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micro exam 3 > RetroViruses, AIDS, & Tumor VIruses > Flashcards

RetroViruses, AIDS, & Tumor VIruses Flashcards

1
Q

who discovered Retroviruses

A

1911 by Peton Rous

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2
Q

first retrovirus

A

Rous Sarcoma Virus

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3
Q

who discovered reverse transcriptase

A

David Baltimore and Howard Temin in 1970

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4
Q

Involvement in finding reverse transcriptase

A

Temin had the theory; baltimore/temin found the enzyme

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5
Q

Isolation of the first retrovirus for human disease

A

1981 by Bob Gallo and associates who isolated HTLV-1

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6
Q

The 4H club risk group for Retroviruses

A

Homosexual men
Heroin addicts
Haitians
hemophiliacs

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7
Q

what did the 4H club die of

A

of normally benign opportunistics infections in the U.S.- AIDS (acquired immune deficiency syndrome

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8
Q

Disocovery of HIV-1

A

1980: MOntagnier and assocaites in paris and Gallo and colleagues at NIH isoluate HIV_1 from patients with lymphadenopathy and AIDS

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9
Q

where was HIV-2 discovered

A

In west africa in 1986

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10
Q

similarity of HIV-1 and HIV-2

A

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

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11
Q

Origin of HIV

A

Evolved from simian virus in Africa (SIV) and spread through the rest of the world due to an increasingly mobile pop and aberrant sex
SIV>HIV-2>HIV-1 and human infection in 1930

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12
Q

how mnay retroviruses are there

A

large and diverse group of viruses

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13
Q

replication cycle similarity of retroviruses

A

Unique, with a DNA intermediate despite using RNA

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14
Q

Retroviruses in vertebrates

A

ubiquitous

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15
Q

do most retroviruses cause damage

A

no, most are benign

but other have significant pathogenicity and cause diseas and cancer

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16
Q

2 subfamilies of Retroviruses

A

Orthoretroviridae

Spumaviridae

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17
Q

Genome of Retroviruses

A

(+)ssRNA

diploid, identical copies

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18
Q

Virion of Retrovirues

A

Enveloped

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19
Q

proteins of Retroviruses

A

Reverse transcriptase (RNA-> DNA, DNA-> DNA
Integrase
Protease

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20
Q

How are Retroviruses characterized historically

A

nucleocapsid strucutre and location in the particle

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21
Q

how are retroviruses classified now

A

genome contents used to classify as simple or complex

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22
Q

Simple retroviruses encode what genes

A

Gag
Pro
Pol
Env

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23
Q

Complex retroviruses encode

A

all what simple retroviruses encode plus more

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24
Q

replication cycle of a Retrovirus

A 
Attachment
Entry
Reverse transcription
Integration
Transcription from provirus
Translation
Assembly
release
Maturation - protease activity
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25
Q

what occures in retrovirus reverse transcription

A

ssRNA genome to dsDNA

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26
Q

what occures in retrovirus integration

A

Virus dsDNA into host making a provirus

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27
Q

how does a retrovirus enter the cell

A

due to membrane fusion at the cellular membrane due to receptor mediated endocytosis

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28
Q

The defining feature of retroviruses

A

Reverese transcription

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29
Q

when does reverse transcription begin

A

initiates once nucleocapside is in cytoplasm (neeed higher level of NTPs)

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30
Q

what prevents reverse transcription

A

Low NTP levels

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31
Q

where does Reverse transcription occur

A

within a large complex similar to nucleocapside

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32
Q

what happens if reverse transcription does not occur for a retrovirus

A

infection cannot progress

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33
Q

why is Reverse Transcriptase promiscuous

A

can fall off one genome copy and then continue on another

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34
Q

Why would promiscuous Reverese transcription be silent

A

When copies are identical

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35
Q

what happens when different genomes are in the virion of a retrovirus

A

many different recombinations

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36
Q

why are Retrocviruses difficult to vacinate

A

since Reverse transcriptase can move from one genome to anther, it changes antigens of the retrovirus

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37
Q

what must a retrovirus have access to, in order to inegrate

A

must access the nucleus

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38
Q

when does a retrovirus access the nucleus during integration

A

access during mitosis - requires dividng cell

also can do importation to infect non-deviding cells

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39
Q

how does a retrovius integrate

A

3 prime end of dsDNA from the virus genome is processed/opened up
Attacks target DNA creating a Nick in it
Host then repares DNA and acidentally adds the Virus genome

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40
Q

How can virus DNA be removed

A

INtegration of Virus DNA is permanent and cannot be removed

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41
Q

what happens if Virus DNA is integrated into the germ-line

A

provius becomes inherited and is called endogenous

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42
Q

what negative effect can integration of retrovirus cause

A

may disrupt host genes causing diseases such as cancer

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43
Q

Oncogenes for integration

A

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

44
Q

effecienct of retrovirus replication

A

many defective viruses are made during replication (v. sloppy)
missing at least one of gag, pol, or env

45
Q

what is required for retrovirus infection to make progeny

A

Require complementary infection

46
Q

what can happen when Retroviruses carry oncogenes

A

oncogenes

47
Q

do all retroviruses cause problems?

