HIV from defination to treatment and prognosis

hiv disease all topics included from defination to treatment

1. HIV: Understanding the Epidemic, Ending the
Stigma.
Presented by
KIRANAKUMARA
Group 20/10

2. HIV: Understanding the Epidemic, Ending the Stigma

The Human Immunavirus (HIV) has been a pervasive global health concern for over four decades, affecting
millions of people worldwide. Despite significant advancements in treatment, prevention, and awareness
efforts, HIV remains a formidable challenge, particularly in marginalized and vulnerable communities. This
presentation aims to provide a comprehensive overview of the HIV epidemic, its impact on individuals,
communities, and societies, and the concerted efforts being made to combat it. Through this discussion, we
hope to promote awareness, reduce stigma, and support those affected by HIV, ultimately contributing to a
global response that is more informed, empathetic, and effective.

3. Human Immunodeficiency Virus (HIV) Infection:
A chronic, life-threatening viral infection caused by the Human Immunodeficiency Virus (HIV), which progressively
destroys the body's immune system, specifically the CD4+ T lymphocytes (T cells). This impairment of the immune
system makes the individual susceptible to opportunistic infections, autoimmune disorders, and certain types of
cancer.
HIV Morphology:
HIV (Human Immunodeficiency Virus) is a member of the Retroviridae family. Its morphology is characterized by:
1. Size: Approximately 120 nanometers (nm) in diameter.
2. Shape: Spherical or icosahedral.
3. Viral envelope: Composed of a lipid bilayer derived from the host cell membrane, embedded with glycoproteins
(gp120 and gp41).
4. Capsid: A cone-shaped core composed of multiple copies of the p24 protein.
5. Nucleocapsid: Contains the viral genome, composed of two single-stranded RNA molecules.
Key Features:
1. Glycoprotein spikes: gp120 and gp41 proteins protrude from the viral envelope, facilitating attachment and entry
into host cells.
2. Capsid symmetry: The capsid exhibits icosahedral symmetry, providing structural stability.
3. Genome organization: The viral genome consists of two identical RNA strands, containing nine genes that
encode 15 proteins.

5. Origins of HIV and its timeline.
The most widely accepted theory is that HIV-1, the most common strain, originated in Kinshasa, Democratic
Republic of Congo, in the 1950s.
A Congo man, later identified as a local bushmeat hunter, is believed to have contracted the virus from an
infected chimpanzee. This event is thought to have marked the zoonotic transmission of HIV-1 from animals to
humans.
1950s-1970s:
- 1959: First reported case of AIDS-like symptoms
- 1976: First reported case of AIDS in the US
- 1977-1980: Gaétan Dugas, a Canadian flight attendant, is later identified as "Patient Zero" and linked to many
early cases of AIDS in the US
1980s:
- 1981: CDC reports cluster of cases of PCP and KS
- 1982: Term "AIDS" coined
- 1983: HIV identified as cause of AIDS
- 1985: First HIV antibody test available

6. 1990s:
- 1991: Magic Johnson announces he has HIV
- 1996: Combination antiretroviral therapy (cART) widely available
2000s:
- 2000: UNAIDS establishes Millennium Development Goals
- 2003: US President's Emergency Plan for AIDS Relief (PEPFAR) launches
2010s:
- 2010: UNAIDS launches "Getting to Zero" campaign
- 2014: UNAIDS launches "90-90-90" targets
2020s:
- 2020: COVID-19 pandemic affects HIV services
- 2021: Progress reported towards "90-90-90" target

7. Gaétan Dugas Earvin "Magic" Johnson
Jr. an American
businessman and former
professional basketball pl
ayer
Dominic D'Souza, a Goan man, was India's
first openly HIV-positive person. He fought
against stigma, founded an NGO, and
advocated for HIV/AIDS rights until
his death in 1992.

