Biology 160
Reading Guide 10: Population Dynamics, HIV
NAME: _______________________________________
This is DUE: ___________________
Come prepared to share your findings with your group.
*As before, please turn in only the Critical Thinking questions on a separate sheet of paper.
Critical Thinking questions: 11, 12, 20, 40, 42, 60, 61a, 68, 69
What you’ll learn in this reading guide:
 Information on DNA Fingerprinting/Profiling to help you with Lab 06
 The human genome and apply this information to the HIV genome
 Introduction to the Theory of Natural Selection and apply it to HIV drug resistance
 Learn what a population is, how it is studied, and apply it to HIV drug resistance
 Learn about HIV life-cycle and growth rate and apply it to HIV drug resistance
 Learn about how pre-existing individual variation can come about through mutations in the DNA and
apply it to HIV drug resistance
** Fill this reading guide out as you are reading the chapters. This will help you to pull out the important
information that will help us to understand how HIV drug resistance occurs.
Readings:  Essential Biology, 4th or 5th Ed. (Simon, Reece, & Dickey)
Ch 12, pg. 226-233 (DNA Technology): 25,000 genes and the proteins they encode!
Ch 1, pg 10-13 (Evolution: Biology’s Unifying Theme): Introduction to Natural Selection
Ch 18 & 19, pg 374-375; 404-405; 408-411 (Intro to Ecology; Population Ecology): What is a
population and how is it studied?
Ch 10, pg 188-194 (Viruses): Life cycles and growth rates
Ch 10, pg 186-187 (Mutations): Individual variation
While reading these chapters, constantly ask yourself, “How is this information helping me to understand
how HIV drug resistance occurs?”
Chapter 12, pg 226-233
The first two pages of this reading are to help to you understand Lab#6 a little better.
1. What is the definition of forensics?
2. What is the definition of DNA fingerprinting?
3. Provide an overview of how an investigation using DNA fingerprinting works:
4. Why might you need to do a PCR reaction for DNA fingerprinting?
5. Remind yourself how PCR (polymerase chain reaction) works, particularly the heat-stable DNA polymerase,
the reagents in the Master Mix needed for the reaction to occur, the sequence-specific primers, and the
amplifying power of PCR. Look at Lab#6 for the best amount of detail.
6. What is a genetic marker?
7. What is repetitive DNA?
8. What is a short tandem repeat (STR)? Look both in your book and in Lab#6.
9. What is STR analysis? Give an example.
10. Gel Electrophoresis: Redraw Figure 12.17 to help you remember a) the DNA is negatively charged and thus
runs toward the positively charged end of the gel, and b) that the gel acts like a sieve and separates out the DNA
according to length, allowing the shorter pieces of DNA to run faster through the gel.
11. So, how could you prove that two samples of DNA came from the same person? Make sure you look at
Lab#6 to review this.
Genomics and Proteomics
OK, so far in this class we have been studying how a single cell works and have learned a lot about its structure,
how it harvests and uses energy, how it senses and reacts to its environment, and how it divides. When we
studied transcription and translation, we mostly focused in on one gene. However, we did touch on how a cell
needed to transcribe and translate many, many genes during interphase of the cell cycle in order for the cell to
duplicate its cytoplasm and DNA. So now we need to step back and see that almost every cell in an organism
has a genome, or a complete set of genes located on its chromosomes that provide the instructions for structure,
growth, development, and interaction with its environment. (Red blood cells are an important exception, as
they lose their nuclei during development. This adaptation enables them to fit through small capillaries more
efficiently.)
So now, if we are going to look at how populations of organisms (for example, a population of HIV
viruses) reacts to a change in its environment (taking an anti-HIV drug), we need to understand that organisms
have a set of genes, or a genome, that controls its structure, growth, development, and interaction with its
environment.
1. What is genomics?
2. Want to take a look at some of the genomes that have been sequenced so far? Go to
http://www.ncbi.nlm.nih.gov/sites/genome and click away.
3. What was the Human Genome Project? (The sequence for human chromosome 14 in the Human Genome
Project was done here in Seattle at the Institute for Systems Biology!)
4. Remember from our mitosis lab that humans have a total of 46 chromosomes in each cell, half of them from
mom, half of them from dad. Two of those 46 chromosomes are called sex chromosomes (the X and Y
chromosomes) because they determine the sex of the individual (male or female). The other 44 are called
autosomes. That means we received 23 chromosomes, 22 autosomes and one sex chromosome, from each
parent. That’s why the text says that there are 24 chromosomes in the human genome: 22 autosomes plus the X
and Y chromosomes equals 24 human chromosomes. We’ll talk more about chromosomes in our next reading
guide.
5. Approximately how many genes are in the human genome?
6. How many genes are in the HIV-1 genome? (You’ll have to look this up outside of the text)
7. What is “Junk DNA”?
8. What are some benefits of having a map of the human genome?
9. Have you heard that Neanderthals may have interbred with modern humans? By sequencing a Neanderthal
genome they compared it with modern human genomes and found some surprising results. Listen to
http://www.sciencefriday.com/program/archives/201005072 if you want to learn more! We’ll talk more about
human evolution in our next unit.
