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Microbiology E-Books > HIV and AIDs I > Flashcards

HIV and AIDs I Flashcards

1
Q

Characterized by immunodeficiency resulting from loss of CD4+ T lymphocytes, and development of lifethreatening opportunistic infections

A

AIDs

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2
Q

One of the most prevalent places of HIV infection in the world is

A

Africa south of the sahara

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3
Q

In infected persons, infectious quantities of HIV (and infected cells, also infectious) are present in blood, CSF, and semen, with smaller quantities in

A

Vaginal secretions and milk

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4
Q

Spread by parenteral exposure to blood, sexual intercourse, perinatally, and rarely from other forms of contact

A

HIV

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5
Q

Before testing was available, many people were infected with HIV via

A

Transfusions

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6
Q

Increase the risk of transmission, by damaging mucosal barriers and locally increasing the number of white blood cells which may become infected

A

Genital tract infections or injuries

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7
Q

Present in human seminal plasma was found to increase infectivity of virions by many orders of magnitude, making this interaction an attractive potential target for drug development

A

Prostatic acid phosphatase fragment

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8
Q

The decline in deths from AIDs after 1995 reflects the development of a

A

Highly-Active Anti-Retroviral Therapy (HAART)

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9
Q

The use of a combination of two RT inhibitors plus a protease inhibitor

A

HAART

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10
Q

The biology of HIV is deeply intertwined with the biology of its

A

Host cells

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11
Q

HIV gene products replicate its genome and form the structural components of

A

New Virions

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12
Q

A recent survey identified over 250 host-cell proteins required for efficient

A

HIV replication

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13
Q

Cytosolic contents are wrapped in a double shell of membrane and delivered to endosomes in

A

Autophagy

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14
Q

Normally function in formation of multi-vesicular bodies and degradation of plasma membrane proteins, are required for budding of HIV virions

A

Proteins of the ESCRT complexes (Endosomal Sorting Complexes Required for Transport)

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15
Q

The primary receptor for HIV is

A

CD4

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16
Q

The cell tropism of HIV is largely determined by the distribution of

A

CD4

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17
Q

A plasma membrane glycoprotein that in structure resembles an immunoglobulin heavy chain, with four immunoglobulin-type domains

A

CD4

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18
Q

CD4 is present on helper T cells and cells of the monocyte/macrophage lineage, including dendritic cells of epithelia, which may be the initial cells infected with

A

Sexually transmitted HIV

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19
Q

HIV binding to dendritic cells may also facilitate infection of

A

T cells

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20
Q

A surface protein of dendritic cells that binds HIV virions to the cell surface

A

DC-SIGN

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21
Q

Attract T cells, which then become infected

A

Dendritic cell chemokines

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22
Q

After infection macrophages can spread HIV, especially to secondary lymphoid organs and the

A

Brain

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23
Q

Can block HIV infection by occupying the receptor

A

Chemokine receptors

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24
Q

About 1% of U.S. Caucasians (and a lower faction of Black and Hispanic Americans) are homozygous for a deletion in the gene for the receptor

A

CCR5

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25
Q

Such persons have slower progression of disease after infection. However, they eventually develop

A

AIDS

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26
Q

The number of CCR5 gene copies varies between individuals - the higher the copy number the more rapid the progression to

A

AIDs

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27
Q

Some CD4- cells can be infected with HIV in vivo, especially brain astrocytes and oligodendrocytes and epithelial cells of the

A

Bowel

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28
Q

Here, the receptor may be a

A

Glycolipid, galactosyl ceramide

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29
Q

The ability of HIV to establish productive infection depends on the state of the cell infected. Monocytes and resting T cells produce little if any

A

Virus

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30
Q

However, these support abundant virus replication

A

Macrophages and activated T cells

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31
Q

The state of the infected cell may affect reverse transcription, integration, or

A

Virus transcription

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32
Q

The HIV promoter binds numerous cellular transcription factors (notably NF-KB) which are activated when T cells are stimulated by cytokines such as