8. UNAIDS 90-90-90 Targets
Launched in 2014, the UNAIDS 90-90-90 targets aim to:
By 2020:
1. 90% of all people living with HIV will know their HIV status.
2. 90% of all people with diagnosed HIV infection will receive sustained antiretroviral therapy (ART).
3. 90% of all people receiving ART will have viral suppression.
Current Progress:
As of 2021:
- 84% of people living with HIV know their status
- 87% of people with diagnosed HIV are on treatment
- 92% of people on treatment have viral suppression
Challenges Ahead:
Despite progress, challenges remain:
- Reaching marginalized communities
- Increasing access to testing and treatment
- Addressing stigma and discrimination
Next Steps:
UNAIDS has set new targets for 2025:
- 95-95-95: Increase the percentages of people who know their status, are on treatment, and have
viral suppression.

9. The global HIV epidemic affects approximately 38 million people living with HIV worldwide, as of 2021. This
number has been steadily increasing over the years, with 1.5 million new HIV infections reported in 2021 alone.
Unfortunately, HIV continues to claim lives, with 650,000 AIDS-related deaths occurring in 2021.
In terms of prevalence, the global adult HIV prevalence stands at 0.7%, as of 2021. However, this number varies
greatly across regions, with sub-Saharan Africa having the highest prevalence at 4.5%. This highlights the
disproportionate impact of HIV on certain populations and regions.
New HIV infections have declined significantly since the peak in 1996, when 3.4 million new infections were
reported. In 2021, this number stood at 1.5 million new HIV infections. However, certain populations continue
to be disproportionately affected, with 75% of new HIV infections occurring among key populations, such as
men who have sex with men, sex workers, and injecting drug users.
EPIDEMIOLOGY

11. Modes of HIV Transmission:
1. Sexual Transmission: HIV can be transmitted through vaginal, anal, or oral sex with an infected person.
2. Blood Transmission: HIV can be transmitted through blood transfusions, sharing needles, or other blood-
to-blood contact.
3. Mother-to-Child Transmission: HIV can be transmitted from an infected mother to her child during
pregnancy, childbirth, or breastfeeding.
4. Occupational Exposure: Healthcare workers can be at risk of HIV transmission through needlesticks or
other occupational exposure.
How HIV Enters the Body:
1. Mucous Membranes: HIV can enter the body through mucous membranes, such as those found in the
vagina, anus, or mouth.
2. Bloodstream: HIV can enter the bloodstream through blood-to-blood contact, such as through needle
sharing or blood transfusions.
3. Open Wounds: HIV can enter the body through open wounds or cuts, especially if they come into
contact with infected blood or bodily fluids.

12. Stage 1: Attachment (Binding)
- HIV gp120 protein binds to CD4 receptors on the surface of immune cells (CD4 T-cells).
- This attachment is specific and allows HIV to target and infect CD4 T-cells.
Stage 2: Entry (Fusion)
- After attachment, HIV gp41 protein mediates fusion of the HIV envelope with the CD4 T-cell membrane.
- This fusion allows HIV to release its genetic material into the cell.
Stage 3: Uncoating and Release of Viral Components
- The HIV capsid (protein shell) enters the cytoplasm of the CD4 T-cell.
- The capsid is then dissolved, releasing HIV proteins and enzymes, including reverse transcriptase (RT), integrase
(IN), and protease (PR).
Stage 4: Reverse Transcription
- RT converts the single-stranded HIV RNA into double-stranded HIV DNA.
- This process is error-prone, leading to high mutation rates and genetic diversity.
HIV Lifecycle:

13. Stage 5: Integration
- IN enables the HIV DNA to integrate into the host cell genome.
- This integration allows HIV to remain dormant or replicate along with the host cell.
Stage 6: Transcription and Translation
- HIV DNA is transcribed into RNA, which is then translated into new viral proteins.
- These proteins are necessary for the assembly of new HIV particles.
Stage 7: Assembly and Maturation
- New viral proteins and RNA assemble into immature HIV particles.
- PR cuts and processes these proteins, allowing the immature particles to mature into infectious HIV virions.
Stage 8: Budding and Release
- Mature HIV virions bud from the infected CD4 T-cell, releasing hundreds of new infectious particles.
- These particles can then infect other CD4 T-cells, repeating the cycle.