10. What is proteomics?
11. Critical Thinking: Why does the total “number of proteins in humans far exceed the number of genes”?
12. Critical Thinking: How is this information helping you to understand how HIV drug resistance occurs?
Chapter 1, pg 10-13 (Evolution: Biology’s Unifying Theme)
13. Who is Charles Darwin and what book did he publish in 1859?
14. What is “descent with modification”?
15. What is the mechanism for descent with modification called?
16. Explain Darwin’s two observations that he used to construct the theory of natural selection.
FACT 1:
FACT 2:
17. What was his conclusion from these two observations?
18. Explain and understand Figure 1.12 Natural selection:
19. What is artificial selection?
20. Critical Thinking: How can natural selection help you to understand how HIV drug resistance occurs?
Chapter 18 & 19, pg 374-375; 404-405; 408-411
So, if natural selection occurs in populations over time, let’s understand exactly what a population is and how
people study them.
21. What is ecology?
22. What are the two major components that the environment is divided into and what do they consist of?
23. What are the four levels of ecology?
24. What does population ecology study?
25. How do ecologists define a population?
26. Describe the four factors that population ecology focuses on.
27. What are some examples of how population ecology research is applied?
28. Is the size of a population always a fixed size or can it vary with what researchers are studying?
29. What is population density?
30. What are two sampling techniques that ecologists use to study population density?
31. What is population dispersion?
32. What are the three types of dispersion?
33. What is the definition of growth rate?
34. Explain the exponential growth model and redraw Figure 19.5 in your description.
35. What are population limiting factors?
36. Explain the logistic growth model and redraw Figure 19.6 to compare it with the exponential growth model.
37. Explain “carrying capacity.”
38. According to the logistic growth model, what would be the growth rate of
a) a small population and why?
b) an intermediate-sized population and why?
c) a large population and why?
39. Describe the two “population-limiting factors that contribute to carrying capacity”:
a) Density-dependent factors
b) Density-independent factors
40. Critical Thinking: Do you think the effects of an anti-HIV drug would be a density-dependent or densityindependent factor in limiting HIV population growth? Why?
41. What is a population cycle?
42. Critical Thinking: How can population ecology help you to understand how HIV drug resistance occurs?
**STOP reading Ch 19 here. We’ll return to the human population in the next reading guide.
Chapter 10, pg 188-194
Now that we’ve read about genomes, natural selection, and populations, we’re ready to understand more about
the particular population that we’ll be focusing on in this reading guide: HIV or the Human Immunodeficiency
Virus. Skim over bacteriophages and plant viruses in this section just so that you know that there exist viruses
that infect all sorts of organisms from bacteria to plants to animals.
43. What is a virus? Is it alive?
44. Redraw Figure 10.28 to familiarize yourself with the structure of the influenza virus.
45. Redraw Figure 10.29 to understand the life-cycle of an enveloped virus. Make sure you can tell the story of
its life cycle.
46. What is a retrovirus?
47. What does reverse transcriptase do?
48. What is a provirus?
49. What does AIDS stand for?
50. What does HIV stand for?
51. What does HIV do that causes AIDS?
52. Redraw Figure 10.31 to understand to the structure of HIV. Know this information.
53. Redraw Figure 10.32 to understand the behavior of HIV nucleic acid during its life-cycle. Know this
information.
54. What are the two types of anti-HIV drugs described in this text?
55. Make sure you can answer the Checkpoint questions throughout your reading. If not, please write your
questions here:
Chapter 5, pg 82 (Enzymes): Reminder – HIV Reverse Transcriptase and HIV Protease are enzymes
56. Think back: What are the ways that inhibitors can inhibit enzyme function?
Chapter 10, pg 193
57. How does the anti-HIV drug AZT work?
58. Since the printing of this text, there have been two more anti-HIV drug types discovered. Take a look at
http://www.thebody.com/content/treat/art6114.html to find out more about anti-HIV drugs and to answer these
two questions:
a) What is Antiretroviral Therapy (ART)?
b) Do anti-HIV drugs kill the virus or just slow down its growth?
59. Next we need to understand more about the growth rate of HIV. Take a look at the following website
http://www.thebody.com/content/art46018.html and then click on “Why Is Understanding Drug Resistance
Important?” to answer the following:
a) What is the approximate growth rate of HIV?
**Technically, HIV is not “alive” so that means that it cannot “die” as stated in this excerpt. However,
the “parent” HIV no longer takes the form of a free virus and becomes a provirus instead (See your drawing of
the HIV life-cycle).
60. Critical Thinking: How can the life-cycle and growth rate of HIV help you to understand how HIV drug
resistance occurs? Hint: Look back at question 16 of this reading guide.
61. Look at http://www.thebody.com/content/art46020.html and answer the following:
a) Critical Thinking: They describe mutations as “changes.” What do you think these changes are?
b) Do these mutations occur all the time during the HIV life-cycle?
Chapter 10, pg 186-187 (Mutations)
62. What is a mutation?
63. Describe what each of the following types of mutations are:
a) silent mutation
b) missense mutation
c) nonsense mutation
d) insertion or deletion mutation
64. What is a reading frame?
65. What are spontaneous mutations?
66. What are mutagens?
67. Make sure you can answer the Checkpoint questions. If not, please write your questions here:
68. Read this page and the next page starting at http://www.thebody.com/content/art46021.html. Then re-read
pg 233 “Can Genomics Cure Cancer?” to answer the following question:
Critical Thinking: How can understanding about mutations help you to understand how HIV drug resistance
occurs?
69. Critical Thinking: What questions do you still have about how HIV drug resistance occurs?