A

TNF

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33
Q

Thus, T cells can not be stimulted to fight HIV without also stimulating its

A

Replication

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34
Q

Infection by HIV can result in a state of

-The provirus is integrated into the host genome but not expressed

A

True viral latency

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35
Q

Such cells persist in the face of an immune response because they produce no viral antigens and, since there is no viral replication, latent HIV is not sensitive to

A

Anti-viral agents

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36
Q

Latently-infected cells may later become activated and produce

A

Virus

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37
Q

HIV and other lentiviruses encode six small proteins not produced by other

A

Retroviruses

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38
Q

Bind to proteinubiquitin ligases, recruit specific host-cell proteins for ubiquitinylation, and promote their destruction by the proteosome

A

Vif, vpr, and vpu

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39
Q

What are the 6 regulatory proteins?

A

Tat, rev, nef, vif, vpu, and vpr

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40
Q

Powerful stimulator (100x) of transcription from the HIV promoter

A

Transactivator (tat)

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41
Q

Inhibits splicing of viral transcripts

A

Rev

42
Q

Named for a putative ‘negative effect’

-Actually stimulates HIV replication and may be responsible for damage to the immune system

A

Nef

43
Q

Persons infected with nef-defective HIV are ‘slow-progressors’ to

A

AIDs

44
Q

Present in virion, required for infectivity

A

Virion Inefectivity Factor (vif)

45
Q

Causes degradation of a DNA cytosine deaminase APOBEC which produces mutagenic damage to reverse transcripts

A

Vif

46
Q

Stimulates virus release from the cell surface by delivering CD4 to the proteosome, and reducing cellsurface tetherin

A

Vpu

47
Q

A protein that binds virions to the cell surface and promotes their endocytosis

A

Tetherin

48
Q

Present in virion, may aid in transport of the viral core to nucleus; blocks cell division cycle in G2, when HIV transcription is more efficient than in G1

A

Vpr

49
Q

Tat is an activator of

A

HIV transcription

50
Q

Binds not to the HIV promoter but to tar (tat response element) of the transcript, which forms a stem-loop structure

A

Tat

51
Q

Tar-bound tat binds cellular proteins which stimulate

A

Transcription

52
Q

One is a protein kinase which phosphorylates the C-terminal domain of

-Facilitates promoter clearance and rapid transcription

A

RNA polymerase

53
Q

Rev prevents splicing of HIV mRNA by binding to

A

Rev Response Element (RRE) and exportins

54
Q

Proteins which transport molecules out of the nucleus

A

Exportins

55
Q

Early after infection, Rev levels are low and most viral transcripts are fully spliced, so that the small regulatory proteins are

A

Translated

56
Q

As Rev accumulates, splicing is blocked, and unspliced and singly-spliced transcripts are able to leave the

A

Nucleus

57
Q

Nef-defective Simian AIDS virus (SIV) failed to produce disease and in fact gave rise to a

A

Protective immune response

58
Q

Expression of Nef in transgenic mice produces an

A

AIDS-like syndrome

59
Q

This suggests that nef may play a key role in

A

AIDS pathology

60
Q

Has an attached fatty acid and is bound to the plasma membrane, where it may alter intracellular signaling from membrane receptors and so alter transcription

A

Mature Nef

61
Q

Down-regulates expression of CD4, MHC antigens, and cytokines, including IL-2 and IFN-γ

A

Nef

62
Q

Induces macrophages to secrete soluble factors which up-regulate proteins on resting T cells, causing them to become susceptible to HIV infection

A

Nef

63
Q

A cellular defense against retroviruses is

A

APOBEC

64
Q

A deaminase that converts cytosine to uracil in viral DNA, creating mutations

A

APOBEC

65
Q

The deaminase is incorporated into new virions and acts on the DNA strands produced by

A

Reverse transcription

66
Q

Incorporated into HIV virions and excludes the deaminase APOBEC

A

Wif

67
Q

One member of this protein family produces an intestine-specific form of Apo-B shorter than the liver form, by converting a cytosine in mRNA to uracil and creating a stop codon

