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week 1 Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

Microbes big to small

A
  • Helminth
  • Protozoa - ekaryotes
  • Fungi
  • Bacteria
  • Virus
  • Prions – smaller than virus, misfolded proteins
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2
Q

Are all microbes pathogenic

A

no, most are not

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3
Q

Classification virusses

A
  • Type of genome
  • Symmetry of the particle
  • Envelope – part of host membrane with proteins sticking out. Is worse fort he virus
  • Segmented genome
    Virus kenmerken
  • No separate kingdom for virusses, did not descend from single prehistoric virus
  • Smallest and most abundend in biosphere
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4
Q

Virome

A

all virusses in the body or certain organ. Detection by deep sequencing

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5
Q

How many bacteria in the body, where are they found

A

Ten times more bacterial cells than normal cells in body – mostly in skin and gut. Mostly Harmless

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6
Q

Zoonoses

A

infections transmitted directly from animals to humans. By uncooked animal products (nematodes, helminths), contact through grooming, petting, bites, scratches, contact urine or faeces, sometimes through vector

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7
Q

Novel zoonoses

A

ongoing increase hman and livestock, decline in natural habitat wild animals, daarom more vulnerable to pathogens transmitted by animals, during contact with domesticated or wild

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8
Q

One health

A

human and animal diseases should not bes een as seperate entities. Toxoplasma, corona etc came all from animals

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9
Q

Spread zoonoses

A

by birds, planes, insects mostly. Also through insect vector or climate change.

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10
Q

Emerging disease

A

appear in a population for the first time, or that may have existed previously but are rapidly increasing

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11
Q

Viromics

A

Technique to find new virusses, sequencing all nucleid acids using next generation sequencing. First enriched for virusses

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12
Q

Conditions viromics

A

low host/bacteria DNA and RNA (filter by size selection or DNase), sequence all virusses, high sensitivity/efficiency

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13
Q

VIDISCA scheme

A
  • size selection – virusses are small, will stay behind, big cells with the pellet
  • DNase – removes free DNA
  • Purification
  • DNA polymerase – create ds DNA (als RNA dan eerst DNA maken, dan dsDNA)
  • Add restriction enzymes that digests every virus; MSE 1 recognizes TTAA, virusses are TA rich
  • Size selection with attachment beads
  • Ligation to anchor (piece of DNA of which you know the sequence) with TTAT
  • Primers
  • PCR
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14
Q

Emulsion PCR

A

small beads with capture probe, grab sequences on primers. Exactly how much DNA is created is known, and exactly how many beads. Beads to DNA ratio is 10:1. oil suspension, water surrounding beads and DNA. This can be amplified using PCR

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15
Q

Why VIDISCA instead of illumina

A
  • Illumina uses clonal amplificaiton on chip with colony formation, using capture probes. Colored nucleotides are added. Those are then sequenced.
  • Nadeel; if all colonies adapt an A, then the machine cannot distinguish anymore, error will occur. Only works great if the product has not the same nucleotide. TTAT sequence after ligation will cause an error
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16
Q

Koch postulates

A
  • Microorganisms must be found in abundance in all organisms suffering from disease , but not in healthy (association of disease)
  • Microorganism must be isolated from diseased and grow in pure culture (culture)
  • The cultured microorganisms should cause disease when introduced into healhy (model)
  • The organism should be re-isolated from the experimentally infected subject
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17
Q

Woodlouse (kakkerlak) turns insects blue why

A

because of the capsule of the virus. Birds eat it, spread

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18
Q

Scale drop virus

A

causes erosion fins, scale loss, pertruding eyes in fish

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19
Q

Vaccine protection

A

protected against infection or disease?

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20
Q

How does immunity by vaccination work –

A

innate DC take up antigen, to lymph node, interaction MHC CD4/8, B cells proliferation, Ab production and memory cells. Memory b cells go to the bone marrow

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21
Q

Sterilizing immunity

A

virus will not enter body, not establish infection.

