HIV and AIDS

Question 1

HIV Lifecycle

Answer 1

+ ssRNA
Attachment and Entry: HIV binds to the CD4 receptor and co-receptors (CCR5 or CXCR4) on the surface of T-helper cells through its envelope glycoprotein gp120.

Fusion: The viral envelope fuses with the host cell membrane, releasing the viral RNA and enzymes into the host cell.

Reverse Transcription: The viral RNA is reverse-transcribed into DNA by the enzyme reverse transcriptase.

Integration: The viral DNA is integrated into the host genome by the enzyme integrase, forming a provirus.

Transcription and Translation: The provirus is transcribed into viral RNA, which is then translated into viral proteins.

Assembly: New viral RNA and proteins assemble into immature virions at the cell membrane.

Budding and Maturation: Immature virions bud from the host cell and mature through the action of the viral protease, becoming fully infectious.

Question 2

Therapeutic Intervention

Answer 2

Nucleoside Reverse Transcriptase Inhibitors (NRTIs): Inhibit reverse transcriptase by incorporating faulty nucleotides.

Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): Bind to reverse transcriptase, inhibiting its function.

Protease Inhibitors: Prevent viral maturation by inhibiting the protease enzyme.

Question 3

Clinical Course of HIV
Stages of HIV Infection

Answer 3

Acute Infection: Rapid viral replication and dissemination, leading to flu-like symptoms.

(Chronic) Clinical Latency: HIV replicates at low levels; the patient may remain asymptomatic for years.

AIDS: Severe immune system damage leading to opportunistic infections and cancers, defining the progression to acquired immunodeficiency syndrome (AIDS).

Question 4

Mutations in HIV and Drug Resistance

Answer 4

High Mutation Rate:

HIV’s reverse transcriptase lacks proofreading ability, leading to frequent mutations.
These mutations can result in the emergence of drug-resistant strains.
Impact on Therapy:

Drug Resistance: Mutations can render antiretroviral drugs ineffective, necessitating changes in therapy.
Combination Therapy: ART uses multiple drugs to reduce the likelihood of resistance development.

Question 5

Vaccine Development for HIV
Challenges:

Answer 5

High Genetic Variability: The rapid mutation rate of HIV complicates vaccine design.

Immune Evasion: HIV targets the immune system and can evade immune responses through latency and antigenic variation.

Lack of Natural Immunity: No known cases of complete immune-mediated clearance of HIV complicate the development of an effective vaccine.

Question 6

Strategies:

Answer 6

Broadly Neutralizing Antibodies (bNAbs): Target conserved regions of the virus.
T Cell-Based Vaccines: Aim to elicit strong cytotoxic T lymphocyte responses to control infection.
Combination Approaches: Use both antibody and T cell responses for broader protection.