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Flashcards in Virology Deck (35):
1

WHat are the two Virus theries?

Evidence for the RNA world theory?

Evidence for Reductionist theory?

RNA world theory
--Life arose with viruses

Reductionist theory
--Viruses came after cellular life; they are reduced versions of cellular organisms


RNA world evidence: Ribozyme- self replicating RNA

Reductionist evidence: Viruses have genes related to those of cellular genes, often pick up cellular genes

2

What are ribozymes?

RNAs that can catalyze specific reactions (similar to enzymes)
-They can even catalyze their own synthesis

3

Natural funcitons of ribsozymes?
3

1. cleave RNA,
2. viral replication,
3. tRNA biosynthesis

4

DNA viruses start off how and end how?
3 Steps



Examples? 3

Start as DNA
then

Transcription to
RNA
then

Translation to
Protein

Ex: Herpes, Smallpox, Mimi

5

RNA viruses start off how and end how?
2 Steps

Examples? 3

Start as RNA
then

Translation
to
Protein

Examples: Rhino, influenza, SARS

6

Retroviruses start off how and end how?
4 Steps


Examples?1

Start as RNA
then

Reverse Transcription to
DNA
then

Transcription to RNA
then

Translation to
Protein

Examples: HIV

7

DNA viral genome Pros?
3

1. Lower mutation rate
2. More stable (can carry more genes)
3. No dsRNA phase

8

DNA viral genome cons?
2

1. Lower mutation rate
2. Slower replication

9

RNA viral genome pros?
2

1. Fast replication rate
2. High mutation rate

10

RNA viral genome cons?
3

1. High mutation rate
2. Limited sequence space (less stable)
3. dsRNA phase

11

Why is HIV so highly mutated even in one single infected body?

They are a retrovirus which means they have a reverse transcriptase step that is different from the orderof the central dogma. This step is also where all the mutations are occurring (1 mutation per virus).

12

What can’t HIV be cured by antiviral drugs?

It integrates into the cell (hides in it) so we cant get rid of it/recognize it

13

Challenges in developing vaccines?
7

1. High mutation rate
2. Integration into the host genome
3. Infects immune privileged region of host
4. Targets immune system
5. Multiple serotypes
6. Costs and time involved in development
7. Vaccine safety concerns

14

When do the earliest synmtpoms of HIV appear?

Earliest symptoms appear at two weeks (if at all)

15

HIV mutation rate is what?

~1 base change per genome

25-30% in circulating HIV strains diveristy

16

What are the most dangerous mutations in viruses?
2

-Some allow a competitive advantage
-Some allow escape from antiviral drugs

17

Which retroviral proteins would you design drugs to target?
4

1. integrase,
2. reverse transcriptase
3. Protease inhibitors
4. Fusion entry inhibitors

18

Describe the nucleotide analong mechanism?

Which drugs are these?
2

nucleoside analog mechanism (prevents adding onto the chain-chain terminator)
-because its so faster for the virus it mostly gets sucked by that instead of our own DNA

NRTI- purine and pyrimidine analogs

19

3TC (Epivir/lamivudine) drug group?

MOA?

Reverse transcriptase inhibitor
-Nucleoside analog
(NRTI)

Cytidine mimic – acts as a chain terminator

20

DLV (Rescriptor/delavirdine) drug group?

MOA?

Reverse transcriptase inhibitor (non-nucleoside)
NNRTI

Binds RT catalytic site, blocking polymerase function

21

DRV (darunavir/Prezista) drug group?

MOA?
2

Protease inhibitor

1. binds the active site preventing the processing of viral protein precursors
2. Compete with the natural substrate

22

EVG (Elvitegravir) drug group?

MOA?

Allosteric integrase inhibitor
INTI

Prevents functional multimers from forming (dimer of dimers = tetramer)

23

MVC (Selzentry/maraviroc) drug group?

MOA?

Entry inhibitor/ CCR5 antagonist

Drug binds receptor (CCR5), preventing HIV from binding
Mutant binds receptor in a different conformation

24

T20 (Fuzeon/entuvirtide) drug group?

MOA?

HIV fusion inhibitor

Mimics viral protein to displace it in the fusion complex– binds gp41 and prevents formation of the entry pore
(prevents the virus from fusing with healthy T cells)

25

Immune-base HIV therapies?
4

1. Therapeutic vaccines (DermaVir, Vacc-4x)
2. Gene therapy (Lexgenleucel-T, SB-728T)
3. Interleukin (IL-7, IL-2)-not indicated anymore
4. Chloroquine (Aralen, Plaquenil)

26

SB-728T gene therapy MOA?

What would the treatment process look like?

Modifies a CD4 T cell CCR5 receptor, making it non-functional
Prevents HIV entry
(only T cells affected and not all blood cells)

Harvest patient T-cells, make the mutation and replicate, put back into patient

27

What can be done to prevent escape mutants?

Multi-drug regime

28

Potential effects of viruses on human evolution
4

1. Immune system diversity
2. ABO blood system (decreased A allele frequency after smallpox epidemic)
3. Endogenous retroviruses (1% of genome)

4. Cell surface mutations (ex. CCR5)

29

In humans, ERVs (endogenous retroviruses) have been associated with:
5

Multiple sclerosis
Schizophrenia
Cancer
Autoimmune diseases
Amyotrophic lateral sclerosis (ALS)

30

Why do viruses start epidemics and then pandemics?
4

1. Increased virulence (severity of disease or ability to spread)

2. Introduction into a novel setting

3. Changes in host susceptibility to the infectious agent

4. Changes in host exposure to the infectious agent

31

Transmission modes for viruses?
6

Iatrogenic
Vertical transfer
Droplet transmission
Vector bourne
Fecal oral route
Sexual transmission

32

What is a characteristic of zoonosis viruses?

Often diseases are adapted to their host and more deadly when they jump hosts (ex. Ebola)

33

What kind of viruses are studied in BSL-4 Facilities?
2

1. Aerosol viruses

2. Severe/fatal viruses with no vaccines or other treatments
-Bolivian and Argentine hemorrhagic fevers
-Marburg virus
-Ebola virus
-Lassa virus
-Crimean-Congo hemorrhagic fever
-Small pox

34

Why is influenza so easily mutated?

influenza is a segmented genome so its great at recombination

35

Why is quicker, earlier HIV treatment essential?

quicker treatment = less viral load for the rest of your life because of less infected cells