomegalovirus retinitis

Clinical
Characteristics of lipodystrophy. A.
Truncal obesity and buffalo hump. B.
Facial wasting

Clinical
Severe, erosive perirectal herpes
simplex in a patient with AIDS

5.3. SYSTEMIC MANIFESTATIONS AND OPPORTUNIST
INFECTIONS
▪ Respiratory System:
▪ Pneumocystis jirovecii Pneumonia (PCP): A severe lung infection caused by the fungus Pneumocystis jirovecii. Symptoms include fever, cough,
difficulty breathing, and low oxygen levels. It is a leading cause of morbidity and mortality in HIV/AIDS patients.
▪ Tuberculosis (TB): An airborne bacterial infection caused by Mycobacterium tuberculosis. HIV/AIDS weakens the immune system, making
individuals more susceptible to TB. Symptoms include persistent cough, fever, night sweats, weight loss, and chest pain.
▪ Bacterial Pneumonia: In HIV-positive patients, bacterial pneumonia can occur due to various bacteria. Symptoms include fever, productive
cough, and difficulty breathing.
▪ Cytomegalovirus (CMV) Pneumonitis: CMV is a common virus, but in immunocompromised individuals, it can cause severe lung infections.
Symptoms include fever, cough, and shortness of breath.
▪ Gastrointestinal System:
▪ Candidiasis (Esophageal Thrush): An infection caused by the fungus Candida. It affects the esophagus and may cause painful swallowing, chest
pain, and white patches in the mouth.
▪ Cryptosporidiosis: An intestinal parasitic infection that leads to severe and chronic diarrhea, abdominal pain, and weight loss.
▪ Mycobacterium avium complex (MAC) infection: MAC is a group of bacteria causing infections in various body systems. In HIV/AIDS patients,
it can cause fever, night sweats, weight loss, and abdominal pain.
▪ Cytomegalovirus (CMV) Colitis: CMV can affect the colon and cause diarrhea, abdominal pain, and fever.

INFECTIONS
▪ Central Nervous System:
▪ Toxoplasmosis: An infection caused by the parasite Toxoplasma gondii. It affects the brain and may lead to headaches,
confusion, seizures, and focal neurological deficits.
▪ Cryptococcal Meningitis: A fungal infection affecting the membranes covering the brain and spinal cord. Symptoms include
headache, fever, neck stiffness, and altered mental status.
▪ Progressive Multifocal Leukoencephalopathy (PML): Caused by the JC virus, PML damages the brain, leading to neurological
deficits, speech problems, and cognitive changes.
▪ HIV-Associated Neurocognitive Disorders (HAND): Refers to a range of cognitive impairments seen in HIV/AIDS patients,
including memory problems, impaired concentration, and motor dysfunction.
▪ Skin and Mucous Membranes:
▪ Herpes Simplex Virus (HSV) Infections: HSV can cause painful vesicles on the lips (oral herpes) or genital area (genital
herpes).
▪ Herpes Zoster (Shingles): Caused by the varicella-zoster virus, shingles presents as a painful rash with blistering along a
dermatome.
▪ Kaposi Sarcoma: A cancer caused by human herpesvirus 8 (HHV-8), leading to red, purple, or brown skin lesions.

INFECTIONS
▪ Blood and Lymphatic System:
▪ Cytomegalovirus (CMV) Retinitis: CMV can cause inflammation of the retina, leading to blurred
vision, floaters, and vision loss.
▪ Non-Hodgkin Lymphoma: HIV/AIDS patients are at increased risk of certain lymphomas, which
present as swollen lymph nodes, weight loss, and night sweats.
▪ Disseminated Histoplasmosis: A fungal infection caused by Histoplasma capsulatum. It can lead to
fever, fatigue, and enlargement of the liver and spleen.
▪ Other:
▪ Mycobacterium avium complex (MAC) Bacteremia: Infections involving MAC bacteria can lead to
fever, night sweats, and weight loss.
▪ Salmonella Septicemia: Caused by Salmonella bacteria, this condition presents with fever,
abdominal pain, and diarrhea.
▪ Candidemia: An infection caused by Candida, leading to fever, chills, and low blood pressure.

