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Infectious Disease > Virology > Flashcards

Virology Flashcards

1
Q

2 theories of how viruses fit into the tree of life?

A
  1. RNA world theory: life arose with the viruses
  2. Reductionist theory: viruses came after cellular life, they are reduced versions of cellular organisms
    * mimiviruses and megaviruses may be the missing link
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2
Q

What are Ribozymes?

A
  • RNAs that can catalyze specific reactions (similar to enzymes)
  • ribozymes (produced in lab) can catalyze their own synthesis
  • natural fans: cleave RNA, viral replication, tRNA biosynthesis
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3
Q

Examples of DNA viruses?

A
  • herpes, smallpox, mimivirus

DNA -> RNA -> protein

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4
Q

Examples of RNA viruses?

A
  • Rhino, influenza, SARS

RNA-> protein

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5
Q

Examples of Retroviruses?

A
  • HIV

RNA -> DNA (through reverse transcriptase) -> RNA -> protein

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6
Q

Pros and cons of a DNA virus

A

pros: lower mutation rate, more stable (can carry more genes), no dsRNA phase
cons: lower mutation rate, slower replication

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7
Q

Pros and cons of RNA virus

A

pros: fast replication rate, high mutation rate
cons: high mutation rate, limited sequence space (less stable), dsRNA phase, degrades faster, humans don’t have dsRNA (easy to identify)

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8
Q

What happens frequently in reverse transcriptase?

A
  • 1 mutation per virus, much more common in retrovirus
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9
Q

What are some challenges in developing HIV vaccines?

A
  • high mutation rate
  • integration into host genome
  • infects immune privileged region of host
  • targets immune system
  • multiple serotypes
  • costs and time involved in development
  • vaccine safety concerns
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10
Q

What is the diversity in HIV strains

A
  • 25-30% in circulating HIV strains

- mutation rate is - 1 base change per genome

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11
Q

What effects can a mutation have on a virus?

A
  • not all mutations are advantageous: some hinder the virus, some prevent virus replication, and some are silent ( have no effect)
  • Some allow a competitive advantage, and some allow escape from antiviral drugs
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12
Q

antiretroviral drug classes

A
  • reverse transcriptase inhibitors (NRTIs)
  • Fusion/entry inhibitors
  • Integrase inhibitors
  • Protease inhibitors
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13
Q

Difference b/t nucleosides and nucleotides?

A
  • nucleosides: sugar+ base
    3 phosphorylation events required for activity

-nucleotide: sugar+base+phosphate, 2 phosphorylation events required for activity

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14
Q

Nucleoside analogs??

A

prevent adding of next nucleoside on to the chain looks like nucleoside but doesn’t have site to bind to next nucleoside so it is a chain terminator

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15
Q

3TC (Epivir/Iamivudine)

A
  • FDA approved 1995
  • reverse transcriptase inhibitor
  • nucleoside analog: mimics cytidine -> acts as a chain terminator
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16
Q

DLV (Rescriptor/delavirdine)

A
  • FDA approved 1997
  • Reverse transcriptase inhibitor (non-nucleoside)
  • binds RT catalytic site, blocking polymerase fxn
17
Q

Reverse transcriptase mutations?

A
  • only takes 1 or 2 mutations of virus to make reverse transcriptase drugs ineffective
18
Q

DRV (darunavir/Prezista)

A
  • FDA approved 2006
    protease inhibitor: binds the active site preventing the processing of viral protein precursors
  • compete with the natural substrate
19
Q

EVG (Elvitegravir)

A
  • FDA approved 2014

- Allosteric integrase inhibitor (prevents functional multimers from forming (dimers of dimers= tetramer)

20
Q

MVC (Selzentry/maraviroc)

A
  • FDA approved 2007
  • entry inhibitor (receptor antagonist)
    drug binds receptor (CCR5), preventing HIV from binding
  • mutant bind receptor in a different conformation
21
Q

T20 (Fuzeon/entuvirtide)

A
  • FDA approved 2003
  • HIV fusion inhibitor
  • mimics viral protein to displace it in the fusion complex (binds p41 and prevents formation of the entry pore)
22
Q

Vacc-4x

A

therapeutic vaccine
in clinical trials 9phase 2)
peptide vaccine -> dropped viral load but didn’t slow CD4 T cell decline

