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Introduction
1. CARS
2. Psych/soc
3. Bio/biochem
3.1 1A: Structure and function of proteins and their constituent amino acids
3.2 1B: Transmission of genetic information from the gene to the protein
3.3 1C: Heredity and genetic diversity
3.4 1D: Principles of bioenergetics and fuel molecule metabolism
3.5 2A: Assemblies of molecules, cells, groups of cells
3.6 2B: Structure and physiology of prokaryotes and viruses
3.6.1 Cell Theory, prokaryote structure and physiology
3.6.2 Virus structure and life cycle
3.7 2C: Processes of cell division, differentiation, and specialization
3.8 3A: Structure and functions of nervous and endocrine systems
3.9 3B: Structure and functions of main organ systems
4. Chem/phys
Wrapping up
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3.6.2 Virus structure and life cycle
Achievable MCAT
3. Bio/biochem
3.6. 2B: Structure and physiology of prokaryotes and viruses
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Virus structure and life cycle

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Virus structure

Viruses are remarkably small, often about 100 times smaller than bacteria and up to 1000 times smaller than eukaryotic cells. Their defining feature is a protein coat housing the genetic material, which can be DNA or RNA, either single- or double-stranded.

Some viruses possess a lipid envelope derived from the host’s membrane, classifying them as enveloped; these exit the host by budding from its membrane. By contrast, nonenveloped viruses rely on the cell bursting to release new viral particles.

Rabies virus structure with ssRNA core, envelope, and helical capsid
Rabies virus structure with ssRNA core, envelope, and helical capsid

Genetic material

Although viruses contain genetic material, they lack organelles and a nucleus. Their nucleic acid is simply packaged within the protective coat. Certain bacteriophages illustrate this structure vividly:

  • A head (capsid) stores genetic material
  • A sheath provides a channel for injecting that material into bacterial hosts
  • Tail fibers attach to the host’s surface.

Viral life cycle

In terms of genomic variation, viruses may store RNA, and those that convert RNA into DNA upon infection are known as retroviruses. Such viruses carry reverse transcriptase to perform this conversion before harnessing the host’s replication machinery.

HIV, a retrovirus, infects helper T cells by attaching to specific receptors on the cell surface, fusing with the plasma membrane, and releasing its genetic material and proteins into the host cell.

HIV virus binding to CD4 receptor on immune cell during viral attachment
HIV virus binding to CD4 receptor on immune cell during viral attachment

Replication

  • Across all viruses, replication depends on a host cell for ribosomes, ATP, and molecular substrates. The viral particle attaches to the host, penetrates the membrane or wall, injects its genetic material, and uses the host’s systems to synthesize viral components.
  • These parts self-assemble into new virions, which exit by lysis or budding.
  • A special phenomenon called transduction occurs when a lysogenic virus inadvertently packages fragments of a previous host’s DNA. After infecting a new cell, the virus injects that leftover DNA, where it can integrate into the new host’s chromosome by recombination. Such horizontal gene transfer contributes to genetic diversity, as do other virus-host interactions that shape evolutionary dynamics.

Prions and viroids: subviral particles

  • Viroids are extremely small, circular, single-stranded RNA molecules without a protein coat; they infect plants and cause various diseases. In contrast, prions are misfolded proteins that act as infectious particles, leading to a range of transmissible and inherited neurodegenerative diseases through protein misfolding. Classic prion diseases include Creutzfeldt-Jakob disease, Gerstmann-Straussler syndrome, and mad cow disease. Emerging research suggests that prion-like mechanisms may also contribute to Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and certain cancers.

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