Systemic
Manifestation of
Opportunist
Infections

5.4. WHO STAGING OF HIV/AIDS
▪ Clinical Latency/Asymptomatic Disease
(Clinical Stage 1)
▪ Asymptomatic
▪ Persistent lymphadenopathy
▪ May last 8–10 years
▪ HIV enzyme-linked immunosorbent assay and
Western blot or immunofluorescence assay will
be positive.
▪ CD4+ count is greater than 500 cells/μL
▪ Mild Signs and Symptoms of HIV (Clinical
Stage 2)
▪ May appear to be healthy for years, and then
minor signs
▪ Candidiasis
▪ Lymphadenopathy
▪ Persistent hepatosplenomegaly
▪ Pruritic eruptions
▪ Herpes zoster
▪ Peripheral neuropathy
▪ CD4+ count falls is between 350-499/ uL

5.4. WHO STAGING OF HIV/AIDS
▪ Advanced Signs and Symptoms of HIV
(Clinical Stage 3)
▪ Cryptosporidiosis
▪ Pulmonary and lymph node tuberculosis
▪ Wasting
▪ Persistent fever (longer than one month)
▪ Persistent candidiasis
▪ Recurrent bacterial pneumonia
▪ CD4+ count 200 – 349 cells/μL
▪ Clinical Stage 4 or AIDS
▪ Pneumocystis carinii pneumonia
▪ Cytomegalovirus infection
▪ Toxoplasmosis
▪ Mycobacterium avium complex
▪ Cryptococcal meningitis
▪ Progressive multifocal leukoencephalopathy
▪ Kaposi sarcoma
▪ CD4+ count is less than 200 cells/μL
▪ Death in imminent

5.5. CDC CLASSIFICATION OF HIV/AIDS
▪The CDC classification of HIV/AIDS into Category
A, Category B, and Category C was introduced in
1993
▪Category A: Asymptomatic or mild symptoms with a CD4
count above 500 cells/mm³.
▪Category B: Symptoms of HIV infection with a CD4 count
between 200 and 499 cells/mm³.
▪Category C: AIDS-defining illnesses or severe symptoms with
a CD4 count below 200 cells/mm³

5.6. AIDS
WHO Definition of AIDS:
▪ The WHO defines AIDS as the final stage
of HIV infection when the immune system
is severely compromised, and the individual
has either a CD4 count below 200
cells/mm³ or specific AIDS-defining
illnesses. 2 major signs in combination
with 1 minor sign:
▪ Major Signs:
▪ Weight loss > 10% body wt.
▪ Chronic Diarrhoea for > 1 month.
▪ Prolonged fever for > 1 month
▪ Minor Signs:
▪ Persistent cough for > 1 month.
▪ Generalized pruritic dermatitis.
▪ History of herpes zoster.
▪ Oropharyngeal candidiasis.
▪ Chronic herpes simplex infection.
▪ Generalized lymphadenopathy

5.6. AIDS
▪ Most common:
▪ Opportunistic infection in HIV/aids is TB
▪ Fungal infection is candidiasis
▪ Cancer: non hodkin lymphoma
▪ 2nd most common cancer: Kaposi sarcoma
▪ Genital cancer: cervical cancer cos of HPV
▪ Hematology manifestation: autoimmune hemolytic anemia
▪ Endocrine disorder: lipodystrophy
▪ Dermatological manifestation: seborrheic dermatitis
▪ Ocular infection: CMV retinitis
▪ CNS manifestation: AIDS dementia complex
▪ Renal manifestation: HIV associated nephropathy associated with focal segmental glomerulosclerosis
▪ Hepatitis: B

5.6:AIDS
▪AIDS RELATED COMPLEX:
▪Fever/fatigue/malaise
▪Night sweats
▪Weight loss more than 10% body weight
▪Unexplained diarrhea
▪Lymphadenopathy on more than 2 non-inguinal
site

5.6. AIDS
▪ AIDS DEFINING: Divided into
Infections and Tumors
▪ Cancer:
▪ NHL
▪ Kaposi sarcoma
▪ Cervical carcinoma
▪ Infections: divided into Bacteria, Viral,
Protozoa, fungal
▪ Bacteria:
▪ Mycobacterium tuberculosis
▪ Norcardia (pneumonia, meningitis)
▪ Salmonella infections.....presents with diarrhea
▪ Viral:
▪ Cytomegalovirus (affects CNS, LUNG, EYE AND
INTESTINE)
▪ Herpes simplex virus
▪ Varicella-zoster virus
▪ Protozoa:
▪ Cryptosporidium
▪ Pneumocystis
▪ Toxoplasma
▪ Fungal:
▪ Candida
▪ Cryptococcus
▪ Coccidioides
▪ Histoplasma

