Biology 1 - Lesson 19: Viruses and the Biology of HIV

Lesson 19: Viruses and the Biology of HIV

Viruses are acellular infectious entities that depend on host cells for replication. They infect a wide range of hosts, featuring diverse genome types (DNA or RNA) and replication styles (lytic, lysogenic, or retroviral). This lesson overviews viral structures and replication cycles, concluding with HIV, a retrovirus that integrates into immune cells and progressively disrupts host defense.

Viral Structure and Classification

While viral forms differ, most include:

  • Capsid: A protein coat shielding the genome (DNA or RNA).
  • Envelope (sometimes): A membrane from the host, bearing viral glycoproteins for attachment.
  • Compact Genome: Typically encodes only core proteins (capsid, polymerases) relying on host cell machinery for replication.

Classification often uses the Baltimore system (Classes I–VII), which focuses on genome composition and mRNA generation routes.

Lytic vs. Lysogenic Cycles

Bacteriophages demonstrate two major replication pathways:

  • Lytic Cycle: Viral replication culminating in cell lysis and release of virions.
  • Lysogenic Cycle: Viral DNA integrates as a prophage into the host chromosome, replicating passively until triggered to enter the lytic pathway.
flowchart TB A[Lysogenic Phase] -->|Trigger| B[Lytic Cycle] A -->|Prophage replicates| A B -->|Assemble virions| C[Cell lysis]
A Mermaid diagram illustrating bacteriophage lysogenic integration vs. lytic replication.

HIV: A Retrovirus Model

The Human Immunodeficiency Virus (HIV) is an enveloped retrovirus infecting CD4+ T lymphocytes. It reverse-transcribes RNA to DNA, integrating into the host genome. Key steps include:

  • Two ssRNA copies + Reverse Transcriptase (RNA→DNA), Integrase (genome insertion), Protease (viral protein maturation)
  • Envelope Glycoproteins (gp120, gp41) to bind CD4/co-receptors (CCR5/CXCR4)
  • Provirus Formation: Integrated viral DNA can remain latent or express viral genes, damaging immune function

D3-based Timeline of HIV Replication (Margins in Code)

The chart below adjusts its domain so text remains within the container’s view:

D3-based timeline with left/right margins inside the code. The container is fully dynamic (width:100%), but internal margins keep text visible without drifting off the left or right.

Antiviral Strategies Targeting HIV

Various drug classes block distinct steps of HIV replication:

  • Reverse Transcriptase Inhibitors: Halt RNA→DNA (e.g., AZT, Efavirenz)
  • Integrase Inhibitors: Prevent proviral DNA insertion (e.g., Raltegravir)
  • Protease Inhibitors: Inhibit protease, blocking viral protein maturation (e.g., Lopinavir)
  • Entry Inhibitors: Interfere with gp41 or CCR5/CXCR4 usage (e.g., Maraviroc)

Combination antiretroviral therapy (cART) is standard, reducing viral load effectively and mitigating resistance.

Relevance of Viral Research

Viruses influence health, ecology, and evolutionary processes. Studies of phages propelled molecular genetics; understanding retroviruses unveiled reverse transcriptase, cDNA, and gene therapy approaches. HIV research has reshaped immunology and highlighted the complexities of virus-host coevolution, fueling novel vaccine and therapeutic advances.

Conclusion

Viruses exhibit compact genomes yet sophisticated replication methods, seen in HIV’s retroviral cycle—reverse transcription, genome integration, and immune system evasion. By unraveling viral strategies, scientists devise targeted drugs, refine vaccine designs, and reveal deeper insights into cellular biology and evolutionary innovation.

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Biology 1 - Lesson 18: Regulation of Gene Expression

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Biology 1 - Lesson 20: DNA Technology and Biotechnology