Deck 28: Hiv Disease and Complications of Immunodeficiency

Question 1

Which group had by 1982 gathered enough epidemiological evidence to suggest that AIDS was caused by a new infectious agent?

A) Pasteur Institute
B) Lister Institute
C) Centers for Disease Control
D) World Health Organization

Answer 1

C

Question 2

How many subtypes of the M group of HIV-1 exist at present?

A) 2
B) 5
C) 10
D) 15

Answer 2

C

Question 3

The prime target(s) of the HIV virus is/are

A) red blood cells.
B) liver cells.
C) T_H cells.
D) macrophages.
E) T_H cells AND macrophages.

Answer 3

E

Question 4

Genetic evidence suggests that the HIV-1 virus mutated to its present form approximately

A) 100-200 years ago.
B) 50-100 years ago.
C) 20-30 years ago.
D) 500-600 years ago.

Question 5

The first human retrovirus (HTLV) was discovered by

A) Kenmore.
B) Temin.
C) Gallo.
D) Baltimore.

Question 6

The double-stranded HIV DNA is inserted into the host DNA by

A) polymerase.
B) integrase.
C) invertase.
D) Nef.

Question 7

Who were the scientists that received the Nobel Prize for their work with reverse transcriptase?

A) Temin, and Baltimore
B) Gallo and Montagnier
C) Kenmore and Temin
D) Gallo and Baltimore

Question 8

Besides HIV-1, which type of HIV is prevalent in parts of Africa and India?

A) HIV-0
B) HIV-2
C) HIV-3
D) HIV-4

Question 9

Which of the following are symptoms of HIV disease?

A) headache
B) sore throat
C) muscle aches
D) fever
E) All of these are symptoms of HIV disease.

Question 10

HIV is a

A) single-stranded RNA virus.
B) double-stranded RNA virus.
C) single-stranded DNA virus.
D) double-stranded DNA virus.

Question 11

Which of the following is/are target(s) of medicines for treating AIDS?

A) polymerase
B) reverse transcriptase
C) protease
D) matrix protein
E) reverse transcriptase AND protease

Question 12

Which of the following is true of gp120?

A) It is a glycoprotein.
B) It forms knobs projecting from the virus.
C) It is partly responsible for binding to the host cells.
D) It transports the viral genome to the host cell nucleus.
E) It is a glycoprotein, it forms knobs projecting from the virus AND it is partly responsible for binding to the host cells.

Question 13

AIDS was first described as a new disease in

A) 1970.
B) 1976.
C) 1981.
D) 1989.

Question 14

Which of the following may have served as the ultimate source of HIV?

A) orangutans
B) apes
C) gorillas
D) chimpanzees

Question 15

Human T Lymphotrophic Virus-III (HTLV-III), upon genetic analysis, actually turned out to be the same as

A) Lymphadenopathy virus (LAV).
B) Epstein-Barr virus (EBV).
C) Herpes virus (HV).
D) lentivirus (LV).

Question 16

Which type of HIV is most prevalent in the United States?

A) HIV-1
B) HIV-2
C) HIV-3
D) HIV-4

Question 17

HTLV-III and LAV were renamed

A) AIDS.
B) HIV.
C) EB.
D) SBE.

Question 18

gp120 binds to
A)

A) protein
B) reverse transcriptase.
C) CD8.
D) CD4.

Question 19

Which scientists were involved in a bitter legal battle over who had contributed what and when to the work on HIV?

A) Dulbecco, Temin, and Baltimore
B) Gallo and Montagnier
C) Kenmore and Temin
D) Gallo and Baltimore

Question 20

Some of the host cell coreceptors for HIV have been found to be

A) lipids.
B) cytokines.
C) chemokine receptors.
D) gp41.
E) cytokines AND chemokine receptors.

Question 21

HIV on objects may be dealt with by

A) commercial, high-level disinfectants.
B) 56ºC for 30 minutes.
C) soap and water.
D) household bleach.
E) commercial, high-level disinfectants, 56ºC for 30 minutes AND household bleach.

Question 22

HIV transmission from mother to newborn can be significantly reduced by using

A) penicillin.
B) disinfectants.
C) erythromycin.
D) AZT.

Question 23

A big limitation of anti-HIV therapy, especially in third world countries, is the

A) side effects.
B) lack of supply.
C) delivery system.
D) cost.

Question 24

Destruction of T_H cells after HIV infection may occur by

A) lysis following HIV replication.
B) attack by CD8⁺ lymphocytes.
C) attack by natural killer cells.
D) a consequence of cell fusion.
E) All of the choices are correct.

Question 25

HAART

A) cures AIDS.
B) may, in some patients, eliminate free virus in the blood.
C) eliminates the provirus.
D) is recommended for acute retroviral syndrome.
E) may, in some patients, eliminate free virus in the blood AND is recommended for acute retroviral syndrome.

Question 26

The first approved protease inhibitor was

A) saquinovir.
B) zalcitabine.
C) lamivudine.
D) didanosine.

Question 27

Side effects of AZT may include

A) anemia.
B) low white blood cell count.
C) vomiting.
D) fatigue.
E) All of the choices are correct.