14. Pathogenesis: How HIV Causes Disease
As HIV replicates and spreads, it causes damage to the immune system and other organs, leading to various
diseases and complications.
Immune System Damage
- HIV infects and kills CD4 T-cells, which are essential for immune function.
- Depletion of CD4 T-cells impairs immune responses, making it harder for the body to fight off infections.
- HIV also infects and damages other immune cells, such as dendritic cells and macrophages.
Opportunistic Infections
- With a weakened immune system, the body becomes susceptible to opportunistic infections (OIs), such as:
- Pneumocystis pneumonia (PCP)
- Tuberculosis (TB)
- Cryptococcal meningitis
- Toxoplasmosis
- OIs can be life-threatening and require prompt treatment.

15. AIDS: Advanced HIV Disease
- AIDS (Acquired Immunodeficiency Syndrome) is the most advanced stage of HIV disease.
- AIDS is defined by the presence of one or more OIs or cancers, and/or a CD4 T-cell count below 200
cells/μL.
- AIDS requires prompt treatment and management to prevent further complications and improve quality
of life.
HIV Pathogenesis: Key Factors
- Viral load: High levels of HIV in the blood increase the risk of transmission and disease progression.
- CD4 T-cell count: Low CD4 T-cell counts indicate advanced HIV disease and increased risk of OIs and
cancers.
- Host genetics: Genetic factors can influence HIV susceptibility, disease progression, and response to
treatment.
- Co-infections: Presence of other infections, such as TB or hepatitis, can worsen HIV disease and increase
the risk of complications.

16. Clinical manifestations of HIV infection:
•Acute HIV Infection (0-6 weeks)
- Fever
- Rash
- Sore throat
- Muscle and joint pain
- Swollen lymph nodes
- Diarrhea
- Headache
- Fatigue
•Chronic HIV Infection (6 weeks-20 years)
- Asymptomatic (no symptoms)
- Persistent generalized lymphadenopathy (PGL)
- Oral candidiasis (thrush)
- Herpes zoster (shingles)
- Herpes simplex
- Human papillomavirus (HPV) infection
•Advanced HIV Disease (AIDS)
- Pneumocystis pneumonia (PCP)
- Tuberculosis (TB)
- Cryptococcal meningitis
- Toxoplasmosis
- Kaposi's sarcoma
- Lymphoma
- Cervical cancer
- Neurological disorders (e.g., HIV-associated dementia)
- Wasting syndrome
•Opportunistic Infections (OIs)
- Bacterial infections (e.g., pneumonia, TB)
- Fungal infections (e.g., PCP, cryptococcal meningitis)
- Viral infections (e.g., herpes simplex, HPV)
- Parasitic infections (e.g., toxoplasmosis,
cryptosporidiosis)

17. Neurological Manifestations
- HIV-associated dementia
- HIV-associated neurocognitive disorder (HAND)
- Neuropathy
- Myelopathy
- Seizures
Dermatological Manifestations
- Rash
- Oral candidiasis (thrush)
- Herpes zoster (shingles)
- Herpes simplex
- Kaposi's sarcoma
- Seborrheic dermatitis
HIV IS PREVENTABLE ,
BUT
AIDS IS
FATAL ,DEADLY!
DR.GOWDA

18. DIAGNOSTICS
Types of HIV Tests:
1. Rapid Tests: Provide results within 15-30 minutes.
2. Laboratory Tests: Provide results within 1-7 days.
3. Home Testing Kits: Allow individuals to test themselves at home.
HIV Testing Methods:
1. Antibody Tests: Detect HIV antibodies in blood or oral fluid.
2. Antigen Tests: Detect HIV p24 antigen in blood.
3. Nucleic Acid Tests (NAT): Detect HIV RNA or DNA in blood.
4. Combination Tests: Combine antibody and antigen tests.
Diagnostic Algorithms:
1. Serial Testing: Repeat testing to confirm results.
2. Parallel Testing: Use multiple tests simultaneously.
3. Confirmatory Testing: Use additional tests to confirm
diagnosis
Interpretation of Results:
1. Positive Result: Indicates HIV infection.
2. Negative Result: Indicates no HIV
infection or early infection.
3. Indeterminate Result: Requires repeat
testing.
Window Period:
1. Acute Infection: HIV may not be
detectable during the first 2-4 weeks.
2. Window Period: Time between HIV
infection and detectability (average 23 days).