6. HIV DIAGNOSIS, INVESTIGATIONS AND
TESTING
6.1. Diagnosis and Differentials
6.2. Baseline Investigation of a newly diagnosed
HIV-seropositive individual
6.3. Types of HIV tests and their accuracy
6.4. Importance of early detection

6.1. DIAGNOSIS AND DIFFERENTIALS
▪ Differentials include:
▪ Infectious Mononucleosis (Mono):
▪ Infectious mononucleosis is a viral infection most commonly caused by the Epstein-Barr virus (EBV).
▪ It presents with symptoms like fever, sore throat, swollen lymph nodes, and fatigue.
▪ Enlargement of the spleen and liver may also occur, and a characteristic rash may develop in some cases.
▪ Influenza (Flu):
▪ Influenza is a contagious respiratory illness caused by influenza viruses.
▪ It presents with high fever, chills, headache, and body aches, often leading to severe fatigue and malaise.
▪ Respiratory symptoms like cough, sore throat, and runny nose are common.
▪ Primary Syphilis:
▪ Primary syphilis is the early stage of syphilis infection caused by the bacterium Treponema pallidum.
▪ It is characterized by the appearance of a painless sore or ulcer (chancre) at the site of infection, such as the genitals, anus, or mouth.
▪ Enlarged lymph nodes near the chancre may also be present.
▪ Tuberculosis (TB):
▪ Tuberculosis is a bacterial infection caused by Mycobacterium tuberculosis, primarily affecting the lungs.
▪ It presents with persistent cough (often with blood), fever, night sweats, and weight loss.
▪ Fatigue, chest pain, and difficulty breathing are also common symptoms.

6.1. DIAGNOSIS AND DIFFERENTIALS
▪ Diagnosis:
▪ HIV is diagnosed by detecting host antibodies, either using rapid point-of-care tests
or in the laboratory, where enzyme-linked immunosorbent assay (ELISA) tests are
commonly conducted.
▪ Most tests can detect antibodies to both HIV-1 and HIV-2. Screening tests may also
include an assay for p24 antigen in addition to antibodies to detect patients with
primary infection before the antibody response occurs.
▪ A confirmatory diagnosis is usually made when two positive antibody tests from two
different immunoassays are obtained. For specific situations, such as diagnosing
infections in infants born to HIV-positive mothers or detecting primary infection
before antibodies develop, nucleic acid amplification tests (such as polymerase chain
reaction, PCR) are used to detect HIV RNA. PCR is more sensitive than p24 antigen
detection for diagnosing primary infectio

6.2. BASELINE INVESTIGATION OF A NEWLY DIAGNOSED
HIV-SEROPOSITIVE INDIVIDUAL
▪ Complete Blood Count (CBC): To assess blood cell counts and screen for anemia or low platelet
count.
▪ Liver Function Tests (LFTs): To assess liver health and detect any liver abnormalities.
▪ Kidney Function Tests: To assess kidney function and identify any renal issues.
▪ CD4+ T-cell Count: To determine the immune status and stage of HIV infection.
▪ Viral Load Test: To measure the amount of HIV virus in the blood, which helps in monitoring the
effectiveness of antiretroviral therapy (ART).
▪ Fasting Blood Glucose: To screen for diabetes or impaired glucose tolerance.
▪ Lipid Profile: To assess lipid levels and cardiovascular risk.
▪ Hepatitis B and C Screening: To detect the presence of hepatitis B or C co-infections.
▪ Sexually Transmitted Infections (STI) Screening: To identify and treat any concurrent STIs.
▪ Tuberculosis (TB) Screening: To rule out TB infection, which can be more severe in individuals with
HIV.