Question 28

Medications that interfere with reverse transcriptase work by

A) binding to the host ribosomes.
B) binding to the reverse transcriptase.
C) mimicking nucleosides.
D) mimicking amino acids.
E) binding to the reverse transcriptase AND mimicking nucleosides.

Question 29

Macrophages

A) are not infected by HIV.
B) often lyse and release HIV.
C) survive and release virus over long periods of time.
D) contain dormant HIV.

Question 30

Symptoms of AIDS appear when

A) CD4+ cell counts are at 1000/microliter of blood.
B) CD8+cell counts are over 1000/microliter of blood.
C) CD4+ cell counts are under 200/microliter of blood.
D) CD8+ cell counts are under 700/microliter of blood.

Question 31

Which of the following is a nucleoside inhibitor?

A) zidovudine
B) stavudine
C) nevirapine
D) 3TC
E) zidovudine, stavudine AND 3TC

Question 32

HIV is genetically very variable due to the

A) reverse transcriptase being "error" prone.
B) incompatibility with the host chromosome.
C) incorporation of plasmid DNA.
D) variability of the integrase.

Question 33

Which of the following is a nonnucleoside inhibitor?

A) zidovudine
B) stavudine
C) nevirapine
D) 3TC

Question 34

What aspect of the virus life cycle makes it most difficult to treat?

A) its use of reverse transcriptase
B) its use of protease
C) the method of virion assembly
D) its incorporation into the host cell chromosome

Question 35

Most lymphomas arise from

A) B lymphocytes.
B) lymph nodes.
C) lymph fluid.
D) red blood cells.

Question 36

HIV may infect

A) intestinal epithelial cells.
B) brain cells.
C) macrophages.
D) T helper cells.
E) All of the choices are correct.

Question 37

Which of the following viruses are found in AIDS-associated B-cell lymphomas?

A) herpes
B) Epstein-Barr virus
C) varicella
D) variola

Question 38

The tumor in AIDS patients which arises from blood or lymphatic vessels is

A) Kaposi's sarcoma.
B) cervix carcinoma.
C) anal carcinoma.
D) lymphoma.

Question 39

After integration into the host chromosome, HIV is referred to as a

A) previrus.
B) provirus.
C) viroid.
D) proteosome.

Question 40

The protease inhibitors

A) act late in the virus life cycle.
B) act early in the virus life cycle.
C) act on viral RNA production.
D) prevent the assembly of the virus.
E) act late in the virus life cycle AND prevent the assembly of the virus.

Question 41

Binding of gp120 to CD4 is all that is needed for entry of HIV into the host cell.

Question 42

Most infections of the Mycobacterium avium complex are from

A) person to person contact.
B) environmental sources.
C) reactivation of latent infections.
D) sexual transmission.
E) environmental sources AND reactivation of latent infections.

Question 43

Cytomegalovirus

A) is always latent.
B) is always lytic.
C) may be latent or lytic.
D) integrates into the host cell DNA.

Question 44

HAART cures AIDS.

Question 45

Macrophages tend to release HIV over long periods of time without death of the cell.

Question 46

The definitive host for Toxoplasma gondii is

A) humans.
B) cats.
C) goats.
D) cows.

Question 47

Mycobacterium avium complex consists of

A) Mycobacterium avium.
B) Mycobacterium tuberculosis.
C) Mycobacterium xenopi.
D) Mycobacterium intracellulare.
E) Mycobacterium avium AND Mycobacterium intracellulare.

Question 48

Pneumocystis is caused by a

A) bacteria.
B) fungus.
C) virus.
D) protozoan.

Question 49

HIV disease implies that the virus is multiplying and is interfering with the normal state of health.

Question 50

Toxoplasmosis is caused by a

A) bacteria.
B) fungus.
C) virus.
D) protozoan.

Question 51

Almost everyone infected with HIV develops HIV disease, eventually ending in AIDS.

Question 52

During which trimester is toxoplasmosis most severe to the fetus?

A) first
B) second
C) third
D) all the same

Question 53

Carcinoma of the uterine cervix and anus is strongly associated with

A) varicella virus.
B) Epstein-Barr virus.
C) herpes virus.
D) human papilloma virus.

Question 54

There are no approved vaccines against HIV.

Question 55

AIDS patients are no more susceptible to infectious disease than immunologically healthy people.

Question 56

Infected macrophages and other antigen-presenting cells are a continuing source of infectious virus.

Question 57

Gag and pol are translated as a unit and split into four segments.

Question 58

Cytomegalovirus is a(n)

A) enveloped double-stranded DNA virus.
B) enveloped single-stranded RNA virus.
C) bullet shaped retrovirus.
D) non-enveloped RNA virus.

Question 59

Mycobacterium avium complex organisms

A) survive phagocytosis.
B) are acid fast.
C) are widespread in the environment.
D) cause persistent bacteremia in immunodeficient people.
E) All of the choices are correct.

Question 60

Which of the following is typically used to treat pneumocystis?

