Here is a brief assignment on HIV AIDS posted on studentnurse.in

Introduction to HIV AIDS:

Immune deficiency may be acquired through the normal process of aging or senescence or by infection of the retroviruses- human immune deficiency viruses (HIV-1 and HIV-2). Infection by HIV leads to the development of the currently most dreadful infectious disease, acquired immunodeficiency syndrome (AIDS). The disease known as HIV AIDS is the consequence of HIV infection, though there is usually a long gap between infection and the manifestation of symptoms.

History of HIV AIDS:

AIDS was first detected by the Centre for Disease Control and Prevention, Atlanta USA in June 1981 among group of 5 gay men suffering from an unusual and rare pneumonia caused by fungus, Pneumocystis jirovecii (previously P. carinii) and a type of skin cancer, called Kaposi’s sarcoma. The association of these diseases with a virus was suspected and the virus was first identified in 1984. It was officially designated as human immune deficiency virus (HIV) in 1986.

Origin of HIV AIDS:

HIVs probably originated from the Simian Immunodeficiency Virus (SIV) which infects monkey and Chimpanzee. The probable location of Origin of HIV is thought to be central Africa. SIV has more similarity to HIV-2 than HIV-1.

Definition of HIV AIDS:

An infectious disease of the immune system caused by a human immune deficiency virus (HIV). AIDS is characterized by a decrease in the number of helper T cells, which causes a severe immunodeficiency that leaves the body susceptible to a variety of potentially fatal infections.
 The case definition for AIDS includes those who (a) test positive for HIV and (b) meet one of the two following criteria:

1. A CD4 T cell number of less than 200/μl  of whole blood (the normal count is 600-1000/μ) or a CD4 T cell/total lymphocytes percentage of less than 14%.
2. A CD4 T cell number of more than 200/μl; and any of the following fungal diseases including candidiasis, coccidioidomycosis, cryptococcosis, histoplasmosis, isosporiasis, Pneumocystis jirovecii pneumonia, cryptosporidiosis, or toxoplasmosis of the brain; bacterial diseases including pulmonary tuberculosis or other Mycobacterium spp. Infections, or recurrent Salmonella septicemia; viral diseases including cytomegalovirus infection, HIV- related encephalopathy, HIV wasting syndrome, chronic ulcers, or bronchitis due to HSV; or progressive multifocal leukoencephalopathy, malignant diseases such as invasive cervical cancer, Kaposi’s sarcoma, Burkitt’s lymphoma, primary lymphoma of the brain, or immunoblastic lymphoma; or recurrent pneumonia due to any agent.
   
   

ETIOLOGY OF HIV AIDS

   HIV is a variation of a virus that can be transmitted to African chimpanzees. Scientists suspect the simian immunodeficiency virus (SIV) jumped from chimps to humans when people consumed chimpanzee meat containing the virus. Once inside the human population, the virus mutated into what we now know as HIV.

RISK FACTORS OF HIV AIDS

Heterosexual intercourse with an HIV infected partner.
Male homosexual relations.
People who received transfusion of blood or blood products contaminated with HIV.
Children born to mother with HIV infection.
Breast fed infants of HIV infected mothers.
Health care workers exposed to needle stick injury.
Injection drug users who share needles.
People who already have STI are more likely to acquire HIV.

INCUBATION PERIOD OF HIV AIDS

It ranges from 6 weeks – 10 years. Antibodies are produced against virus and detectable in blood between 6 weeks to 6 months. It is also called window period.

PATHOPHYSIOLOGY OF HIV AIDS

1. The pathophysiological process of HIV/AIDS can be summarized as follows:
   Viral Entry and Replication:

1. The primary targets for HIV are cells having CD4 receptors. E.g. T-Helper cells (Both Th1 and Th-2), macrophages, and dendritic cells.
2. The virus binds to CD4 receptors on the surface of these cells with the help of its glycoprotein spikes ( Gp120) and enters the cell with the help of co-receptors, primarily CCR5 and CXCR4.
3. Once inside the host cell, the viral RNA is reverse transcribed into DNA by the enzyme reverse transcriptase.
4. The viral DNA is integrated into the host cell’s genome with the help of integrase and becomes provirus.

