# HIV/AIDS

> CIE A-Level Biology · 9700
> Source: https://www.owlsprep.com/study/cie-9700-u10-hiv-aids/

This sub-topic covers the structure, replication, and clinical progression of HIV infection leading to AIDS, aligned to CIE A-Level Biology 9700 requirements. We also explore control strategies and the global impact of the HIV/AIDS pandemic.

**Prerequisites:** [Virus structure](https://www.owlsprep.com/study/cie-9700-u01-virus-structure/); [The human immune system](https://www.owlsprep.com/study/cie-9700-u11-immune-system/)

## Learning objectives

- Describe the structure and classification of HIV
- Explain the replication cycle of HIV in human helper T cells
- Distinguish between HIV infection and AIDS
- Explain how HIV causes progressive immunodeficiency
- Discuss control strategies and the global impact of HIV/AIDS

## Structure and Classification of HIV

HIV (Human Immunodeficiency Virus) is classified as an enveloped retrovirus, meaning it carries its genetic material as single-stranded RNA and has an outer lipid membrane derived from host cells.

**HIV** — A pathogenic retrovirus that infects human CD4+ helper T cells, causing progressive damage to the adaptive immune system

*Notation:* Human Immunodeficiency Virus

*Example:* Two main strains exist: HIV-1 (virulent, most common globally) and HIV-2 (less virulent, mostly restricted to West Africa)

- **Envelope**: Outer lipid bilayer with embedded glycoproteins *gp120* (binds CD4 receptors) and *gp41* (mediates membrane fusion)
- **Capsid**: Protein coat that encloses viral genetic material and enzymes
- **Genome**: Two identical copies of single-stranded RNA
- **Viral enzymes**: Reverse transcriptase, integrase, and protease, all required for replication

**Worked example:** Describe how HIV's structure allows it to enter helper T cells

1. 1. The viral glycoprotein gp120 on the HIV envelope binds specifically to the CD4 receptor on the surface of helper T cells
2. 2. This binding causes a conformational change that allows gp41 to fuse the viral envelope with the host cell's plasma membrane
3. 3. The viral capsid is then released into the cytoplasm of the helper T cell

> **Exam tip:** Always name the specific glycoproteins gp120 and gp41 when describing entry; CIE examiners require this specific detail for full marks.

## HIV Replication Cycle

HIV follows a unique replication cycle that allows it to integrate into the host genome and remain latent for many years, evading both the immune system and antiviral drugs.

**Reverse Transcription** — The process by which retroviruses convert their single-stranded RNA genome into double-stranded DNA, catalysed by the viral enzyme reverse transcriptase

1. Attachment and entry: gp120 binds CD4, envelope fuses, capsid enters the host cytoplasm
2. Reverse transcription: Reverse transcriptase synthesises double-stranded DNA from the viral RNA template
3. Integration: Viral DNA enters the nucleus and is inserted into the host genome by integrase (no new viruses are produced during latency)
4. Transcription and translation: Host cell machinery produces viral RNA and viral proteins
5. Assembly: New capsids assemble around viral RNA and enzymes
6. Budding: New virions bud from the host membrane, gaining their envelope. Protease cleaves polyproteins to produce mature infectious virions

**Worked example:** Explain why reverse transcriptase is an effective target for antiviral drugs

1. 1. Reverse transcriptase is a viral enzyme that is not produced or required by uninfected human host cells
2. 2. Drugs that inhibit reverse transcriptase block the conversion of viral RNA to DNA, preventing HIV from integrating into the host genome and producing new virions
3. 3. Since the enzyme is not present in human cells, the drug has minimal impact on normal host function, making it a selective and effective therapeutic target

## Progression from HIV to AIDS

HIV infection does not cause AIDS immediately. There is a characteristic multi-stage progression of disease that can last 10+ years in untreated people.

1. Acute infection: 2-4 weeks post-exposure, flu-like symptoms, high viral load
2. Clinical latency: Asymptomatic stage, low-level viral replication, lasts 5-15 years on average untreated
3. Symptomatic infection: Viral load increases, CD4+ helper T cell count drops, immune function weakens, mild opportunistic infections develop
4. AIDS: Final stage, defined as CD4 count < 200 cells per mm³ of blood, with severe life-threatening opportunistic infections

HIV causes AIDS by progressively destroying CD4+ helper T cells, which are critical for coordinating the adaptive immune response. Without enough helper T cells, the body cannot fight off other pathogens.

