Retroviruses, AIDS, & Tumor Viruses Flashcards

1
Q

when was AIDS first identified and what acronym was used to describe those infected?

A

-late 1970s-early 1980s: Homosexual men, heroine addicts, Haitians, and hmeophiliacs (4H risk group) began dying of normally-benign opportunistic infections in the US, defining a new disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where is the origin of HIV?

A

appears to have evolved (genetic evidence) from simian virus in Africa (SIV) and spread through the rest of the world due to an increasingly mobile population and aberrant sexual behaviors

eating and harvesting ape meat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe the retrovirus class

A
  • large and diverse group of viruses
  • unique replication cycle
  • ubiquitous in vertebrates
  • many are benign, cause little to no impact on the host cell or host animal
  • others have significant pathogenicity cause disease and cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what genus and subfamily do HIV-1 and HIV-2 come from?

A
  • genus: lentivirus

- subfamily: orthoretroviridae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

spumaviruses (subfamily of retroviruses) do not cause human disease, however, what kind of structures do they make inside the cell

A

foamy structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

**what type of viruses are retroviruses?

A
  • retroviridae: 2 subfamilies (othroretroviridae, spumaviridae)
  • genome: (+) ssRNA: diploid, identical copies
  • virion: enveloped
  • proteins:
    • reverse transcriptase (RNA->DNA, DNA->DNA)
    • integrase
    • protease
  • *antivirals go after one of these proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how were retroviruses once classified?

A

by nucleocapsid structure & location in the particle

  • A type: shell & hollow center, immature particle
  • B type: circular NC, eccentric location
  • C type: circular NC, central location
  • D-type: cylindrical NC, central location (AIDS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

simple retroviruses only encode the ___, ___, ___, and ____ genes

A

gag, pro, pol, env

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the replication cycle like for retroviruses?

A
  • attachment: membrane fusion @ cell surf when it inserts itself doesn’t discriminate
  • entry
  • REVERSE TRANSCRIPTION: ssRNA genome to dsDNA
  • INTEGRATION: virus dsDNA into host making provirus
  • transcription from provirus
  • translation
  • assembly
  • release by budding
  • maturation: protease activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why is retrovirus replication an exception to the rule?

A

because makes dsDNA intermediate and uses the nucleus even though it is (+)ssRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when does the reverse transcription of retroviruses occur?

A

initiates once nucleocapsid is in cytoplasm

  • need high levels of NTPs present otherwise no transc.
  • low NTP levels prevent reverse transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where does the reverse transcription of retroviruses occur?

A

-occurs within a large complex similar to nucleocapsid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

can infection progress if reverse transcription does not occur?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F: reverse transcription in retroviruses is not promiscuous among genome copies

A

FALSE: “silent” when copies are identical
many different recombinations when different genomes are in the virion

**adds to high mutation=hard to develop vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe the integration process in retrovirus replication

A
  • must access the nucleus during mitosis b/c requires dividing cells
  • importation (mech unknown): can infect nondividing cells
  • 3’ end processing of dsDNA
  • attack target DNA, nick created
  • host repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

is the integration process in retrovirus replication permanent?

A

yes, no mech to remove it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when is the provirus considered “endogenous” in retroviruses?

A

if integrated into the germ-line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

integration can cause cancer. what are some integration identified oncogenes?

A
  • TFs
  • secreted growth factors
  • growth factor receptors
  • cell signal transduction pathways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

many defective viruses are made during replication what are they typically missing?

A

at least one: gag, pol, or env

however, require complementary infection to make progeny

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how is it that most retroviruses are benign?

A
  • not cytopathic
  • chronic infections exert small demand on cell and host resources (few percent of cell RNA and protein)
  • do cause viremia and elicit an immune response, but host animals live normal lives for many months or years
  • viruses are never limited by the host response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

*describe slow retroviruses

A

(eg leukemia viruses)

  • effect is like high-level mutagenesis
  • eventually results in tumorigenesis
  • replication, integration event affects cell growth regulation factor leading to cancer
22
Q

*describe cytopathic retrovirues

A
  • minority of retroviruses carry cytopathic genes
  • cause tissue damage directly
  • genes for cell lysis
23
Q

*describe acute transforming viruses

A
  • induce rapid tumor formation
  • carry host genes: mitogenic and antiapoptotic
  • often replication defective b/c host gene replaces an essential gene (produce oncogenes–>cancer)
24
Q

what are the 4 types of human T-cell leukemia (HTLV)

A

HTLV1-4

25
Q

what type of virus is HTLV?