6.3. TYPES OF HIV TESTS AND THEIR ACCURACY
▪ Rapid Point-of-Care Tests:
▪ These tests are performed at the point of care, such as community health clinics, outreach centers, or homes.
▪ Rapid tests provide results within a short time, usually within 20 to 30 minutes.
▪ They are often based on detecting HIV antibodies in a small blood sample obtained through a fingerstick or oral fluid.
▪ While rapid tests are convenient and offer quick results, they may have slightly lower sensitivity compared to laboratory-based tests.
▪ Enzyme-Linked Immunosorbent Assays (ELISA):
▪ ELISA tests are laboratory-based tests and are commonly used for initial HIV screening.
▪ They detect HIV-specific antibodies in the blood sample.
▪ ELISA tests are highly sensitive and accurate, but they require specialized laboratory equipment and may take a few hours to a few days for
results.
▪ Western Blot Test:
▪ The Western blot is a confirmatory test used to verify positive ELISA results.
▪ It identifies specific HIV antibodies in the blood sample and is considered highly specific.
▪ The Western blot test is typically used when there is a need to confirm the HIV diagnosis after positive ELISA results.

▪ Nucleic Acid Amplification Tests (NAAT) or Polymerase Chain Reaction (PCR):
▪ NAAT/PCR tests detect the presence of HIV genetic material (RNA) in the blood.
▪ They are highly sensitive and are particularly useful in detecting HIV infections during the early stages when antibody tests may not be
conclusive.
▪ These tests are often used for diagnosing HIV in infants born to HIV-positive mothers.
▪ Fourth-Generation Tests:
▪ Fourth-generation tests are a combination of antibody and antigen tests.
▪ They detect both HIV antibodies and the p24 antigen (a viral protein) in the blood.
▪ Fourth-generation tests offer earlier detection of HIV infections compared to antibody-only tests.
▪ They are widely used as screening tests due to their improved sensitivity during the acute phase of infection.
▪ Home HIV Testing Kits:
▪ Home HIV testing kits are available for purchase over-the-counter or online.
▪ These tests use a sample of oral fluid or blood obtained at home and then mailed to a laboratory for analysis.
▪ Results are typically provided by phone or through secure online portals.
▪ Home testing kits can offer convenience and privacy but may have limitations in terms of counseling and support services.

6.4. IMPORTANCE OF EARLY DETECTION
▪ It allows for timely initiation of antiretroviral therapy (ART), which can suppress the viral load, preserve
immune function, and improve long-term outcomes.
▪ Early treatment reduces the risk of HIV transmission to sexual partners or from mother to child during
childbirth and breastfeeding.
▪ Timely diagnosis enables healthcare providers to offer counselling and support to the individual, helping them
cope with the emotional and social challenges of living with HIV.
▪ Patients who should be offered and recommended HIV testing:
▪ Sexually active individual
▪ Men who have sex with men
▪ Partners of HIV positive individuals
▪ Pregnant women
▪ Health workers
▪ Patients with TB: Cause TB and HIV usually coexist
▪ Patients from high prevalence regions or high risk populations

7. MANAGEMENT:
7.1. Antiretroviral Therapy (ART)
7.2. Innovative Treatment Approaches
7.3. Vaccines and Cure research
7.4. Management of complications: Opportunistic
infections and prophylaxis

7.1. Antiretroviral Therapy (ART):
7.1.1. Goals
7.1.2. Classes of antiretroviral drugs
7.1.3. Initiation and monitoring of ART
7.1.4. Complications and management

7.1: ANTIRETROVIRAL THERAPY (ART)
▪ Antiretroviral Therapy (ART) is the cornerstone of HIV
treatment.
▪ It involves the use of a combination of antiretroviral drugs to
suppress the replication of the HIV virus in the body, allowing
the immune system to recover and function more effectively.
▪ ART is highly effective in reducing viral load, maintaining
immune function, and improving the overall health and quality
of life of people living with HIV/AIDS

7.1.1: GOALS
▪ Clinical goals : Prolongation of life and improvement in quality of life
▪ Virological goals : Greatest possible reduction in viral load for as long as
possible to an undetectable level (<50 copies/mL)
▪ Immunological goals : Immune reconstitution that is both quantitative and
qualitative. Improve the CD4 count (above a level of 200 cells/mm3)
▪ Therapeutic goals : Rational sequencing of drugs in to achieve: clinical,
virological and immunological goals while maintaining treatment options,
limiting drug toxicity and facilitating adherence
▪ Reduction of HIV transmission in individuals by suppression of viral load

