Biology 1 - 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.
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:
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.