A

deltaretrovirus

26
Q

what is the HTLV-1 prevalence?

A

millions of people around the world are infected

27
Q

how is HTLV transmitted?

A

person to person:

  • mother to child via breastfeeding (endemic areas)
  • sharing needles for drug users
  • blood transfusions
  • sexual transmission (less efficient)
28
Q

how is HTLV spread within the host?

A
  • highly cell associated/budding out of cell so “hitching a ride”
  • primary mode for spread is contact between infected and naive cells
29
Q

adult T-cell lymphoma/leukemia has a LONG latent period, how long is it?

A

30-50 years

30
Q

which T cells does HTLV-1 infect?

A

memory T cells

31
Q

what triggers the transcription of provirus in HTLV-1 disease?

A

antigen activation triggers it

32
Q

what proteins in HTLV-1 stimulate cell proliferation?

A

Virus Tax protein and others

33
Q

in HTLV-1 cells become ________ generating tumors

A

transformed

with or without protein expression

34
Q

what is HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP)?

A
  • following transfusions
  • infected T cells enter the central nervous system
    • active astrocytes
    • recruit inflamm cells causes further tissue damage
35
Q

what are the symptoms of HAM/TSP?

A
  • onset typically 3 years after infection
  • starts with bladder control issues
  • progress to lower back pain, leg weakness, or stiffness in the hips
  • men suffer impotence or erectile dysfunction
36
Q

how can HTLV-1 be prevented?

A

eliminate breast feeding for HTLV-1 positive mothers

incr. screening for blood products

37
Q

what treatment is there for HTLV-1?

A
  • ATLL:treat the lymphoma/leukemia with chemotherapy regardless of HTLV infection
  • HAM/TSP: corticosteroids, interferon yield temporary relief of symptoms
38
Q

describe human immunodeficiency virus

A
  • two main types: 1 & 2
  • Lentivirus
  • Id’ed due to immune deficiency occurring in previously healthy young gay men
  • Id’ed in 1984
  • specific pops were at risk (4H’s)
39
Q

is the HIV prevalence worldwide?

A

yes

40
Q

where is HIV prevalence highest at?

A

sub-Saharan Africa

41
Q

what is the AIDS incidence like?

A

high rise until 1994 when the AZT(antiviral) was put on the market

42
Q

what is the primary mode of transmission and the most likely way it is passed between person to person?

A

sexual transmission and male to male>male to female>female to male

43
Q

is AIDS latent for a long time?

A

yes 6mos-25 years

44
Q

infection begins virus containing _____ or body fluid to a _______ surface or blood

A

blood, muscosal

45
Q

which immune cells does HIV target?

A

memory T cells (CD4+)

46
Q

when does the initial acute infection of HIV first occur?

A

2 weeks after infection: mucocutaneous ulceration and weight loss more indicative of HIV infection

47
Q

what is GALT and what is it a result of?

A
  • gut associated lymphoid tissue

- result of acute HIV infection (reservoir)

48
Q

does HIV lead to chronic infection

A

yes, ongoing virus replication & T cell depletion

49
Q

T/F: opportunistic infections incr. with HIV infection

A

TRUE

50
Q

how is HIV prevented?

A

sexual behavior and protection, blood screening

51
Q

what is the treatment for HIV?

A

no vaccine

antiviral treatments:

  • nucleoside reverse transcriptase inhibitors (NTI)= azidothymidine (AZT)
  • protease inhibitors
  • non-nucleoside RT inhibitor
  • highly active antiretroviral therapy: combine 3 treatment options
52
Q

IMPORTANT POINTS OF RETROVIRUSES

A
  • enveloped particle
  • diploid (+)ssRNA
  • unique replication cycle:
  • reverse transcription
  • integration into host DNA
  • transmitted by sexual contact, blood transfusions, IV drugs
  • -signif cause of certain types of cancer
  • virus that causes AIDS