19. Treatment guidelines for HIV:
Antiretroviral Therapy (ART):
1. Initiation: Start ART as soon as possible after diagnosis.
2. Regimens: Use a combination of 2-3 medications from different classes.
3. Classes: Nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors
(NNRTIs), protease inhibitors (PIs), integrase strand transfer inhibitors (INSTIs), and entry inhibitors.
Treatment Goals:
1. Viral Suppression: Achieve and maintain an undetectable viral load.
2. CD4 Recovery: Increase CD4 T-cell count.
3. Prevention of Opportunistic Infections: Prevent and treat opportunistic infections.
ART Regimens:
1. First-Line Regimens: Tenofovir (TDF) + emtricitabine (FTC) + efavirenz (EFV) or rilpivirine (RPV).
2. Second-Line Regimens: Zidovudine (AZT) + lamivudine (3TC) + lopinavir/ritonavir (LPV/r).
3. Third-Line Regimens: Individualized regimens based on resistance testing.

20. Treatment Considerations:
1. Pregnancy: Use ART regimens that are safe during pregnancy.
2. Children: Use pediatric-specific ART regimens.
3. Co-infections: Consider co-infections such as TB, hepatitis B, and hepatitis C.
4. Resistance: Monitor for resistance and adjust regimens accordingly.
Monitoring and Follow-up:
1. Viral Load: Monitor every 3-6 months.
2. CD4 Count: Monitor every 3-6 months.
3. Clinical Evaluation: Perform regular clinical evaluations.
4. Resistance Testing: Perform resistance testing as needed.
Prevention of Opportunistic Infections:
1. PCP Prophylaxis: Use trimethoprim-sulfamethoxazole (TMP-SMX) for PCP prophylaxis.
2. Toxoplasmosis Prophylaxis: Use TMP-SMX for toxoplasmosis prophylaxis.
3. TB Prophylaxis: Use isoniazid (INH) for TB prophylaxis.

21. Preventions:
1. Safe Sex Practices: Use condoms consistently and correctly.
2. Needle Exchange Programs: Use sterile needles and syringes.
3. Pre-Exposure Prophylaxis (PrEP): Take antiretroviral medication
daily to prevent HIV infection.
4. Post-Exposure Prophylaxis (PEP): Take antiretroviral medication
within 72 hours of exposure to prevent HIV infection.
5. Blood Safety: Screen blood donations for HIV.
6. Mother-to-Child Transmission Prevention: Provide antiretroviral
therapy to pregnant women and their infants.
Vaccinations:
1. HIV Vaccine: Currently, there is no licensed HIV vaccine. However,
several candidates are in various stages of clinical trials.
2. HPV Vaccine: Human papillomavirus (HPV) vaccine can prevent
HPV-related cancers and genital warts, which are more common in
people with HIV.
DR.GOWDA
DO NOT DRIVE
WITHOUT
HELMETS!

22. Advances in Treatment and Prevention:
1. Long-Acting Antiretroviral Therapy (ART): Development of long-
acting ART formulations to improve adherence.
2. HIV Vaccine: Continued research and development of an
effective HIV vaccine.
3. Pre-Exposure Prophylaxis (PrEP): Expanded access to PrEP and
development of long-acting PrEP formulations.
4. Post-Exposure Prophylaxis (PEP): Improved access to PEP and
development of more effective PEP regimens.
Addressing Health Disparities:
1. Increased Access to Care: Improving access to HIV testing,
treatment, and prevention services, particularly in marginalized
communities.
2. Cultural Competence: Providing culturally competent care to
address the unique needs of diverse populations.
3. Addressing Stigma and Discrimination: Continuing efforts to
address stigma and discrimination, which can prevent individuals
from seeking care.

23. REMEMBER, PROTECTION IS ALWAYS
BETTER THAN CURE!,
YES PROTECTION!