Table of contents
- 1. Introduction to Biology2h 40m
- 2. Chemistry3h 40m
- 3. Water1h 26m
- 4. Biomolecules2h 23m
- 5. Cell Components2h 26m
- 6. The Membrane2h 31m
- 7. Energy and Metabolism2h 0m
- 8. Respiration2h 40m
- 9. Photosynthesis2h 49m
- 10. Cell Signaling59m
- 11. Cell Division2h 47m
- 12. Meiosis2h 0m
- 13. Mendelian Genetics4h 41m
- Introduction to Mendel's Experiments7m
- Genotype vs. Phenotype17m
- Punnett Squares13m
- Mendel's Experiments26m
- Mendel's Laws18m
- Monohybrid Crosses16m
- Test Crosses14m
- Dihybrid Crosses20m
- Punnett Square Probability26m
- Incomplete Dominance vs. Codominance20m
- Epistasis7m
- Non-Mendelian Genetics12m
- Pedigrees6m
- Autosomal Inheritance21m
- Sex-Linked Inheritance43m
- X-Inactivation9m
- 14. DNA Synthesis2h 27m
- 15. Gene Expression3h 20m
- 16. Regulation of Expression3h 31m
- Introduction to Regulation of Gene Expression13m
- Prokaryotic Gene Regulation via Operons27m
- The Lac Operon21m
- Glucose's Impact on Lac Operon25m
- The Trp Operon20m
- Review of the Lac Operon & Trp Operon11m
- Introduction to Eukaryotic Gene Regulation9m
- Eukaryotic Chromatin Modifications16m
- Eukaryotic Transcriptional Control22m
- Eukaryotic Post-Transcriptional Regulation28m
- Eukaryotic Post-Translational Regulation13m
- 17. Viruses37m
- 18. Biotechnology2h 58m
- 19. Genomics17m
- 20. Development1h 5m
- 21. Evolution3h 1m
- 22. Evolution of Populations3h 52m
- 23. Speciation1h 37m
- 24. History of Life on Earth2h 6m
- 25. Phylogeny2h 31m
- 26. Prokaryotes4h 59m
- 27. Protists1h 12m
- 28. Plants1h 22m
- 29. Fungi36m
- 30. Overview of Animals34m
- 31. Invertebrates1h 2m
- 32. Vertebrates50m
- 33. Plant Anatomy1h 3m
- 34. Vascular Plant Transport2m
- 35. Soil37m
- 36. Plant Reproduction47m
- 37. Plant Sensation and Response1h 9m
- 38. Animal Form and Function1h 19m
- 39. Digestive System10m
- 40. Circulatory System1h 57m
- 41. Immune System1h 12m
- 42. Osmoregulation and Excretion50m
- 43. Endocrine System4m
- 44. Animal Reproduction2m
- 45. Nervous System55m
- 46. Sensory Systems46m
- 47. Muscle Systems23m
- 48. Ecology3h 11m
- Introduction to Ecology20m
- Biogeography14m
- Earth's Climate Patterns50m
- Introduction to Terrestrial Biomes10m
- Terrestrial Biomes: Near Equator13m
- Terrestrial Biomes: Temperate Regions10m
- Terrestrial Biomes: Northern Regions15m
- Introduction to Aquatic Biomes27m
- Freshwater Aquatic Biomes14m
- Marine Aquatic Biomes13m
- 49. Animal Behavior28m
- 50. Population Ecology3h 41m
- Introduction to Population Ecology28m
- Population Sampling Methods23m
- Life History12m
- Population Demography17m
- Factors Limiting Population Growth14m
- Introduction to Population Growth Models22m
- Linear Population Growth6m
- Exponential Population Growth29m
- Logistic Population Growth32m
- r/K Selection10m
- The Human Population22m
- 51. Community Ecology2h 46m
- Introduction to Community Ecology2m
- Introduction to Community Interactions9m
- Community Interactions: Competition (-/-)38m
- Community Interactions: Exploitation (+/-)23m
- Community Interactions: Mutualism (+/+) & Commensalism (+/0)9m
- Community Structure35m
- Community Dynamics26m
- Geographic Impact on Communities21m
- 52. Ecosystems2h 36m
- 53. Conservation Biology24m
21. Evolution
Introduction to Evolution and Natural Selection
0:47 minutes
Problem 8e
Textbook Question
Textbook QuestionWithin a few weeks of treatment with the drug 3TC, a patient's HIV population consists entirely of 3TC-resistant viruses. How can this result best be explained? a. HIV can change its surface proteins and resist vaccines. b. The patient must have become reinfected with a resistant virus. c. A few drug-resistant viruses were present at the start of treatment, and natural selection increased their frequency. d. HIV began making drug-resistant versions of its enzymes in response to the drug.
Verified step by step guidance
1
Understand the nature of HIV and its ability to mutate: HIV is a virus known for its high mutation rate, which allows it to quickly adapt to environmental pressures such as antiviral drugs.
Recognize the role of natural selection in viral populations: When a drug like 3TC is used, it creates a selective pressure on the virus population. Viruses that are susceptible to the drug are killed, while any resistant variants survive and reproduce.
Identify the initial presence of resistant viruses: Even before treatment, it is likely that a few viruses in the vast population may carry mutations that confer resistance to the drug.
Consider the growth of the resistant population: As the treatment kills off the susceptible viruses, the few resistant ones will continue to replicate and eventually come to dominate the population.
Evaluate the options given in the problem: Based on the understanding of viral mutation and natural selection, determine which option best explains the scenario where the HIV population becomes entirely resistant to 3TC within a few weeks.
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Key Concepts
Here are the essential concepts you must grasp in order to answer the question correctly.
Natural Selection
Natural selection is a fundamental mechanism of evolution where organisms better adapted to their environment tend to survive and produce more offspring. In the context of HIV treatment, if a few drug-resistant viruses are present before treatment, they can survive the selective pressure of the drug, leading to an increase in their frequency in the population over time.
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Viral Mutation and Resistance
Viruses, including HIV, can mutate rapidly due to their high replication rates. These mutations can lead to drug resistance, where some viral strains develop the ability to survive despite the presence of antiviral drugs. This phenomenon is critical in understanding how a patient's HIV population can become entirely resistant to a drug like 3TC within a short period.
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Reinfection and Viral Diversity
Reinfection occurs when an individual is infected with a different strain of a virus after an initial infection. In the case of HIV, the presence of multiple strains can lead to increased viral diversity, which may include drug-resistant variants. However, in this scenario, the rapid emergence of resistance is more likely due to pre-existing resistant strains rather than reinfection.
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