A) AZT
B) pentamidine
C) penicillin
D) trimethoprim-sulfmethoxazole

Question 61

HIV may induce rapid cell division in some cell types. Would rapid cell division favor mutation and induction of possible cancerous lesions?

A) No-we have proofreading and repair capabilities in our DNA synthesis enzymes that prevent mutations. Just because more cell division is occurring doesn't mean more mutation would occur.
B) Yes-especially as all of these cells are infected with HIV as they are newly made. Since HIV integrates into the host cell chromosome, each time it does so it has a small chance to cause a cancerous state.
C) Yes-spontaneous mutation is a random event. Sometimes it is corrected, but rarely it goes forward. Technically, then, each and every new cell formed is a chance for induction of a cancerous state. If you increase the number of cells formed, you increase the chance for that induction event.
D) No-part of the HIV lifecycle also hijacks the DNA synthesis machinery. Since it's hijacked, there's no way that it could be used to produce mutations in the host cells that would lead to cancerous states.

Question 62

The vast majority of Mycobacterium avium complex infections in immunologically normal people are asymptomatic.

Question 63

What is the best reason (most useful reason for the largest number of people) why having the ability to recognize differing strains of HIV-1 would aid in epidemiological studies?

A) Since HIV mutates so rapidly, being able to trace different strains allows us to better trace who gave the virus to whom first. This is especially useful in legal issues related to intentional HIV infection.
B) It doesn't-HIV is HIV. It doesn't matter which strain a person has-it only matters that we know who is infected and who isn't.
C) By recognizing different strains, we can fine-tune the treatments for each individual to best suppress the progress of the illness.
D) Being able to observe how the virus mutates as it progresses through a population of susceptible individuals, some of whom are treated and some of whom have not been treated, allows us to better understand how the virus changes over time in order to better fight it with new drugs/therapies.

Question 64

How might the progression of HIV have been different in the US if it appeared in 1928 rather than 1978?

A) It would have been slower because blood transfusions were rare.
B) It would have been slower because people were less likely to engage in sexual intercourse with as many separate partners across their lifespan.
C) It would have been slower because travel to and from other countries (and often even simply other states) was less common.
D) All of these options are correct statements-the overall progression of the illness would most likely have been slower.

Question 65

Live vaccines are generally unsafe to give to an AIDS patient.

Question 66

If AIDS was present in Africa in the 1950's, what is the most likely reason why did it not appear in the United States until the 1970's?

A) It wasn't until the 1970's that large-scale humanitarian aid (including susceptible workers) began to move into Africa from Western countries.
B) Travel to and from Africa was relatively rare in the 1950's. This would mean that it would have been very improbable that an infected individual would have come to the US from Africa and begun spreading the illness.
C) The virus needed a longer period of time to mutate in order to become more virulent and spread more easily. Even in the 1950's in Africa, it most likely wasn't able to be transmitted very easily from person to person (yet).
D) Sexual practices and behaviors were different in the 1950's than they were in the 1970's. This led to less sexual intercourse outside of monogamous married relationships, and less likelihood of spread of the illness between people.

Question 67

Highly effective vaccines have been produced. Why can't we seem to develop an effective vaccine for HIV?

A) The best protective effect would be a stimulation of antibodies from B cells and production of infected cell killing cytotoxic CD8⁺ T cells, most likely from a live attenuated form of HIV used as a vaccine. Both of these cell types require the help of CD4⁺ helper T cells. HIV infects and destroys the very cells required to produce a strong protective immune response to a vaccine (CD4⁺ helper T cells). This would make the use of a live, attenuated virus as a vaccine impractical.
B) HIV goes latent quite quickly in every one of the cells it infects. This latency makes it extremely difficult to completely eradicate from an individual, even if a protective immune response were able to be induced by a vaccine.
C) HIV vaccines of any kind would be far too dangerous to test on human beings. Without human testing, we can't be sure of their effectiveness in order to begin using them for human protection.
D) The best protective effect would be achieved solely by production of anti-HIV antibodies from B cells. However, B cells become infected with HIV and are destroyed. A vaccine would destroy the very cells we need to stimulate to best fight the infection.

Question 68

A CDC epidemiologist presents a report to Congress that suggests it is more important to focus on funding for prevention/treatment of HIV infection research than on AIDS itself. Is she right or wrong, and why?

A) She's wrong-AIDS is the stage of the illness that kills people. All funding should be directed towards preventing people from dying from AIDS.
B) She's right-once people progress to AIDS, you really can't do much for them. We would be better off if we spent research money on preventing and treating HIV infection before it progresses to full-blown AIDS. All of the research money should be shifted to that aspect.
C) She is right-but we can't completely ignore the end-stages of the illness. We would be better off spending money to find new ways to prevent new individuals from being infected, or by trying to keep people from progressing to the AIDS state once they are infected. However, we cannot completely abandon efforts to treat and prolong survival and quality of life in people who have progressed to the end stages of the illness.
D) In reality, since only approximately 3% of the US population is infected with HIV, it makes far more sense to shift research spending to diseases that have more of an impact on the population (cancer, diabetes, etc.). If anything, both HIV and AIDS research funding should be cut dramatically.