Final Exam Flashcards

1
Q

HIV is a(n) __________ virus.

A

Sense RNA

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2
Q

What’s the function of the capsid and the matrix?

A

it maintains the viral structure and protects the genetic material

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3
Q

What is the function of gp120?

A

It allows the virus to bind to it’s host cell

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4
Q

What’s the function of gp41?

A

it helps the viral envelope fuse with the host cell membrane

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5
Q

What’s the function of integrase?

A

it integrates DNA copy of viral genome into the host cell’s DNA

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6
Q

What’s the function of protease?

A

it chops up proteins to produce mature versions of HIV (viral) proteins

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7
Q

What’s the function of reverse transcriptase?

A

it reads viral DNA and produces a DNA copy

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8
Q

Name three molecules found on human cells that HIV can use as a receptor or co-receptor.

Name at least one type of human cell that expresses the molecules you named in the previous question.

A

CD4, CCR5, CXCR4

helper t-cell

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9
Q

The first thing that happens when HIV binds to a host cell is that _______ binds to __________.

A

gp120; cd4

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10
Q

A series of events happens between gp120 binding to CD4 and entry of HIV into its host cell. Describe this series of events. As part of your description, include the roles of gp41 and CCR5.

A

gp120 binds to CD4 causing the gp120 to bind to the coreceptor (either CCR5 or CXCR4). gp41 then drills down into the host cell, which causes everything to fold down and allow for fusing of the membrane of HIV and the membrane of the host cell. Now HIV can enter

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11
Q

HIV enters its host cell by…

A

fusing its envelope together with the membrane of the host.

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12
Q

Outline the sequence of events that happens during HIV viral replication (between the time it fuses with its host cell to the time new viruses leave the host cell).

A

once HIV fuses with the membrane of the host cell and gains entry into it, the matrix and capsid of HIV dissolve, releasing the RNA of the HIV virus. The RNA is reversed transcribed to make a DNA copy and integrate with the DNA of the host cell. It then directs the host cell to make new viruses. gag proteins are chopped to produce more matrix and capsid proteins, and then the virus buds out of the host cell, taking some of the envelope with it, as well as the gp proteins.

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13
Q

What is the gag protein? What does the gag protein make?

A

its a group antigen - it makes more HIV proteins (capsid and matrix proteins).

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14
Q

HIV can cause latent infections and it can also produce a stage of disease called clinical latency. What do the two types of latencies have in common?

A

latent infection: when the HIV virus has integrated into the host cell DNA but is not being actively transcribed.

clinical latency: same as the above, but the DNA IS being actively transcribed and our immune system is eliminating most of the viruses so that there is not a significant increase in the body.

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15
Q

HIV tends to infect _______ CD4+ cells.

A) naive
B) activated

A

activated

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16
Q

Explain why HIV tends to infect activated CD4 cells

A

HIV infects the cell with a lot more cytokine receptors (a.k.a. the activated CD4 cells).

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17
Q

HIV tends to cause latent infections in _________ CD4+ cells.

A

memory

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18
Q

Explain why HIV tends to cause latent infections in memory cells

A

memory cells are resting cells - there’s not much activity happening within the cell. it can hang out in the blood for a relatively long time.

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19
Q

What triggers latent HIV viruses to become actively replicating?

A

when the memory helper t-cell sees an antigen and becomes activated

20
Q

What role might antibodies play in slowing HIV infection?

A

some of them can bind to the HIV viruses to prevent them from binding to a host cell

21
Q

What’s the role of cytotoxic T-cells in slowing HIV infection?

A

it can kill the helper t-cell infected with the HIV virus

22
Q

When HIV leaves its host cell, it does not lyse (kill) the cell. Despite this, the numbers of CD4+ cells tend to decrease over time in someone who has HIV infection. Explain what causes this decrease in CD4+ cell numbers.

A

cytotoxic t-cells kill host cells that are infected with the HIV virus, and the CD4 molecules are on the host cells.

23
Q

Suppose that a person has a really low number of CD4+ cells. Explain what effect this would have on the activity cytotoxic T-cells.

A

cytotoxic t-cells need to be activated by healthy helper t-cells (containing the CD4 molecules). Therefore, the lack of CD4 molecules means a lack of healthy helper t-cells to activate cytotoxic t-cells.