A

Vif

68
Q

Another member of the Vif family causes hypermutation of

A

Ig-gene

69
Q

A host protein used by HIV to defend itself

A

Cyclophilin

70
Q

Cyclophilin was named because it binds the immunosuppressant

A

Cyclosporin A

71
Q

Mammalian cells contain ‘restriction factors’, proteins which bind CA proteins of infecting virions and block

A

Virus Replication

72
Q

Binds Cyclophilin; it is incorporated into virions and, in an as-yet-unknown way, blocks a ‘restriction factor’

A

HIV CA

73
Q

Typically follows exposure to HIV by 4-8 weeks. Symptoms are non-specific and may include (from most to least common) fever, lymphadenopathy, rash, pharyngitis, myalgia, diarrhea, headache, nausea, hepatosplenomegaly, peripheral- or CNS symptoms

A

Acute HIV infection

74
Q

Acute HIV infection typically presents how long after initial infection?

A

4-8 Weeks

75
Q

In acute disease there is rapid viral replication and high-level

A

Viremia

76
Q

Can be found in the blood during acute HIV infection?

A

Infectious virus and CA (p24) antigen

77
Q

After a few weeks, HIV-specific CTL appear and a strong cell-mediated immune response clears virus from the

A

Bloodstream

78
Q

Anti-HIV antibodies (seroconversion) may not appear until

A

2-6 Months after infection

79
Q

Gut lymphoid tissue is a major site of early

A

HIV replication

80
Q

Massive early loss of T cells creates “holes” in the T-cell repertoire as clones of memory cells are eliminated by the

A

Virus

81
Q

T cells with anti-HIV specificity may be especially susceptible to

A

Infection and killing

82
Q

Binds integrin α4β7

A

HIV SU protein

83
Q

The receptor which causes memory T cells to ‘home’ to mucosal lymphoid tissue

A

Integrin α4β7

84
Q

This in turn up-regulates the membrane protein

A

LFA-1

85
Q

Promotes cell-cell association of T cells and may promote cell-to-cell spread of HIV

A

LFA-1

86
Q

Untreated, the median interval between seroconversion and development of AIDS is

A

10.5 years

87
Q

This period is known as the

A

Asymptomatic period

88
Q

Patients do not feel ill, and unless diagnosed, do not curtail activities that transmit the virus to others

A

Asymptomatic period

89
Q

During the asymptomatic period, plasma viremia is typically low due to production of

A

Anti-HIV antibodies

90
Q

During the asymptomatic period, dendritic cells trap these immune complexes and remove virus from the circulation; however this may facilitate infection of dendritic cells and/or transfer of virus to

A

T cells

91
Q

Plasma virus load determines the speed of progression to

A

Symptomatic disease

92
Q

Which cell type has the longest half-life when treated with HIV drugs?

A

Infected macrophages and dendritic cells

93
Q

During the ‘asymptomatic period’ there is slow but steady alteration of the

A

Immune system

94
Q

Early there is B-cell dysregulation, polyclonal B-cell proliferation, and proliferation of

A

CD8 T cells

95
Q

Later, although the total concentration of circulating lymphocytes does not change, the ratio of CD4+ to CD8+ cells progressively

A

Declines

96
Q

Within the TH population, we see an

A

Increase in TH2 cells and decrease in TH1 cells

97
Q

T-cell proliferation and CMI are compromised and may ultimately lead to failure of the anti-HIV

A

CTL response

98
Q

Response of T-cells to previously-encountered antigens also declines, perhaps because HIV preferentially infects

A

Memory T cells

99
Q

Lymphadenopathy, fever, weight loss, persistent diarrhea, and Candida infection (the “AIDS-related” complex or ARC), are the initial manifestations of

A

Immune-system failure?

100
Q

Defined by rapid decline of CD4+ lymphocytes, rapid increase in plasma viremia, and development of opportunistic infections

-The last stage of HIV disease

A

AIDS

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