7.1.2: CLASSES OF ANTIRETROVIRAL DRUGS
▪ Approved antiretroviral (ARV) HIV drugs are divided into seven drug
classes based on how each drug interferes with the HIV life cycle. These
seven classes include the nucleoside reverse transcriptase inhibitors
(NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs),
protease inhibitors (PIs), fusion inhibitors, CCR5 antagonists, post-
attachment inhibitors, and integrase strand transfer inhibitors (INSTIs).
The choice of an HIV treatment regimen depends on a person's
individual needs.
▪ Type A/Entry inhibitors
▪ Ibalizunamb
▪ Enfuvertide
▪ Maraviroc

▪ Type B/ Reverse Transcriptase Inhibitors
▪ NRTI [Nucleoside reverse transcriptase Inhibitors]
▪ They are pseudo nucleosides which binds to the viral ssRNA at the complementary DNA site and block further
DNA elongation
▪ E.g:
▪ Zidovudine
▪ Stavadine
▪ Didanosine
▪ Zalcitabine
▪ Tenofovir
▪ Abacavir
▪ Lamivudine (longer acting)
▪ Emtriutabine (once a day)
▪ These two are the safest and widely used in this category, no problem with any organ

▪ Type B/ Reverse Transcriptase Inhibitors
▪ NNRTI [Non-Nucleoside reverse transcriptase Inhibitors]
▪ Non-competitive Inhibitor of reverse transcriptase
▪ They prevent base insertion
▪ They do not need Phosphorylation
▪ Affect HIV I
▪ E.G
▪ Eja Vironz (most popular and safest)
▪ Neveradine
▪ Delavirdine
▪ Etra Virine (Newer)
▪ Rilpl Virine (newer)
▪ Dalpi Virine (newer)

▪ Type C/Integrase Inhibitors
▪ Prevents the integration of Viral and Host DNA
▪ Examples:
▪ Raltigrovir
▪ Elvita gravir
▪ Doluta gravir
▪ They are considered as most of the most potent and most effective HIV drugs
▪ Type D/Protease Inhibitors
▪ In the host cell, viral proteins are formed in long inactive form, which are to be broken down into active particles which is
mediated by proteases
▪ These inhibitors inhibits the breaking down of large viral protwins into small active viral proteins
▪ Examples:
▪ Rotinavir
▪ Indinavir
▪ Saqinavir
▪ AtiziNavir

7.1.3. INITIATION AND MONITORING OF ART
▪ Monitoring of efficacy of art:
▪ Clinical improvement
▪ Weight gain.
▪ Decrease severity of HIV related disease.
▪ Increase in Total Lymphocyte count.
▪ Improvement in biological markers of HIV.
▪ CD 4 + T – Lymphocyte count.
▪ Plasma HIV – RNA levels.
▪ Treatment should be monitored by measuring viral load, which should drop tenfold in the first 4–8 wks of
ART. Within 6 mths, viral load should be below the limit of detection (usually 400–1000 copies/mL. CD4
count rises with treatment and falls with treatment failure, and can be used for monitoring in countries
where viral load is unavailable
▪ Adherence to ART is crucial for its effectiveness. Patients are advised to take their medications as
prescribed, without missing doses.
▪ Consistent adherence helps maintain viral suppression and reduces the risk of developing drug resistance

Initiation of art based on cd4 count and WHO clinical staging:

7.1.4. COMPLICATIONS AND MANAGEMENT
▪ There are mostly two complication: IRIS and Drug Resistance
▪ Immune reconstitution inflammatory syndrome (IRIS): IRIS is a paradoxical worsening or
manifestation of pre-existing infections or inflammatory conditions that occurs shortly after starting
ART.
▪ It happens due to the restoration of the immune system, leading to an exaggerated inflammatory
response against latent or subclinical infections. IRIS can be seen in individuals with advanced HIV
disease who have a low CD4+ T-cell count at the time of ART initiation. Common conditions associated
with IRIS include tuberculosis, cryptococcal meningitis, and cytomegalovirus retinitis.
▪ Management:
▪ Anti-inflammatory medications: Corticosteroids are the mainstay of treatment for moderate to severe IRIS.
Prednisone is commonly used with an initial dose of 1-1.5 mg/kg/day (maximum 60 mg/day) for 2-4 weeks,
followed by a gradual taper over 4-6 weeks.
▪ Aspirin: Aspirin may be used as an adjunct to control inflammation and reduce symptoms in mild cases of IRIS.