24
Q

What’s the difference between the following terms: HIV infection, HIV disease, AIDS

A

in HIV infection, signs/symptoms are not present

in HIV disease, signs/symptoms are present

in AIDS, CD4 levels drop below 200 cells per micro liter of blood, and signs/symptoms of immunodeficiency are present

25
Towards the beginning of acute phase of disease, explain what causes the number of CD4+ cells to decrease while the number of viruses increase.
Our own CD4 cells (infected with HIV) are being killed off by cytotoxic t-cells, allowing the number of HIV viruses to increase.
26
consider what occurs at towards the end of acute phase. Why do the numbers of viruses drop, and why do the numbers of CD4+ cells go up?
Our immune system is activated in a way that is able to handle the virus by producing antibodies to fight it off.
27
During asymptomatic phase, why do the number of viruses in a person’s body remain nearly constant, while the number of CD4+ cells gradually decrease?
the HIV virus is being killed at the expense of the CD4 molecules that are fighting it off. Our immune system still has control over the virus to keep it from replicating out of control. Some of the viruses are also in the memory cells.
28
During AIDS phase, there is a sudden (and drastic) increase in the number of HIV viruses in a person’s blood. What causes this sudden spike?
There are not enough helper t-cells to activate cytotoxic t-cells. HIV replicates out of control
29
Describe 3 ways that the presence of HIV is detected in a person’s body. Which of the methods can detect HIV infection in the shortest amount of time after the person was exposed to the virus?
1. you can look to see if a person has antibodies against HIV (longest) 2. look for presence of HIV nucleic acids in a person (shortest) 3. look for presence of HIV antigen
30
ELISA is a ________ based method for determining whether someone has HIV infection.
antibody
31
explain how an ELISA works to detect HIV infection.
bottoms of wells are coated with capsid protein of HIV. then a serum sample of a person is placed in the wells. if a person is positive, antibodies from the serum sample would attach to the antigens/proteins at the bottom of the wells/plate. This does not happen if a person is not HIV positive. The plate is washed, and everything that is not an antigen stuck to an antibody will wash away too. Secondary antibodies are added to the plate, and if the plate contains the serum sample of an HIV positive person, these antibodies will stick to the Fc portion of the antibodies already in the wells. Substrate is then added, and it recognizes and binds to the secondary antibodies, producing a yellow color that indicates someone is HIV positive. 
32
The rapid oral test for detecting HIV infection is a ______ based detection method.
antibody
33
Describe two general challenges that make it difficult to develop an HIV vaccine that completely protects against infection.
1. HIV has a high rate of mutation | 2. Neutralizing epitopes on HIV are blocked
34
What are “neutralizing epitopes”?
a portion on the HIV virus that does a really good job of protecting our cells from becoming infected with the virus if antibodies stick to it
35
The neutralizing epitopes on the HIV virus are relatively ______ for antibodies to bind.
difficult
36
Attenuated and inactivated vaccines are very ___________ to fully protect people against HIV one day.
unlikely
37
why are attenuated and inactivated vaccines unlikely to protect people against HIV?
there's a high mutation rate for HIV and attenuated vaccines can revert back into their pathogenic form. Inactivated cells can never get into our cells and activate a cytotoxic t-cell or produce memory cytotoxic t-cells. It cannot generate protective immunity.
38
________ vaccines are better at causing people to produce memory cytotoxic T-cells.
attenuated
39
Explain why attenuated vaccines are better at inducing the production of memory cytotoxic T-cells.
the virus (though weakened) is being used, which can activate an immune response. Whereas the inactivated vaccine does not use a live virus and cannot produce any memory cytotoxic t-cells at all.
40
Name and describe three types of vaccines that show the most promise for one day protecting people against HIV against.
1. DNA vaccines - plasmid DNA contains genes for HIV envelope, gag, and reverse transcriptase 2. Synthetic peptide vaccines - synthetically made gp120 3. Virus vector vaccines - using a non- HIV virus to deliver HIV genes to a person being vaccinated 
41
Describe 5 classes of drugs that are currently used to help treat/manage HIV infection.
1. inhibiting HIV binding to CCR5 2. inhibiting fusion of HIV envelope with host cell membrane 3. Reverse transcriptase inhibitor 4. Inhibiting integration of HIV DNA into host DNA 5. inhibiting cleaving of GAG to make capsid and matrix proteins (protease inhibitors)
42
_________ is a more common cause of HIV infection worldwide.
HIV-1
43
_________ is more virulent and easily spread.
HIV-1
44
When it comes to genetic sequences, HIV-1 and HIV-2 are ______________.
different
45
What group of HIV-1 is the most common cause of infections worldwide?
Group M (M= main)
46
About ______ years passed between the time HIV-1 Group M is thought to have first entered the human population, and the time AIDS was first described.
60 years (1920 - 1981)
47
Briefly describe two things that would allow SIV to change over time into a virus that is capable of infecting humans.
HIV evolved from SIV as a result of mutations and reassortment. monkeys that originally carried the virus were hunted and eaten by larger monkeys, and eventually chimpanzees. Humans were believed to have eaten those chimpanzees that were infected with HIV, leading to HIV-1 M&N (maybe O)in humans. Gorillas came into contact with the body fluid of chimpanzees, and humans were came into contact with the bodily fluid of a gorilla positive for HIV, leading to HIV-1 P (maybe O).