05c: Retroviruses/HIV Flashcards

1
Q

HTLV-1 and HTLV-2 are examples of (X) viruses that cause which diseases?

A

X = retroviruses;

T-cell leukemias (HTLV = human T-cell leukemia virus)

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2
Q

HIV-1 and HIV-2 are examples of (X) viruses that cause which diseases? Which strain is less virulent?

A

X = retroviruses;

AIDS (HIV = human immunodeficiency virus); HIV-2 less virulent

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3
Q

T/F: The DNA sequence that defines HIV-1 is most related to that which defines HIV-2.

A

False - no such thing as “single” DNA sequence that defines HIV

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4
Q

Retroviruses are (enveloped/non-enveloped) viruses, about (X) nm in diameter.

A

Enveloped;

X = 100

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5
Q

Retrovirus structure: inner shell is composed of (X) proteins and inner core composed of (Y) proteins. What’s contained within the core?

A
X = matrix
Y = capsid
  1. Genome (2 copes of (+) sense mRNA)
  2. Proteins (Reverse transcriptase, Integrase, Protease)
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6
Q

T/F: HIV-1 genome is more complex than most retroviruses.

A

True - Encodes additional gene products (regulate virus replication and play role in pathogenesis)

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7
Q

HIV: The (X) gene product functions as transcriptional transactivator. It can be released from infected cells and induce which processes in uninfected cells?

A

X = tat

  1. Alter gene expression
  2. Apoptosis
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8
Q

HIV: The (X) gene product downregulates CD4 and MHC-1 expression.

A

X = nef

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9
Q

Long-term non-progressors of HIV (are/aren’t) viremic. Some harbor HIV-1 variants that have mutant of (X) gene product.

A

Are (but not pathogenic);

X = nef

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10
Q

Worldwide, most common method of HIV-1 transmission is:

A

M to F sex contact

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11
Q

What are the routes of HIV-1 infection?

A
  1. Sexual
  2. Parenteral
  3. Perinatal
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12
Q

Primary receptor for HIV-1 is (X), found on (Y) cells. Which viral protein attaches to (X)?

A
X = CD4
Y = T-helper lymph and macrophages

gp120

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13
Q

The major HIV-1 co-receptors are (X).

A

X = CCR5 and CXCR4

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14
Q

HIV-1 establishes low-level infection in which cell types?

A
  1. DCs

2. Langerhan’s cells

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15
Q

T/F: Macrophages are the cells thought to facilitate HIV-1 dissemination from mucosa to lymph nodes.

A

False - DCs and Langerhan’s cells

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16
Q

Individuals thought to be resistant to HIV-1 infection are (homo/hetero)-zygous for which gene alteration?

A

Homozygous;

Deletion in CCR5 gene

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17
Q

A group of long-term non-progressors of HIV-1 expresses high levels of (X), which compete with the virus for (Y).

A
X = chemokines (MIP-1a, MIP-2b, RANTES)
Y = CCR5 binding
18
Q

List the steps in HIV-1 life cycle that have been targeted by anti-retroviral drugs.

A
  1. Receptor binding
  2. Entry
  3. Integration
  4. Proteolytic maturation
19
Q

HIV-1: (X) co-receptor is expressed on T-cells and macrophages. (Y) co-receptor is preferentially expressed on T-cells.

A
X = CCR5
Y = CXCR4
20
Q

HIV-1: drugs block entry of virus into cell by preventing (X) from..

A

X = gp41

Adopting fusion-competent conformation

21
Q

Reverse transcriptase synthesizes (X) from (Y). AZT and other anti-retroviral drugs block this step via which mechanism?

A
X = dsDNA
Y = ssRNA

They’re nucleoside analogs that compete with normal nucleoside (terminate DNA chain elongation)

22
Q

Non-nucleoside inhibitors of reverse transcriptase function as anti-retroviral drugs via which mechanism?

A

Bind RT near active site and block its activity

23
Q

HIV-1: lack of proofreading activity of (X) polymerase(s) contribute to viral variants.

A

X = RNA-dependent DNA Pol (reverse transcriptase) and RNA polymerase II

24
Q

T/F: HIV-1, like most retroviruses, cannot productively infect non-dividing cells.

A

False

25
Q

For most retroviruses, entry of DNA into nucleus requires (X). HIV-1 has (Y) protein that allows DNA transport in absence of (X).

A
X = nuclear membrane breakdown (during cell division)
Y = CA
26
Q

T/F: Assembled HIV-1 virions, released from cell, are mature.

A

False - contain uncleaved polyproteins (must undergo proteolytic maturation)

27
Q

High rates of (X) during HIV-1 infection result in extensive sequence heterogeneity and outgrowth of viral strains with higher (Y) capacity.

A
X = replication, mutation, and recombination
Y = replicative and pathogenic
28
Q

In acute HIV-1 infection, there’s a sudden drop, followed by rebound increase, in (CD4 cells/viral load).

A

CD4 cells

29
Q

In acute HIV-1 infection, there’s a sudden spike, followed by sudden drop, in (CD4 cells/viral load).

A

Viral load

30
Q

In acute HIV-1 infection, (CD4 cells/viral load) initially spikes. (X) cells also spike, but then steadily decline.

A

Viral load;

X = HIV-1 specific CTL

31
Q

During latent phase of HIV-1 infection, replication is (stopped/slow).

A

Still very high! (10^8 to 10^9 virions/day)

32
Q

List examples of HIV-1 induced T-cell abnormalities.

A
  1. Lack of Ag response
  2. Impaired proliferation
  3. Impaired IL-2 expression (T cell growth)
  4. Shift from Th1 (CM) to Th2 (humoral) profile
33
Q

List examples of HIV-1 induced macrophage abnormalities.

A

Impaired chemotaxis, phagocytosis, and cytokine production

34
Q

List the general mechanisms by which HIV-1 kills.

A
  1. Direct killing (cytotoxicity)
  2. Syncytium formation
  3. Immune attack/apoptosis
35
Q

Worldwide HIV-1 epidemic has epicenters in which countries?

A
  1. Sub-saharan Africa
  2. India
  3. China
  4. Russia
36
Q

T/F: Significant exposure to body fluids from HIV+ person has 30% transmission risk.

A

False - 0.3%! (Very low).

30% transmission risk for HBV

37
Q

CDC recommends primary assay for HIV test that detects (X).

A

X = HIV p24 Ag and HIV Ab

38
Q

CDC recommends secondary assay for HIV test. If primary assay is (negative/positive), the secondary assay detects (X). What’s the point of this second assay?

A

X = HIV-1/HIV-2 Ab

Differentiate between HIV-1 v. HIV-2

39
Q

T/F: Patients can opt-out of screening tests for HIV.

A

True

40
Q

T/F: Written consent is required for HIV testing.

A

False - general consent for medical care is sufficient

41
Q

List some side effects of HAART.

A
  1. Fat redistribution
  2. Hypercholesterolemia
  3. Other specific drug adverse effects