23
Q

SB-728T gene therapy

A

in phase 1/2 trials
modifies a CD4 T cell CCR5 receptor, making it non-functional, prevents HIV entry
- harvest patient T cells, make mutation and replicate, and put back into pt
- this mutation occurs naturally and confers HIV resistance
- expensive and time consuming

24
Q

Interleukin

A

IL-7: trial abandoned b/c IL-7 increased the number of CD4+ T cells but that increased viral load too

IL-2: increased number of CD4+ T cells but didn’t significantly decrease clinical events or death, even when combined with antiretrovirals

25
Q

Chloroquine

A
  • antimalarial
  • drops pH in vacuoles
  • disrupts Env protein gp120, inhibits maturation
  • drops viral load, doesn’t affect T cells so doesn’t stop T cells from decreasing
26
Q

What can be done to prevent escape mutants?

A 
- combo drugs
Atripla (3)
Complera (4)
Stribild (4)
Triumeq (3)
Combivir (4)
27
Q

Difference b/t viral and human evolution

A
  • humans: complicated, multiple polymerases, error prone, and non-error prone sites, at most 1 mistake/ 100 million, proofreading and correcting machinery, and we only have a couple kids in a lifetime
  • viruses: often 1 mistake per genome, no proofreading, often whole populations knocked out, billions of genomes made per day
28
Q

Potential effects of viruses on human evolution

A
  • immune system diversity
  • ABO blood system (decreased A allele frequency after smallpox epidemic)
  • endogenous retroviruses (1% of genome)
  • cell surface mutations (ex: CCR5)
29
Q

What does it mean that viruses are a part of us?

A
  • they are a part of our regulation of host gene expression
  • they take part in placental formation
  • reason why there is immunosuppression during pregnancy
  • promoters, enhancers and proteins can be coopted by the host for its own purposes (placenta formation)
  • can be fixed or mobile, and no human endogenous retroviruses (ERVs) are capable of replication
30
Q

What are endogenous retroviruses (ERVs) associated with in humans?

A
  • MS
  • schizophrenia
  • cancer
  • autoimmune diseases
  • amayotrophic lateral sclerosis (ALS)
31
Q

Mutation in humans that allow them to be resistant to HIV infection?

A

-mutation prevents an HIV corrector from being made by the cell, and therefore HIV can’t infect people with this mutation (CCR5 delta 32 mutation) -> positive selection for this mutation

32
Q

Hypothesis for why mutation has been selected in specific regions (Europe, Asia, North Africa)?

A
  • either plague (bacteria) or smallpox (virus)
33
Q

How can humans drive viral evolution?

A
  • each infection is a population
  • zoonosis: virus mutating to be able to pass from one species to another
  • humans as an enviro: immune system and viral recombination
  • antiviral drugs: promote resistance and mutations
34
Q

difference b/t epidemic and pandemic?

A
  • epidemic: greater than expected incidence “outbreak”
    ex: SARS, Dengue
  • pandemic: spread over a large geographical area (b/t continents) ex: HIV, smallpox, H1N1 (seasonal flu not a pandemic)
35
Q

Why do viruses start epidemics and then pandemics?

A
  • increased virulence (severity of disease or ability to spread)
  • intro into novel setting
  • changes in host susceptibility to the infectious agent
  • changes in host exposure to the infectious agent
36
Q

Transmission modes of viruses?

A
  • iatrogenic (blood transfusion)
  • vertical
  • vector borne
  • droplet
  • fecal-oral
  • sexually
37
Q

Zoonosis?

A
  • disease that can pass from another species to humans or humans to another species
  • often diseases are adapted to their host and more deadly when they jump hosts (ex: Ebola)
  • Many viruses can pass from animal reservoir to humans, but have difficulties transmitting human to human
  • issues: domestication, deforestation, bush meat
38
Q

BSL-4 viruses

A
  • aerosol viruses
  • severe/fatal viruses w/ no vaccines or other txs:
  • bolivian and argentine hemorrhagic fevers
  • marburg virus
  • ebola virus
  • lassa virus
  • crimean-congo hemorrhagic fever
  • small pox

Infectious Disease (27 decks)

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