A

NO, can be benign

48
Q

are most retroviruses cytopathic

A

no

49
Q

effect of benign retroviruses on the cell

A

little impact to cell replication and physiology

Chronic infection exert small demand on cell and host resources

50
Q

How does the host respond to a benign retrovirus

A

can cause Viremia and elicit an immune response, bt host animals may live normal lives for months and years
never eliminated by the host

51
Q

Types of Retroviruses that cause disease

A

Slow Retroviruses
Cytopathic retroviruses
Acute transforming viruses

52
Q

what is the effect of a slow retrovirus

A

Like High-level mutagenesis

53
Q

Eventual result of a slow retrovirus

A

Results in humorigenesis

54
Q

how many Retroviruses carry cytopathic genes

A

Minority

55
Q

What do Cytopathic retroviruses do

A

Cause tissue damage directly

56
Q

what do Acute transforming viruses do

A

Induce rapid tumor formation

57
Q

How do Acute transforming viruses lead to rapid tumor formation

A

carry host genes (mitogenic or antiapoptiotic

Replication defective because host gene replaces an essential gene

58
Q

Types of Human T-Cell Leukemia Virus (HTLV)

A

4:1,2,3,4

59
Q

what type of HTLV is most often associated with humans

A

HLTV-1

60
Q

what type of virus is HTLV

A

Deltaretrovirus

61
Q

how does HTLV first isolated

A

in patients with cutaneous T-cell lymphoma in the 1970s

62
Q

what forms when the Retrovirus first assembles

A

an immature virus

63
Q

what happens to turn an immature virus into a mature one

A

proteases allow the immature to become mature and now it can replicate and infect

64
Q

how many people are infected with HRLV-1

A

Millions of people world wide

65
Q

How is HTLV-1 transmitted person to person

A

mother to child via breastfeding (endemic areas)
Sharing needles for drugs users
Blood transfusions
Sex transmission (less efficient)

66
Q

How can HTLV-1 be transmitted within the host

A

Cell Associated via contact between infected and naive cells

67
Q

What disease does HTLV-1 cause

A

Adult T-cell Lymphoma/Leukemia (ATLL)

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

68
Q

what must HTLV-1 be exposed to to cause Adult T-cell Lymphoma/Leukemia

A

Following mucosal exposure

69
Q

how often does HTLV-1 cause ATLL

A

204% of cases

70
Q

latent period for ATLL

A

30-50 years

71
Q

What does HTLV-1 infect to cause ATLL

A

Infect memory T-cells

72
Q

what triggers transcription of provirus HTLV-1

A

Antigen activation

73
Q

what triggers cell proliferation with HTLV-1

A

Virus Tax Proteins and others

74
Q

what does HTLV-1 do with ATLL

A

Cell become transformed generating tumors with or without virus protein expression

75
Q

How often does HAM/TSP occure when infected with HTLV-1

A

1-2% of cases

76
Q

how would someone get HAM/TSP

A

following transfusions

77
Q

what does HAM/TSP infect

A

T-cells

78
Q

once HAM/TSP infects T cells what happens

A

enter the CNS
Activate AStrocytes, microglial cells
Recruit inflammatory cells- further tissue damage

79
Q

when does HAM/TSP occure

A

3 years after infection

80
Q

progession of HAM/TSP

A

starts with bladder control issues
Progress to lower back pain, leg weakness or stiffness in hip
men suffer impotence or erectile dysfunction

81
Q

Preventing HTLV-1

A

eliminate breastfeeding for HTLV-1 positive moms

INcrease screening for blood products

82
Q

How to Treat ATLL

A

treat the lymphoma/leakemia with chemotherapy regardless of HTLV infections

83
Q

how to treat HAM/TSP

A

Corticosteriod, interferon yielding temporary relief of symtpoms

84
Q

types of HIV in humans

A

type 1 and type 2

85
Q

type of Virus is HIV

A

Lentivirus

86
Q

how was HIV discovered

A

due to immune deficiency occurring in previously healthy young gay men in 1984

87
Q

who is most likely to get HIV

A

Homosexuals
Injection drug users
Hemophiliacs
Transfusion recipients

88
Q

extent of HIV

A

World wide pandemic with significant impact

89
Q

how bad is HIV in sub-saharan africa

A

it really is decreasing life expectancy

90
Q

first drug to fight aids

A

AZT

91
Q

what does AZT target as an aids med

A

reverse transcriptase

92
Q

HIV transmission

A

Sex transmission (Primary route)
Parenteral
mother to infant

93
Q

odds of getting HIV in sex

A

Female to male: 1:600-1:3000
Male to female - 1:200 - 1:2000
Male to Male - 1:10 to 1:1600

94
Q

odds of getting HIV parenterally

A

Transfusion - 95%

needle sharing - 1:150

95
Q

odds of getting HIV from mom to infant

A

No AZT - 1:4

AZT - less than 1:10

96
Q

Latent period for AIDS

A

6 months to 25 years

97
Q

How does HIV infection begin

A

Begins in virus containing blood or body fluid to a mucosal surface or blood

98
Q

what does HIV target

A

memory T-cells (CD4+)

99
Q

when does Acute infection with HIV occure

A

2 weeks aftetr infection

100
Q

signs of HIV infection

A

Mucocutaneous ulceration and weight loss

101
Q

what is seeded as a rusult of an acute infection (reservoir)

A

GALT

102
Q

Rounds of infection in GALT

A 
1st Primary infection where it accutely affects the T cell population
dormancy
T cells eventually begin to drop
Constituional symptoms
Opportunistic disease
Death
103
Q

Common Opportuistic infections due to HIV

A 
CAndida
Coccidioidomycosis
Cryptococcus
Cytomegalovirus
Kaposi
sarcoma
Tuberculosis
Taxoplasmosis
Wasting due to HIV infection
104
Q

Prevention of HIV

A

sex behavior and protection

Blood screening

105
Q

Treating HIV

A

No vaccine

Antiviral treatments

106
Q

what antivirals are used to treat HIV

A

Nuceloside reverse transcriptase inhibitors (NRTI)- azidothymidine (AZT)
Protease Inhibitors - Ritonavir
Non-nucleoside RT inhibitors (NNRTI) - Efavirenz
Highly Active Antiretroviral Therapy (HAART) - combines 3 of the treatment options

micro exam 3 (15 decks)

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