HIV

Human Immunodeficiency Virus (HIV)

Overview

  • Acquired Immunodeficiency Syndrome (AIDS)

  • 1-2% of every 1000 women giving birth are HIV+

Risk Factors

  1. Multiple sexual partners

  2. Unprotected vaginal/anal sex

  3. Existing STI’s

  4. Intravenous drug use

  5. Unsafe injections, blood transfusions, tissue transplantation

  6. Accidental needle stick injuries (especially among health workers)

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Characteristics of HIV

  • Type: Retrovirus (RNA: transfers to DNA via reverse transcription)

  • Key Proteins:

    • GP 41: Fusion with host cell membrane

    • GP 120: Attachment to target receptor

Target Cells

  • CD4(+) cells: T-Helper cells, Monocytes, Macrophages, Microglial cells, Dendritic cells

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HIV and How It Works

HIV is a retrovirus, meaning it has RNA as its genetic material. Unlike human cells, which follow the normal process of DNA → RNA → Proteins, HIV reverses this process using a special enzyme called reverse transcriptase. It converts RNA → DNA, which is then used to produce new viruses. This process is called reverse transcription.

HIV Structure & Key Proteins:

  • Lipid bilayer (outer covering)

  • GP41 – Helps the virus fuse with human cells.

  • GP120 – Helps the virus attach to its target cells.

HIV Targets the Immune System:

HIV primarily infects CD4(+) cells, which are important for immunity. These include:

  • T-helper cells

  • Monocytes → Macrophages

  • Microglial cells (brain immune cells)

  • Dendritic cells (under the skin)

By attacking these cells, HIV weakens the immune system, making the body vulnerable to infections.

How HIV Infects Cells & Why It’s Hard to Cure

How HIV Enters the Body:

HIV attaches to CCR5 receptors on macrophages using its active site.

T-helper cells, which don’t have CCR5, use CXCR4 receptors instead.

GP41 helps the virus fuse with the host cell, allowing infection.

Why HIV is Hard to Cure:

HIV mutates rapidly, especially its GP120 protein, making vaccine development difficult (antigenic variation).

It takes about 7 years for HIV to develop into AIDS.

Some Northern Europeans have natural immunity due to a CCR5 mutation.

Key HIV Drugs:

Maraviroc blocks CCR5, preventing infection.

Enfuvirtide - destabilize/disrupts GP41, stopping fusion with cells.

HIV Structure & Key Enzymes:

Capsid (outer shell) – Made of p24 protein, a marker for HIV in blood tests.

HIV contains double RNA molecules and three key enzymes:

  • Reverse Transcriptase – Converts viral RNA into DNA.

  • Integrase – Merges viral DNA with the host cell’s DNA.

  • Protease – Cuts long viral proteins into functional parts.

HIV Types:

  • HIV-1 – Most common worldwide, highly transmissible.

  • HIV-2 – Found mainly in West Africa, less transmissible.

Mechanism of Infection

  1. Virus contacts host cell

  2. Utilizes CCR5 (on macrophages) and CXCR4 (on T-Helper cells) for attachment

  3. Initiates fusion process

Development of AIDS

  • Takes approximately 7 years

  • Northern European race has natural immunity due to CCR5 mutation

  • Medication: Maraviroc (to inactive CCR5)

Challenges in Vaccine Development

  • Antigenic variation due to GP 120

Treatment

  • Enfuvirtide: destabilizes GP 41

HIV Types

  • HIV 1: Most common globally, highly transmissible

  • HIV 2: Primarily found in Western Africa

Important Facts

  • Anal sex poses the highest risk for HIV transmission.

  • The receptive partner (bottom) is at higher risk than the insertive partner (top).

  • Kissing is not a mode of transmission.

  • Use sterile equipment for tattoos and body piercings.