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Micro unit 2 > L5 > Flashcards

L5 Flashcards

1
Q

4H club” risk group retrovirus

A

Homosexual men, heroine addicts, Haitians, and hemophiliacs (“4H club” risk group) began dying of normally-benign opportunistic infections in U.S., defining a new disease, “acquired immune deficiency syndrome” (AIDS)

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2
Q

1986: HIV-2 discovered in West Africa. HIV-2 RNA is

A

sequence similar (40%) to HIV-1. HIV-2 is mostly a heterosexual disease.

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3
Q

HIV appears to have evolved (genetic evidence) from

A

simian virus in Africa (SIV) and spread through the rest of the world due to an increasingly mobile population and aberrant sexual behaviors. Theory: SIV > HIV-2 > HIV-1 with initial human infection ~ 1930.

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4
Q

Retroviruses Have a unique

A

replication cycle

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5
Q

Retroviruses are

A

Ubiquitous in vertebrates

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6
Q

Retroviruses - Many are

A

benign, causing little to no impact on the host cell or host animal

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7
Q

Retroviruses can have significant

A

pathogenicity causing disease and cancer

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8
Q

retroviruses Spumaviruses do not cause

A

human disease

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9
Q

Retroviruses make

A

Make “foamy” structures insidethe cell

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10
Q

Retroviridae: two subfamilies

A

Orthoretroviridae

Spumaviridae

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11
Q

Retrovirus genome

A

Genome: (+)ssRNA

Diploid, identical copies

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12
Q

Retrovirus Virion:

A

enveloped

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13
Q

Historically, retroviruses were characterized by

A

nucleocapsid structure & location in the particle

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14
Q

Retrovirus Genome contents now used to classify retroviruses as

A

simple or complex

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15
Q

Simple retroviruses only encode the

A

Gag, Pro, Pol, and Env genes

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16
Q

Retrovirus Replication Cycle

A 
Attachment
Entry
Reverse transcription
ssRNA genome to dsDNA
Integration
Virus dsDNA into host  making provirus
Transcription from provirus
Translation
Assembly
Release
Maturation – protease activity
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17
Q

Reverse transcription Defining feature of

A

retroviruses

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18
Q

RT Initiates once nucleocapsid is in

A

cytoplasm

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19
Q

RT needs higher levels of

A

NTPs present

Low NTP levels prevent reverse transcription

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20
Q

RT Occurs within a

A

large complex similar to nucleocapsid

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21
Q

Infection cannot progress

A

if reverse transcription does not occur

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22
Q

Reverse transcription is

A

promiscuous between genome copies

Silent” when copies are identical

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23
Q

Many different recombinations when different genomes are in the

A

virion

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24
Q

Retrovirus Integration

A

Must access the nucleus
Access during mitosis – requires dividing cells
Importation (mechanism unknown) – can infect non-dividing cells

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25
Q

Retroviruses have 3’ end

A

processing of dsDNA

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26
Q

Retrovirus Attack

A

target DNA, nick created

Host repair

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27
Q

Integration of virus DNA is

A

permanent, no mechanism to remove it

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28
Q

If integrated into the germ-line then

A

provirus is inherited and is called “endogenous”

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29
Q

Integration may disrupt

A

host genes causing disease such as cancer

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30
Q

Integration identified oncogenes

A

Transcription factors
Secreted growth factors
Growth factor receptors
Cell signal transduction pathways

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31
Q

Many defective viruses are made during

A

replication

32
Q

Defective viruses are missing at least one of

A

gag, pol, or env

33
Q

Retrovirus Require complementary infection to make

A

progeny

34
Q

Can carry host genes,

A

tumorigenic when they carry oncogenes

35
Q

Many retrovirus infections are

A

benign

36
Q

Retroviruses usually

A

Usually not cytopathic

37
Q

Retroviruses usually have

A

Little impact to cell replication & physiology

38
Q

Chronic infections exert small demand on

A

cell and host resources (few percent of cell RNA and protein)

39
Q

Retroviruses Do cause

A

viremia and elicit an immune response, but host animals can live normal lives for many months or years

40
Q

Viruses are never eliminated by the

A

host response

41
Q

Slow retroviruses (e.g., leukemia viruses)

A

Effect is like high-level mutagenesis

Eventually results in tumorigenesis

42
Q

Cytopathic retroviruses

A

Minority of retroviruses carry cytopathic genes

Cause tissue damage directly

43
Q

Acute transforming viruses

A

Induce rapid tumor formation
Carry host genes – mitogenic or antiapoptotic
Often replication defective because host gene replaces an essential gene

