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UBC Microbiology 212 > Virology Chapter 12 > Flashcards

Virology Chapter 12 Flashcards

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1
Q

What is the most common type of HIV

A

HIV-1

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2
Q

what are examples of the mucosal route

A

epithelial of the vagina, penis or rectum
macrophages and dendritic cells at mucosal surface

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2
Q

HIV enters the body via what route

A

mucosal route

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3
Q

Why can macrophages and dendritic cells can also be infected by HIV

A

because they express CD4 protein

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4
Q

HIV -1 is transmitted through direct contact of a mucus membrane or the bloodstream with a biological fluid, like;

A

blood, semen, vaginal fluid, pre-cum, breast milk

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5
Q

HIV-1 primarily infects CD4, macrophages, dendritic cells, but infection can extend to

A

microglia cells in the brain

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6
Q

T cells with CD4 markers are called

A

Helper T cells

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7
Q

What is the function of Helper T cells

A

to activate macrophages to kill pathogens, and to activate B cells to make antibodies

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8
Q

Is HIV infected through sweat, tears or toilet seats?

A

NO

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9
Q

What do HIV-infected macrophages do that causes the recruitment of more primary target cells.

A

secrete chemokines to attract CD4 T lymphocytes, recruiting more primary target cells

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10
Q

What do dendritic cells do to “deliver” hIV to T helper cell

A

it traps HIV on their surfaces (bind to gp120) but it DOESN’T get infected

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11
Q

HIV infection can be described in 3 stages:

A

acute infection, clinical latency and AIDS

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12
Q

what are the stages measured by?

A

CD4 T cell count and HIV viral load (virus in the blood)

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13
Q

Describe acute infection

A

non-specific symptoms or no symptoms at all

symptoms: fever, headache, swollen lymphnodes, sore throat, nausea, vomiting, diarrhea, joint pain, muscle aches, skin rash, night sweats

they last for several days / weeks

what occurs:
rapid viral replication, so a lot of viral particles in the blood, and less CD4 T cells

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14
Q

Why is acute HIV infection often misdiagnosed as influenza?

A

because the early symptoms are very similar to influenza

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15
Q

What is the incubation period of HIV

A

2-4 weeks
asymptomatic
slight decline in CD4 T lymphocytes

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16
Q

What is seroconversion

A

production of antibodies to the virus and marks the start of latency stage

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17
Q

so, what marks the beginning of the latency stage

A

seroconversion: with the production of anti-HIV antibodies

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18
Q

how long is the latency stage

A

2 weeks - decades
patients can be asymptomatic for long time

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19
Q

Describe the latency stage

A

HIV is actively replication in lymphoid organs
Low levels of virus in the blood stream due to anti-HIV antibodies
CD4 T cells normal
Lots of virus in dendritic cells (hideaway) - they can infect and activate CD4 T cells

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20
Q

What indicates the AIDS stage

A

When CD4 numbers decline below 200µl, immune system collapse, so the body is more susceptible to opportunistic pathogens
-»» death

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21
Q

AIDS isn’t the only cause of death to HIV people, whats the other cause

A

Myocobacterium tuberculosis

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22
Q

HIV virus load tests measure the

A

amount of HIV in the blood stream

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23
Q

What is the main goal of anti-viral drugs

A

to reduce the viral load to an undetectable leave (below the level of detection)