7.1.4. COMPLICATIONS AND MANAGEMENT
▪ Antiretroviral drug resistance
▪ Prevention of drug resistance: Encouraging and supporting adherence to ART is crucial in preventing the development of drug
resistance.
▪ Regular viral load monitoring: Frequent viral load testing allows for early detection of treatment failure and the development of drug
resistance mutations.
▪ Examples of Alternative Drugs for Drug-Resistant ART regimen: If drug HIV:
▪ Efavirenz Resistance:
▪ Alternative NNRTIs: Etravirine or Rilpivirine.
▪ Protease Inhibitors: Darunavir or Atazanavir boosted with ritonavir or cobicistat.
▪ Lamivudine/Emtricitabine Resistance:
▪ Alternative NRTI: Tenofovir disoproxil fumarate (TDF) or Tenofovir alafenamide (TAF).
▪ Tenofovir Resistance:
▪ Alternative NRTIs: Zidovudine, Abacavir, or Stavudine (caution with Stavudine due to potential toxicities).
▪ Lopinavir/Ritonavir Resistance:
▪ Alternative Protease Inhibitors: Darunavir or Atazanavir boosted with ritonavir or cobicistat.
▪ Integrase Inhibitor Resistance (e.g., Raltegravir or Dolutegravir):
▪ Alternative Integrase Inhibitors: Elvitegravir or Bictegravir (both require boosting with cobicistat).

DIFFERENT ARTs
THAT BLOCKS THE
LIFE CYCLE OF HIV

7.2. INNOVATIVE TREATMENT APPROACHES
▪Highly Active Antiretroviral
Therapy:
▪2 NRTIs plus either a NNRTI or
Protease inhibitor or Integrase
Inhibitors

7.3. VACCINES AND CURE RESEARCH
▪ Vaccine Development: Scientists have made substantial progress in understanding the complex biology of the HIV
virus. Numerous vaccine candidates have been tested in clinical trials. Although we haven't yet achieved a licensed
preventive vaccine, some candidates have shown promising results in providing partial protection and priming the
immune system to control the virus.
▪ Cure Research: The search for an HIV cure is a challenging task due to the virus's ability to integrate into the host's
genetic material. "Functional cures" that achieve long-term remission without the need for continuous treatment have
been reported in a few cases. However, a true "sterilizing cure" that completely eliminates the virus from the body
remains elusive.
▪ Gene Editing Techniques: Recent advancements in gene-editing technologies, such as CRISPR-Cas9, offer new hope
for targeted interventions to eliminate HIV reservoirs from the body.
▪ Long-acting Therapies: Research is ongoing to develop long-acting antiretroviral therapies that reduce the burden of
daily medication for HIV-positive individuals.
▪ Cure Research Challenges: Eradicating HIV from the body is complicated due to viral latency, the ability of the virus to
hide in dormant cells, and the potential for viral rebound after stopping treatment. Overcoming these challenges requires
continued dedication and resources.
▪ Reasons of failure of Anti-HIV Vaccine
▪ The changing nature of GP120:
▪ Genetic mutation in GP120 gene, is making it difficult for the antibodies to recognize it
▪ It has many antigenic variants and the human body fail to form antibodies against each and every variant

7.4. MANAGEMENT OF COMPLICATIONS: OPPORTUNISTIC
INFECTIONS AND PROPHYLAXIS
 Opportunistic infections and prophylaxis
• HIV infected adults with CD4 <250 cells/mm3 OR
• WHO clinical stage 3 or 4 irrespective of CD4 count
• Prophylaxis for opportunist infections based on c4 count
1. Less than 200, Pneumocystic carinni pneumonia => co-trimoxazole
2. Less than 100, Toxoplasmosis => co-trimoxaxole
3. Less than 75, Mycobacterium avium complex => Clarithromycin/azithromycin
4. Less than 50, Cytomegalovirus => ganciclovir
• This therapy helps to protect against pneumocystis, toxoplasmosis and isospora belli
• Also:
 Avoidance of contaminated water.
 Barrier contraception.
 Avoidance of animal-borne infection (cats)
 Malaria vector control in endemic areas.
 Vaccination against pneumococcus, seasonal influenza and hepatitis B is useful once CD4 counts are >200
cells/mm3

