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BIOL 2402 NAME _____________________________
This is a case study in two parts. First you must watch an HBO movie called “And the Band Played On”. It is available on HBOgo and YouTube. I also have several copies of the movie on DVD. After that you will answer the questions related to HIV and AIDS. You may use any resource but you MUST NOT plagiarize. Copy and Paste will get you a zero. You must answer the questions in your own words and in your own hand-writing. You may work with your group members but remember—NO PLAGIARIZING!!!
First you will watch the HBO movie “AND THE BAND PLAYED ON”. It dramatizes the events that took place in the early years of the AIDS crisis. While watching the movie answer the questions below and then you will go a little deeper into the virus and the disease.
1. Who wrote the book that the movie was based on?
a. Bobbi Campbell
b. Randy Shilts
c. Don Francis
d. Robert Gallo
e. Luc Montanier
Write a short “biography” of the author of the book. Why did he feel the need to write this book? What happened to him?
2. Who was at the forefront of the American effort to isolate and identify the virus?
a. Luc Montanier 
b. Robert Gallo 
c. Francoise Barre-Sinoussi 
d. William Darrow 
e. Don Francis 
Write a short biography of this person. Include any pertinent facts about his/her career. 
3. Who was at the forefront of the French effort to isolate and identify the virus?
a. Luc Montanier 
b. Robert Gallo 
c. Francoise Barre-Sinoussi 
d. William Darrow 
e. Don Francis 
Write a short biography of this person. Include any pertinent facts about his/her career. 
4. Who was Patient Zero?
a. Bobbi Campbell
b. Gaetan Dugas
c. Mary Guinan
d. Sister Heimulluer
e. William Darrow
Why was this person called that? Was this person the first to have AIDS? Include any pertinent information about this person.
5. Who worked for the CDC?
a. Luc Montanier 
b. Robert Gallo 
c. Francoise Barre-Sinoussi 
d. William Darrow 
e. Don Francis
Write a short biography of this person. Include any pertinent facts about his/her career.
The following is a story about John and his cousin Albert. 
John’s cousin, Albert, had a bad case of pneumonia for several weeks. Albert took antibiotics but they did not seem to be able to clear up the infection. The doctor finally took a sputum sample, which led to a biopsy of Albert’s lung tissue. The tests revealed the fungus Aspergillus caused the pneumonia. Because this fungus is more likely in individuals with weakened immune systems, the doctor ordered additional tests. It was soon determined that Albert was HIV positive and had developed acquired immune deficiency syndrome (AIDS). His viral load was 2 million and his CD4 cell count was 11. 
John was very concerned when he heard the news because he and his family were around Albert while he was coughing and sneezing from the pneumonia. John is worried that the family might have been exposed to the human immunodeficiency virus (HIV). Obviously John and his family need to know more about how the virus is transmitted and how it harms those who are infected.
1. List and explain the major routes of HIV transmission. Was John or his family at risk from Albert? What would tell John and his family?
2. What does HIV positive mean and how is a person tested for HIV? 
3. What is the difference between being HIV positive and having AIDS? AIDS can be divided in the acute and chronic phases. Describe each. What is the typical timeline for each? What is the prognosis if left untreated? 
4. What is meant by viral load? Albert’s viral load was 2 million? What does that mean for Albert? What is meant by having an undetectable viral load?  Discuss Albert’s condition.
5. Place the following in the correct order using the diagram (circle one). 
HIV Life Cycle:

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A. The new polypeptides are converted into functional HIV proteins by the enzymatic actions of protease.
B. The HIV DNA form is inserted into the host’s genome by the enzymatic action of integrase.  Once inserted into the host genome, HIV is called a provirus.  
C. HIV uses a receptor on its surface called gp160 to bind to T cells.  The T cells that gp160 interacts with are CD4 (or T4).  Once bound to the cell surface the virus enters the cell
D. Once the newly synthesized HIV proteins are synthesized in the host cell, the HIV virus is then assembled into new virus particles.  Hundreds or thousands of viruses may be produced within a single cell.
E. Once the HIV is in the host cell, the virus releases the 2 RNA strands that comprise the HIV genome.  The HIV genome is converted from RNA to DNA by the enzymatic action of Reverse Transcriptase (RT).
The good news is that drugs have been developed that successfully treated HIV-positive patients, giving them extended lifespans, allowing the immune system to regain control, and decreasing virus loads.  
The bad news is that HIV is a smart virus; HIV has developed mechanisms to overcome drug treatments. Through a micro-evolutionary process, HIV variants that are resistant are able to replicate and produce more virus.  
Over time, in the presence of an antiviral drug, random mutations may develop that allow these variants to be resistant to the effects of the drug. These variants continue to replicate in human T cells in a person even in the presence of the drug. Thus, the effectiveness of the drug decreases over time.  
6. What was the first drug developed to treat HIV/AIDS? How did it work? What were the side-effects? What were the costs associated with the drug? 
7. What drugs are typical used today? How do they work? Often multiple drugs are prescribed simultaneously? What are advantages? What do the different drugs of today target? What are typical costs?
8. Generally treatments to HIV are based on inhibiting enzymes necessary for HIV replication. Based on the HIV life cycle (above), propose “new” potential anti-HIV treatments.  
The CDC and some doctors are recommending PREP for individuals at risk of becoming HIV positive. On the other hand some people say it is not 100% fool-proof and is too expensive. Some insurance companies refuse to pay for it. 
8. What is PREP? How does it work? How effective is it? What is the typical cost?
In many patients, over the course of many years, the virus undergoes many mutations, which continually challenges the T cells to keep up by producing clone after clone of cells. Eventually, too many CD4 T helper cells are killed. 
9. Describe how mutations could lead to drug resistance in the RT enzyme.  What happens to the patient when resistant strains develop? What treatment options are available?
10. If you worked for a government agency whose job it is to reduce HIV/AIDS in the general population, what sort of things would you spend on money on? What would you do to slow the spread of drug resistant strains? 

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