2. Viral Replication and Cell Death:

2. Infected cells start producing new viral particles (virions), leading to the destruction of the host cell. The infected and uninfected cells can then fuse to produce multinucleate giant  cells called syncytia.
3. The release of virions from infected cells can cause the death of CD4+ T cells.

3. Immune System Activation and Inflammation:

3. HIV triggers an immune response, resulting in chronic immune system activation and inflammation.
4. Elevated levels of immune activation contribute to the exhaustion and depletion of CD4+ T cells.

4. Depletion of CD4+ T Cells:

4. HIV specifically targets and kills CD4+ T cells, which are essential for coordinating the immune response.
5. As the infection progresses, the number of CD4+ T cells declines, compromising the immune system’s ability to mount an effective defence against infections.

5. Opportunistic Infections:

5. With the decline in CD4+ T cell count, the individual becomes susceptible to opportunistic infections that would typically be controlled by a healthy immune system.
6. Opportunistic infections may include fungal, bacterial, viral, and parasitic infections.

6. Cancers:

6. Individuals with advanced HIV/AIDS are at an increased risk of certain cancers, such as Kaposi’s sarcoma, non-Hodgkin lymphoma, and invasive cervical cancer.

7. Progression to AIDS:

7. AIDS (Acquired Immunodeficiency Syndrome) is diagnosed when the CD4+ T cell count falls below a certain threshold, and/or the individual experiences specific opportunistic infections or cancers.
8. AIDS represents the advanced stage of HIV infection, characterized by severe immunodeficiency and increased vulnerability to life-threatening illnesses.

CLINICAL MANIFESTATIONS OF HIV AIDS:

The symptoms of HIV and AIDS vary, depending on the phase of infection.

Early stage/ Primary HIV infection:

Lasts for a few weeks, and is accompanied by a brief illness that resembles flu which includes: fever headache, Rash, Body and joint aches, Tiredness, Sore Throat.

Clinically asymptomatic stage:

Lasts for an average of ten years and is symptom-free but there may be enlarged glands.

Symptomatic HIV infection

Rapid weight loss and Chronic Diarrhoea with no identifiable cause (wasting syndrome), Recurring fever or profuse night sweats, Extreme and unexplained tiredness, Prolonged swelling of lymph glands in armpits, groins, or neck, anus, or genitals, Oropharyngeal candidiasis, Kaposi’s Sarcoma (Cherry red, firm, painless nodular lesion arising from the endothelium of blood vessels), Persistent cough for more than a month.

Progression from HIV to AIDS

Severe weakened immune system give rise to multiple Opportunistic infections, and eventually leading to an AIDS diagnosis.

Complications OF HIV AIDS:

Kaposi’s sarcoma, non-Hodgkin lymphoma, and invasive cervical cancer. HIV-Associated Nephropathy (HIVAN), Immune Reconstitution Inflammatory Syndrome (IRIS), Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), AIDS associated dementia / Encephalopathy.

DIAGNOSTIC EVALUATIONS of HIV AIDS:

The diagnostic evaluation for HIV typically involves a combination of laboratory tests and clinical assessments. Here are key components of the diagnostic process:

1. HIV Antibody Test:

1. ELISA Test (Enzyme-Linked Immunosorbent Assay): This blood test detects antibodies to HIV. If the result is positive, it is usually followed by a confirmatory test.
2. Western Blot Test: This test confirms the presence of antibodies to specific HIV proteins. A positive result on the Western Blot confirms HIV infection.
3. Rapid HIV Tests: These are quick tests that provide results in about 20 minutes. They are often used in outreach and testing programs.