8. PREVENTION AND RISK REDUCTION:
8.1. Primary Prevention
8.2. Secondary Prevention

8.1: PRIMARY PREVENTION
▪ Primary prevention focuses on implementing measures to prevent individuals from acquiring HIV in the first place.
▪ Safe Sex Practices
▪ Needle Exchange Programs
▪ Pre-Exposure Prophylaxis (PrEP)
▪ Education and Awareness Campaigns
▪ Safe Sex Practices: Practicing safe sex, particularly using condoms consistently and correctly, remains one of the most effective
ways to prevent sexual transmission of HIV. It is crucial to educate individuals about the importance of safe sex and make
condoms widely accessible.
▪ Needle Exchange Programs: For individuals who inject drugs, needle exchange programs play a role in reducing the risk of HIV
transmission through contaminated needles. These programs provide clean needles and syringes, thereby reducing the sharing of
infected equipment.
▪ Pre-Exposure Prophylaxis (PrEP): PrEP is a preventive medication regimen for individuals at high risk of acquiring HIV. It
involves taking antiretroviral drugs daily to reduce the chances of infection. PrEP has proven highly effective when used as
prescribed.
▪ This is for HIV discorbant couple who wants to have a child (a partner –ve and the other +ve) and not for health workers or Sexworkers cos they
don’t know when they will be exposed to HIV
▪ So they start pre exposure prophylaxis prior to conceiving
▪ They take combination of Tenofivir + Embricitamine

8.2: SECONDARY PREVENTION
▪ Secondary prevention strategies are focused on individuals who are already at risk of HIV transmission,
aiming to prevent further spread or progression of the disease
▪ Early Detection and Treatment
▪ Post-Exposure Prophylaxis (PEP)
▪ PEP is a short course of antiretroviral medication given to individuals who have had a potential exposure to HIV (e.g.,
unprotected sex, needlestick injury)
▪ The first dose should be given as soon as possible, preferably within 6–8 hrs; after 72 hrs PEP is ineffective. Dual NRTIs are
usually recommended, with a PI or efavirenz if exposure is high-risk. HIV antibody testing should be repeated at 6, 12 and
24 wks after exposure
▪ Start within 72 hours of exposure
▪ Duration of treatment is 28 days – 30 days
▪ 2NRTIs are recommended for low risk exposure like needle stick injury common in health care workers
▪ 2NRTIs + 1Protease/1Integrase inhibitors are given High risk exposures

9. HIV/AIDS IN SPECIAL POPULATIONS:
9.1. HIV in children and adolescents
9.2. HIV in older adults
9.3. HIV in pregnant women

9.1: HIV IN CHILDREN AND ADOLESCENT
▪ Unique Considerations: Pediatric HIV presents some unique
challenges. Children may acquire HIV from their infected mothers
during pregnancy, childbirth, or breastfeeding. Timely identification
of HIV in infants is critical to initiating appropriate treatment.
▪ Treatment Challenges: Pediatric antiretroviral drugs are formulated
differently from those used in adults. Dosing and administration need
to be adjusted for children based on their age and weight.
▪ Adherence: Ensuring adherence to medication can be challenging in
children and adolescents. Involving parents, guardians, and providing
psychosocial support is essential for successful treatment outcome

9.2: HIV IN OLDER ADULTS
▪ Age-Related Complications: Older adults living with HIV may
face age-related health issues compounded by the effects of the
virus and long-term antiretroviral use. Conditions such as
cardiovascular disease, bone density loss, and cognitive
impairment need to be addressed comprehensively.
▪ Late Diagnosis: HIV is often overlooked in older adults, leading
to delayed diagnosis and treatment initiation. Healthcare
providers should maintain a high index of suspicion and offer
routine HIV testing, especially in high-risk populations.