44
Q

Human T-Cell Leukemia Virus Four distinct types (1, 2, 3, 4)

A

HLTV-1 most often associated with humans

45
Q

HTLV

A

Deltaretrovirus

46
Q

HTLV First isolatedin patient with

A

cutaneous T-cell lymphomain the late 1970s

47
Q

HTLV-1 Transmission - person to person

A

Mother-child via breastfeeding (endemic areas)
Sharing needles for drug users
Blood transfusions
Sexual transmission (less efficient)

48
Q

HTLV-1 transmission Within the host

A

Highly cell associated

Primary mode for spreadis contact between infected and naïve cells

49
Q

HTLV- 1 Adult T-Cell Lymphoma/Leukemia (ATLL)

A

Following mucosal exposure

50
Q

HTLV-1 disease occurs

A

Occurs in 2-4% of cases

51
Q

HTLV-1 latent period

A

30-50 years

52
Q

HTLV-1 infects

A

Infects memory T-cells

53
Q

HTLV-1 Antigen activation triggers

A

transcription of provirus

54
Q

HTLV-1 Virus Tax protein & othersstimulate

A

cell proliferation

55
Q

HTLV-1 Cells become transformed

A

generating tumors

With or without virusprotein expression

56
Q

HTLV-1 Associated Myelopathy / Tropical Spastic Paraparesis (HAM/TSP)

A

Two disease now shown to be the same

Occurs in 1-2% of cases

57
Q

HTLV-1 disease occurs

A

Following transfusions

58
Q

Infected T-cells enter the

A

central nervous system

Activate astrocytes, microglial cells
Recruit inflammatory cells causes further tissue damage

59
Q

HTLV-1 HAM/TSP Symptoms

A

Onset typically 3 years after infection
Starts with bladder control issues
Progress to lower back pain, leg weakness or stiffness in hips or knees
Men suffer impotence or erectile dysfunction

60
Q

HTLV-1 prevention

A

Eliminate breastfeeding for HTLV-1 positive mothers

Increased screening for blood products

61
Q

HTLV-1 Treatment is specific to the disease

A

ATLL – treat the lymphoma/leukemia with chemotherapy regardless of HTLV infection
HAM/TSP – corticosteriods, interferon yield temporary relief of symptoms

62
Q

Human Immunodeficiency Virus type

A

Lentivirus

Virus identified in 1984

63
Q

HIV Identified due to immune deficiency occurring in previously healthy

A

young gay men

64
Q

HIV Specific populations were

A

most at risk

Homosexuals, injection drug users, hemophiliacs, transfusion recipients

65
Q

HIV Impact

A

Highest in sub-Saharan Africa

66
Q

HIV transmission Sexual transmission

A

primary route)

67
Q

HIV transmission Parenteral

A

Transfusion – 95%

Needle sharing – 1:150

68
Q

Mother to infant HIV transmission

A

No AZT – 1:4

AZT – less than 1:10

69
Q

Aids latent periord

A

6 mths to 25 yrs

70
Q

HIV Infection begins virus

A

containing blood or body fluidto a mucosal surface or blood

71
Q

HIV targets

A

memory T-cells (CD4+)

72
Q

HIV Initial acute infection

A

usually 2 weeks afterinfection

Mucocutaneous ulcerationand weight loss more indicative of HIV infection

73
Q

HIV Gut Associated Lymphoid Tissue (GALT) seeded as a result of

A

acute infection (reservoir)

74
Q

Chronic infection established

A

Ongoing virus replication & T-cell depletion

75
Q

HIV: Opportunistic infections

A 
increase
Common infections
Candida
Coccidioidomycosis
Cryptococcus
Cytomegalovirus
Kaposi sarcoma
Tuberculosis
Toxoplasmosis
Wasting due to HIV infection
76
Q

HIV Prevention

A

Sexual behavior and protection

Blood screening

77
Q

HIV Treatment

A

No vaccine
Antiviral treatments
Nuceloside reverse transcriptase inhibitors (NRTI) – e.g., azidothymidine (AZT)
Protease inhibitors – e.g., Ritonavir
Non-nucleoside RT inhibitor (NNRTI) – e.g., Efavirenz
Highly Active Antiretroviral Therapy (HAART) – combines three of the treatment options

Micro unit 2 (12 decks)

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