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Explain the biochemistry of AIDS according to mbbs first year in short

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I have enough content from the biochemistry textbook. Let me continue reading a bit more for the drug/treatment part, then compose the answer.
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I have solid textbook content. Now let me compose the answer directly - this is a conceptual explanatory question, so per the medical-library instructions the library search suffices without needing a PubMed search.

Biochemistry of AIDS (MBBS 1st Year - Short Notes)

Causative agent: HIV (Human Immunodeficiency Virus) - HIV-1 (worldwide) and HIV-2 (Africa, parts of India). It is a retrovirus with a single-stranded RNA genome.

1. Entry into the host cell

  • Viral coat glycoprotein gp120 binds to the CD4 receptor on helper T-lymphocytes (and macrophages/dendritic cells).
  • A conformational change lets gp120 bind a chemokine coreceptor (CCR5/CXCR4).
  • The viral envelope (via gp41) fuses with the host membrane, and the core "uncoats," releasing viral RNA and enzymes (reverse transcriptase, integrase, protease) into the cytoplasm.

2. Reverse transcription

  • Reverse transcriptase (RNA-dependent DNA polymerase, encoded by pol gene) copies viral RNA into single-stranded DNA, then makes it double-stranded.
  • This is the key biochemical step unique to retroviruses - it runs "backwards" (RNA to DNA) compared to normal transcription.

3. Integration

  • Viral integrase inserts the double-stranded DNA into the host genome, forming a provirus that persists for the life of the cell (explains the long latent period, often 8-10 years before AIDS develops).

4. Transcription and translation

  • Host RNA polymerase transcribes the provirus.
  • Early spliced transcripts give regulatory proteins: Tat (activates/boosts transcription of viral genes), Rev (exports unspliced RNA from nucleus), Nef (assists particle assembly).
  • Once Rev accumulates, full-length unspliced RNA leaves the nucleus to serve as (a) the new viral genome and (b) mRNA for structural proteins - envelope proteins gp41/gp120 (from env) and core proteins (from gag, made as a polyprotein).

5. Assembly and budding

  • The viral protease cleaves the gag polyprotein into individual core proteins as new particles bud from the cell membrane.
  • Budding virions acquire their lipid envelope (containing gp41/gp120) from the host cell membrane itself.

6. Immunologic consequence

  • Progressive destruction/depletion of CD4+ helper T-lymphocytes (normal ~1000/µL).
  • When CD4 count falls below ~200/µL, the disease reaches an advanced (AIDS) stage, with opportunistic infections (e.g., TB, PCP).

Biochemical basis of antiretroviral drugs (as taught alongside this topic)

Drug classTargetExampleMechanism
NRTIs (nucleoside analogs)Reverse transcriptaseLamivudine, ZidovudineGet incorporated at 3' end of growing DNA chain, terminate elongation
NNRTIsReverse transcriptaseEfavirenzBind directly to enzyme, inhibit its action (non-competitively)
Protease inhibitors (PIs)Viral proteaseIndinavirBlock cleavage of the gag polyprotein, preventing formation of mature infectious particles
Combination ("multidrug"/HAART) therapy targeting different enzymes delays resistance and controls viral load, though it does not cure the infection.
  • Basic Medical Biochemistry - A Clinical Approach, 6e, p. 462-464
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