9.3: HIV IN PREGNANT WOMEN
▪ All pregnant women should be recommended for HIV screening. ART has reduced the
risk of mother-to-child transmission of HIV to <1%.
▪ Caesarean section reduces the risk of transmission but makes no difference to risk in
those on ART. HIV is also transmitted by breastfeeding but risk can be reduced by
treating the infant with antiretroviral.
▪ Prevention of Mother-to-Child Transmission (PMTCT): Preventing transmission of
HIV from mother to child is a priority. Antenatal care, HIV testing, and provision of
appropriate antiretroviral medication during pregnancy and childbirth can significantly
reduce transmission rates.
▪ Breastfeeding Considerations: In regions with high HIV prevalence, the risk of
mother-to-child transmission through breastfeeding must be balanced against the
nutritional benefits of breastfeeding. Safe infant feeding practices should be promoted

10. PSYCHOSOCIALAND MENTAL HEALTH
EFFECTS
10.1. Stigma and discrimination
10.2. Support services and counselling

10.1:STIGMAAND DISCRIMINATION
▪ There is a cyclical relationship between stigma and HIV; people who experience stigma and
discrimination are marginalized and made more vulnerable to HIV, while those living with HIV are
more vulnerable to experiencing stigma and discrimination.
▪ Myths and misinformation increase the stigma and discrimination surrounding HIV and AIDS.
▪ Roughly one in eight people living with HIV is being denied health services because of stigma and
discrimination.
▪ Adopting a human rights approach to HIV and AIDS is in the best interests of public health and is key to
eradicating stigma and discrimination.
▪ UNAIDS and the World Health Organization (WHO) cites fear of stigma and discrimination as the main
reason why people are reluctant to get tested, disclose their HIV status, and take antiretroviral drugs
(ARVs).
▪ One study found that participants who reported high levels of stigma were over four times more likely
to report poor access to care. This contributes to the expansion of the global HIV epidemic and a higher
number of AIDS-related deaths.

10.2: SUPPORT SERVICES AND COUNSELLING
▪ In March 2016, UNAIDS and WHO’s Global Health Workforce
Alliance launched the Agenda for Zero Discrimination in
Healthcare.
▪ This works towards a world where everyone, everywhere, can
receive the healthcare they need with no discrimination, in line
with The UN Political Declaration on Ending AIDS.
▪ Zero discrimination is also at the heart of the UNAIDS vision,
and one of the targets of its Fast-Track response.
▪ WHO and UN has recognized December 1st as World AIDS Day
for support to HIV/AIDs patient and sensitisation

11:PROGNOSIS
▪ The prognosis, or prospect of recovery, for HIV-positive and AIDS
patients has improved tremendously over the past 20 years, but still
depends on multiple factors.
▪ The most important include the patient’s access to HIV specialists and
proper drug treatments.
▪ At this time, there is still no cure for AIDS, but combinations of various
drugs can slow down the virus’s progress, often allowing patients to live
longer, healthier lives.
▪ The time to develop AIDS after HIV infection depends on the individual’s
health status, behaviors, and how soon he or she seeks treatment.
▪ In most cases, treating HIV infections or AIDS as early as possible is the
best way to improve prognosis.

12. CONCLUSION:
12.1. Key points
12.2. Q&A session

12.1: KEY POINTS
▪ HIV is a virus that attacks the immune system, leading to the development of AIDS,
which makes the immune cells compromised
▪ HIV/AIDS has a profound global impact, affecting millions of people worldwide.
▪ Antiretroviral therapy (ART) is the cornerstone of HIV management, suppressing viral
replication and improving overall health.
▪ Early detection and treatment are crucial for better outcomes and reducing the risk of
transmission to others.
▪ Opportunistic infections pose significant threats to individuals with weakened immune
systems, and prompt diagnosis and management are essential.
▪ Prevention strategies, including safe sex practices, needle exchange programs, PrEP,
and education campaigns, helps in reducing new infections.
▪ Special populations, such as children, older adults, and pregnant women, have unique
considerations and require tailored care.

13. REFERENCES
▪ Harrison’s Principle of Internal Medicine 20th Edition
▪ Davidson’s Essentials of Internal Medicine 2nd Edition
▪ Davidson’s Principle and Practice of Medicine 24th Edition
▪ HIV/AIDS by www.mednotes.in
▪ HIV/AIDS by Prof. OP Rajoura
▪ HIV/AIDS by Stupiremed
▪ Anti-HIV drug by www.mednotes.in

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