**Worked example:** Explain why people with untreated AIDS are at very high risk of active tuberculosis

1. 1. Untreated HIV infection destroys large numbers of CD4+ helper T cells, severely impairing immune function
2. 2. *Mycobacterium tuberculosis* (the TB bacterium) is normally controlled by the immune system in latent infection
3. 3. When the immune system is damaged by AIDS, latent TB can reactivate, and new TB infections cannot be controlled, leading to life-threatening active TB disease

## Control and Global Impact of HIV/AIDS

HIV/AIDS remains one of the world's most significant global public health issues, with approximately 38 million people living with HIV globally as of 2024. A range of strategies are used to control its spread.

- Transmission prevention: Condom use, antiretroviral treatment (ART) that reduces viral load to undetectable levels (preventing transmission), clean needle programs, screened blood supplies
- Treatment: ART combines multiple drugs that target different stages of HIV replication, suppresses viral load, prevents progression to AIDS
- Prevention of mother-to-child transmission: ART given to pregnant people with HIV reduces transmission risk to <1%
- Vaccines: No effective licensed vaccine currently exists

**Worked example:** Explain why developing an effective HIV vaccine has been so difficult

1. 1. Reverse transcriptase has no proofreading activity, so HIV has a very high mutation rate during replication
2. 2. This leads to rapid evolution of viral surface proteins like gp120, allowing the virus to evade antibodies induced by a vaccine
3. 3. HIV also integrates as latent proviral DNA into the host genome, where it is hidden from the immune system even if vaccine-induced immunity is present

> **Exam tip:** Always state that ART does not cure HIV, it only controls replication. This is a common marking point in extended response questions.

## Common pitfalls

- **Wrong:** Calling AIDS a virus, or HIV the disease
  - Why it fails: Confuses the causative agent with the resulting clinical condition, which loses easy marks
  - Correct: HIV is the virus that causes infection; AIDS is the late-stage immunodeficiency condition caused by untreated HIV infection
- **Wrong:** Forgetting to name specific HIV enzymes or glycoproteins
  - Why it fails: CIE requires specific named molecules for full marks in structure/replication questions
  - Correct: Always name gp120, gp41, reverse transcriptase, integrase and protease when describing HIV
- **Wrong:** Stating HIV directly kills patients
  - Why it fails: HIV does not cause death directly; it acts by weakening the immune system
  - Correct: HIV destroys CD4+ helper T cells, causing immunodeficiency that allows opportunistic pathogens to cause fatal infections
- **Wrong:** Claiming antiretroviral therapy cures HIV infection
  - Why it fails: ART cannot eliminate integrated latent viral DNA from host cells
  - Correct: ART suppresses viral replication, reduces viral load to undetectable levels, and prevents progression to AIDS, but does not cure HIV infection

## Cheatsheet

| Feature | Key CIE Required Detail |
| --- | --- |
| Virus type | Enveloped retrovirus, ssRNA genome |
| Surface glycoproteins | gp120 (binds CD4), gp41 (fusion) |
| Viral enzymes | Reverse transcriptase, integrase, protease |
| HIV vs AIDS | HIV = causative virus; AIDS = late stage disease |
| AIDS definition | CD4 count < 200 cells mm⁻³, severe opportunistic infections |
| ART action | Inhibits replication, does not cure HIV |

## What's next

HIV/AIDS is a core topic for CIE A-Level Biology, frequently tested in both multiple choice and extended response questions. Mastering this sub-topic builds on your understanding of viruses and immunology, and prepares you to explore other globally significant infectious diseases and strategies for controlling them. This knowledge is also foundational for answering questions on public health and the evolution of drug resistance, which often appear in Paper 4.

- [Tuberculosis](https://www.owlsprep.com/study/cie-9700-u10-tuberculosis/)
- [Malaria](https://www.owlsprep.com/study/cie-9700-u10-malaria/)
- [Antibiotics and Antibiotic Resistance](https://www.owlsprep.com/study/cie-9700-u10-antibiotics-and-antibiotic-resistance/)

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