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24
What are the problems in developing an HIV vaccine
The immune system produces antibodies and CTL responses during acute phase, but they don;t eliminate the virus. Lack of animal model testing / human volunteers is dangerous lowkey
25
Why attenuated viruses cannot be a suitable candidate for HIV vaccine
because it has the potential of reversion
26
Why inactivated viruses cannot be a suitable candidate for HIV vaccine
because the inactivation process denatures the epitope on the glycoprotein that is needed to be neutralized by antibodies to prevent attachment
27
What are potential vaccine candidates for HIV
subunit, synthetic peptides, DNA vaccines
28
Why is developing medications that target virus infections is harder than developing antibiotics?
because the virus is using the host cell for its replication, so the medication would have to enter into the host cell cytoplasm and selectively interfere virus replication cycle without harming the host cell
29
so, the goal of creating anti-viral meds is to identify...
virus specific molecules or processes (proteins / enzymes) that can be targets
30
31
The treatment for HIV is called
antiretroviral therapy (ART)
32
the goal of ART is to
suppress plasma HIV-1 RNA levels to <50 copies/mililitres
33
What are the 3 main categories of antiviral medications currently used against HIV-1
reverse transcriptase inhibitors integrase inhibitors protease inhibitors
34
what are the other categories of antiviral medication
fusion inhibitors CCR5 antagonists Post-attachment inhibitors
35
What is ART? And what's an example of it
treatment with 2 or more antiviral medications e.g: 2 nucleoside RT inhibitors and 1 protease inhibitor
36
Antiviral medications can also be used to prevent infection in a person that is not yet infected with HIV, what are the names (2)
PrEP and PEP (pre-exposure prophylaxis, post-exposure prophylaxis)
37
When is PrEP taken
Before HIV exposure (everyday)
38
When is PEP taken
72 hours after POSSIBLE exposure
39
PrEP is for people who don't have HIV but are...
at risk of getting it from sex / injection
40
PEP is for people who don't have HIV but may have been exposed to
during sex, sharing needles, sexual assault, work through needlestick
41
PrEP is the use of....
daily oral anti-retroviral therapy by HIV negative people to reduce the risk of acquiring HIV infection
42
How would you measure whether the HAART was effective? (Highly active antiretroviral therapy)
RT-PCR FACS
43
If the result of this test indicate that the viral load was undetectable, does this means that the person is cured of HIV?
No, it just means that the virus is undetected
44
Should this person discontinue their HAART (when HIV is not detected)
no, they must continue
45
What are the two types of approaches that have been used in affecting RT function
nucleoside analogs and non-nuceloside analogs
46
What type of RT inhibitor is AZT (azidovudine)
A nucleoside analog
47
How is AZT activated in the cell?
Cellular enzymes convert it to AZT-Triphosphate
48
What must happen to nucleoside analogs for them to become active in the cell
They must be converted to nucleotide analogs by the addition of a phosphate group
49
How do nucleoside analogs mimic natural nucleotides
They resemble nucleotides and can be added to a growing nucleic acid chain
50
What is missing in nucleoside analogs that prevent further chain elongation
They lack the 3' OH group
51
What effect does the absence of the 3'OH group have on DNA synthesis
No other nucleotide can be added after the analog, leading to chain termination
52
How do nucleoside analogs inhibit viral replication
they act as chain terminators and stop viral DNA polymerase
53
Why can nucleoside analogs cause side effects in human cells
they inhibit mitochondrial DNA Polymerase
54
The 3' group of AZT-TP contains .... instead of hydroxyl group
azide group
55
How does AZT-TP inhibit reverse transcription
RT incorporates AZT-TP instead of dTTP, and its azide group at the 3' position prevents DNA chain elongation
56
How do non-nucleoside RT inhibitors work
they bind to a different site on RT changing its shape causing it to not work
57
At what stage in the HIV life cycle do RT inhibitors act
early, before viral RNA is copied into DNA
58
Why do RT inhibitors help prevent permanent HIV infection of a cell?
Because they block the formation of viral DNA, which is needed for integration into the host genome
59
What do protease inhibitors (plug drugs) do
stop virus maturation after assembly and release, causing no functional RT or IN inside the particle
60
what happens to a virus particle when it infects a cell, but it's affected by a protease inhibitor
it will not be able to reverse transcribe because it doesn't have functional RT and IN, so it's eventually degraded
61
protease inhibitors blocks the cleavage of...
Gag-Pol Polyprotein, which prevents the release of RT and IN
62
Integrase inhibitors block which stage of the viral replication cycle
integration of the virus DNA into cell genome
63
What do integrase inhibitors do
it binds to integrase so the enzyme cannot work, so it can't produce viral mRNA and genomic RNA
64
Entry inhibitors are also known as
Chemokine receptor blockers
65
What is an example of a chemokine receptor blocker
CCR5 receptor antagonist
66
What is CCR5 receptor antagonist designed for
to interfere with the binding between gp120 and co-receptor CCR5
67
To wrap up, what are the ARTs that PREVENT UNINFECTED HEALTHY CELLS FROM BEING INFECTED
RT inhibitors, IN inhibitors, Chemokine blockers
68
what are the ARTs that are used for when the cell is infected, but we want to make sure that new virus progeny can't infect new cells
Protease inhibitors (so that RT and IN can't work when the virus infects the next host)
69
An undetectable viral load means that HIV cannot....
be transmitted through sex, breastfeeding, perinatal transmission
70
What is the window period for: Nucleic Acid Test (NAT): Antigen/Antibody Lab Test: Rapid Antigen/Antibody Test: Antibody Test:
10-33 days 18-45 days 18-90 days 23-90 days
71
Antibody tests check for....
HIV antibodies in the blood / oral fluid Blood drawn from vein is more sensitive
72
Antigen/Antibody tests can detect both....
HIV antibodies and HIV antigens in the blood
73
If a person has HIV, a virus antigen called..... is produced before antibodies develop
p24
74
NAT tests...
look for HIV in the blood via finger prick
75
Why is the loss of CD4 T cells significant in the pathogenesis of AIDS? How does the immune system become depleted of CD4 T cells?
the loss is significant because they are helper t cells that without it, the adaptive immune response is impaired CD4 T cells depleted by CTLs if they display the virus protein on MHC class 1 proteins. They may also die if they fuse together to form syncytia
76
Several anti-viral drugs that are effective against HIV are nucleotide analogs. In the laboratory, the replication process of the viral genome is terminated when it is incubated the presence of these drugs. Do these drugs prevent HIV infection or limit the spread of HIV in the patient? Why is it possible that these drugs can be used without disrupting normal host functions?
They prevent infection They can be used because human cells don't have an enzyme that can read RNA as a template to make a nucleic acid, so its safe!
77
What other parts of HIV replication cycle could be targets of anti-viral drugs? Do these drugs prevent HIV infection or HIV spread? Why is it possible that these drugs can be used without causing damage to the host?
(a) RT inhibitors (AZT) lack open 3'OH end, preventing infection of the host cell. It can be used because it doesn't interact with normal cell DNA/DNA pol (b) Protease inhibitor blocks protease, so Gag-Pol Polyprotein cannot be cleaved, so no functional RT and IN (c) Integrase inhibitors blocks integrase, so cannot integrate DNA into host (d) Chemokine receptor blockers block co-receptor so it can't bind to gp120 so cannot conformational change and reveal gp41 (fusion peptide)
78
A “successful” viral pathogen (from the virus’ point-of-view) ensures its passage to another host before it kills its current one. Explain how HIV can be considered a “successful” human viral pathogen while a virus such as Ebola is not.
HIV is successful because it maximizes the amount of time a victim is alive and capable of spreading the virus to new hosts. Moreover, the host is not made too ill during this time. If one looks at the progression of HIV, it can be years before HIV begins to causes excessive damage on the host. In that time, the host can continue carrying out activities that allow for HIV to spread. On the other hand, Ebola is too viscous. It kills its hosts so fast that the chances of successfully infecting other people are greatly decreased. Humans are not the natural host for the virus and are considered a “dead end host” (an unfortunate term) for Ebola virus infections.

UBC Microbiology 212 (23 decks)

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