2. Nucleic Acid Tests (NAT):

2. Polymerase Chain Reaction (PCR): This test directly detects the presence of HIV genetic material (RNA) in the blood. It is highly sensitive and can detect HIV earlier than antibody tests.
3. Nucleic Acid Sequence-Based Amplification (NASBA) and Reverse Transcription Loop-Mediated Isothermal Amplification (RT-LAMP): These are other types of NATs used for HIV detection.

3. p24 Antigen Test:

3. This test detects the presence of the p24 antigen, a protein associated with HIV, in the blood. It can be used in combination with antibody tests for early detection.

4. CD4 T-Cell Count:

4. A blood test that measures the number of CD4 T cells in the immune system. This helps assess the stage of HIV infection and the need for antiretroviral therapy (ART).

5. Viral Load Test:

5. Measures the amount of HIV RNA in the blood, indicating the level of active virus replication. This test helps monitor the effectiveness of antiretroviral treatment.

6. Drug Resistance Testing:

6. If HIV treatment is initiated, testing for drug resistance helps determine the most effective combination of antiretroviral drugs.

7. Screening for Opportunistic Infections:

7. Tests for common opportunistic infections (e.g., tuberculosis, hepatitis) are often performed to assess overall health and guide treatment decisions.

8. Clinical Assessment:

8. A thorough medical history, physical examination, and evaluation of symptoms are essential components of the diagnostic process.

TREATMENT of HIV AIDS:

There is no cure for HIV/ AIDS, but a variety of drugs can be used in combination to control the virus. But these medicines only restrict further growth of HIV virus and keep the health of immune system stable, but is not an exact cure.
Treatment of HIV-AIDS primarily includes:

1. Anti-retroviral therapy
2. Prophylaxis for opportunistic infections
3. Treatment of opportunistic infections.

The standard treatment for HIV/AIDS and involves the use of a combination of antiretroviral drugs to suppress the replication of the HIV virus in the body. The strategy to accomplish this is called highly active anti-retroviral therapy (HAART) and is carried out by administering at least three anti-retroviral drugs at once to inhibit the replication of HIV and prevent the development of drug-resistant strains.

Classes of HIV/ AIDS antiretroviral Drugs:

Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs):
These drugs interfere with the reverse transcriptase enzyme, which is essential for the replication of the HIV virus. NRTIs are incorporated into the growing viral DNA chain, causing premature termination. Examples include Azidothymidine (AZT), also called zidovudine, lamivudine, tenofovir, and abacavir.

Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs):

NNRTIs bind directly to the reverse transcriptase enzyme, blocking its activity. They do not require activation like NRTIs. Examples include efavirenz, nevirapine, and rilpivirine

Protease Inhibitors (PIs):

Protease is an enzyme that plays a crucial role in the maturation of the HIV virus. PIs block the activity of this enzyme, preventing the production of infectious viral particles. Examples include lopinavir, atazanavir, and darunavir.

Fusion Inhibitors:

Fusion inhibitors prevent the entry of HIV into host cells by blocking the fusion of the viral and cellular membranes. Enfuvirtide is an example of a fusion inhibitor.

CCR5 Antagonists:

CCR5 antagonists block the CCR5 co-receptor on the surface of CD4 T cells, preventing HIV from entering the cell. Maraviroc is an example of a CCR5 antagonist.

Post-Attachment Inhibitors:

This newer class of drugs, represented by ibalizumab, works by binding to the CD4 receptor on the surface of CD4 T cells, preventing HIV entry.

Maturation Inhibitors:

Maturation inhibitors, such as fostemsavir, interfere with the final stages of the HIV replication cycle by blocking the maturation of the viral capsid.

Pharmacokinetic Enhancers:

Drugs like ritonavir and cobicistat are used as pharmacokinetic enhancers. They inhibit enzymes that metabolize other antiretroviral drugs, increasing their concentrations in the body.
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