Online Lesson–Viruses


Mastery of this lesson will allow you to:

  1. Describe the anatomy of the human immunodeficiency virus (HIV);
  2. Explain how viral protein GP120 and cell membrane proteins CD4 and coreceptors (CCR5 or CXCR4) interact to allow HIV to infect cells;
  3. Explain why HIV targets only certain cell types, primarily T4 (helper) lymphocytes, macrophages, monocytes and dendritic cells;
  4. Describe the action and explain the significance of viral enzyme reverse transcriptase;
  5. Describe the action and explain the significance of viral enzyme integrase;
  6. Describe how HIV proteins are produced within infected cells;
  7. Describe the action and explain the significance of viral enzyme protease.

This lesson consists of a series of readings and activities from the text and various websites followed by a collection of questions. Some questions require a straightforward understanding of the material, whereas others are more challenging. Answer the questions as best you can. The key is available here.

Readings and Exercises:

Read the virus chapter in your text (Freeman 5th edition, Chapter 36), and watch the video from the Howard Hughes Medical Institute (HHMI) on the HIV life cycle. Use that information to answer the following questions.

  1. What is the difference between the viral capsid and the viral envelope?
  2. Out of what type of chemical is the capsid made? What is the envelope made of?
  3. In what part of the HIV virion (virus particle) would one find GP 120?
  4. Challenge: Would it be correct to characterize HIV as diploid? Why or why not?

In your text, read section, “How Do Viruses Enter a Cell?,” study figure 35.11 and refer again to the HHMI HIV life cycle video to answer the following questions.

  1. To what protein expressed on the surface of human cells does HIV bind?
  2. What HIV protein binds to the protein in the previous question?
  3. Challenge: Some people have a mutation in the gene coding for the chemokine receptor, CCR5. Genes with that mutation produce a version of the CCR5 protein that cannot be inserted into the cell membrane and therefore will not be expressed on the cell surface. Describe what effect, if any, such a mutation would have on a person’s susceptibility to HIV.
  4. Challenge: Explain why human helper T cells, monocytes and macrophages are the cells primarily in danger of being infected by HIV.

Study pages 778-782 and figures 35.12, 35.13, 35.14 and 35.15 in your text. Use this information and the HIV life cycle video to answer the following questions.

  1. HIV viruses do not contain any DNA, yet HIV DNA ends up being incorporated into the nucleus of a host cell. How does that happen? What enzymes are involved, and precisely what do they do?
  2. Challenge: Perhaps the most important reason why we do not have effective cures or vaccines against HIV is that the virus evolves extremely rapidly. Explain why HIV has this massive evolutionary capacity. (HINT: The key insight will be a connection between our study of natural selection in the previous unit and an important property of reverse transcriptase noted in the HHMI video.)
  3. Challenge: What effect would a drug that inhibited integrase have on production of HIV DNA? What effect would such a drug have on transcription and translation of HIV genes?
  4. The HIV genome has genes for viral envelope proteins—that is, proteins like GP 120 that are expressed on the envelope surface. These proteins are first expressed on the surface of the cell prior to the virion leaving the cell. Describe the events leading to such a protein’s expression on the cell surface from the moment the gene is fully transcribed to the moment it arrives at the cell membrane. What organelles are involved and what are their roles in this process?
  5. Newly constructed bacterial viruses tend to escape from their host by causing the host cell to rupture and die. Is this how HIV leaves its host cell—that is, does HIV cause the host cell to burst?
  6. Why is an HIV virion not immediately infectious when it first leaves the cell?

Bonus: Watch the videos about AZT and protease inhibitors at the HHMI website. Use that information to answer the following questions.

  1. The anti-HIV drug AZT is structurally very similar to what type of molecule?
  2. What effect would AZT have on HIV’s ability to produce viral DNA? What effect would it have on HIV’s ability to transcribe its genes, or leave the host cell?
  3. Challenge: Why is AZT not been effective as a cure for HIV?
  4. What effect would Ritonavir have on HIV’s ability to leave the host cell?
  5. Describe precisely how Ritonavir inhibits the life cycle of HIV.
  6. Challenge: The gene for what HIV protein would have to be mutated in an HIV strain that was resistant to Ritonavir?