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22
Q

Do vaccines give sterilizing immunity

A

no, not all vaccines protect against infection. vaccines protect against disease through immune memory. First peak after 2 weeks, second peak uses b and t cells after activation, takes longer

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23
Q

Types of vaccines

A
  • Life attenuated – can infect and replicate, but wont make as sick as usual
  • Killed whole organism – immune sees everything, but cannot replicate
  • Toxoid – only for bacteria, wont get sick
  • Little bit of virus that you need
  • Virus like particles – will not give any disease
  • outer membrane vessicle
  • protein polysachharide conjugate
  • viral vectored
  • nucleic acid
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24
Q

Recombinant viral vectors vaccine werking–

A

pox, adeno, CMV. Capsid or embril (lipid membrane) with genetic material inside, cell will describe genetic material, will be pesented on mhc. Virus within virus

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25
Q

mNRA vaccine werking

A

bilipid layer particle with genetic material

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26
Q

how covid 19 vaccine could be produced in less than a year

A
  • production and trials at faster speed; normally test in animal models, clinical trials, production and selling. With sars cov clinical phase was shorter because of sars, phase 1,2,3 at the same time and production started already, afterwards approved.
  • Learnt lessons from other viruses; spike proteins attach to receptors, fusion proteins have pre fusion and post fusion state. Ab herkennen vaak post fusion state. Stabilization of pre fusion proteins by breaking a helix with prolines. Covid19 is not unique, same spikes, fusion proteins etc
  • Newer and quicker antgen delivery, rna and viral vector
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27
Q

Mutation antigenic drift

A

small mutations

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28
Q

Antigenic shift

A

new stain by mixing strains from different species

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29
Q

Mpox basics

A
  • dsDNA
  • relatively large genome
  • contains several viruses known to be pathogenic to humans; variola, cow pox, vaccinia, mpox
  • normal host is small rodents
  • stable 1-2 mutations per year
  • mpox has a central conserved genome with varying ends
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30
Q

first outbreak in NL mpox

A

started with reading literature, similar symptoms, it’s still spread throughout Africa

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31
Q

mpox in the 80s

A
  • smallpox vaccination reduced household transmission
  • mostly children
  • mortality unvaccinated 11,3%
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32
Q

mpox in America in 2003

A
  • linked to import rodents ghana that infected prairie dogs (ground squirrels) and humans
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33
Q

mpox in amsterdam

A
  • at the same time as us
34
Q

clinical findings mpox prior to 2022

A
  • papules and ulcers
  • limited human to human
  • zoonotic
  • no sexual transmission
  • No anogenital lesions reported until 2017 in Nigeria
  • monomorphic
  • mortality 1-10%
  • children and woman
35
Q

What we have learned from smallpox vaccination

A
  • First/second generation; live attenuated vaccinia virus (form cow skin)
  • Third generation vaccination; modified vaccinia virus MVA replication incompetent
36
Q

After 2022 clinical findings mpox

A
  • Sexually transmitted
  • More polymorphic clinical phase (different phase of skin lesions; wounds, pustules)
  • 99% men, 94% msm, 21% hiv+
37
Q

Vaccination against mpox

A
  • First generation smallpox vaccines – 85% reduction of SAR
  • Experiences with MVA vaccine mpox outbreak 2022 – ex vivo Ab titers and neutralization of MPXV
    -58% mpox serious cases
38
Q

smallpox vaccination generations

A
  • First/second generation: live attenuated
    vaccinia virus (cel culture from cow skin)
  • Third generation: modified vaccinia virus (MVA)
    replication incompetent
39
Q

Tiled amplification based design

A

2 pools together with 88 amplicons, parts can be sequenced. For low genome copy numbers and most reads are on target, reducing background noise.
Sequencing is used for mapping of cases, see where infection came from

40
Q

how do most emerging pathogens emerge

A

zoonotic

41
Q

Factors to consider

A
  • Host proteins or structures needed for virus relication
  • Host immune defences should be circumvented or downregulated
42
Q

What we can learn from emerging viral diseases

A
  • New; adaptation processes should be obvious at molecular leel
  • Compare virus infection and replication in different host systems
  • Analyse mutations in viral genomes
43
Q

Evolving and adapting how to analyse –

A

positive selection? Nucleotide sequence comparison, dN/dS ratio

44
Q

Ebola EBOV why emerging

A

humans

45
Q

Dengue DENV why emerging

A

climate factors/human/addictional insect (a albopictus)

46
Q

Chikungunya CHICKV why emerging

A

increased novel insect (aedes albopictus)

47
Q

Ebola

A
  • Envelope
  • -ssRNA (antisense, non coding)
  • Filoviridae
  • Filovirus
  • Genome
  • Found in bats, humans, monkeys, shrews and duikers, guinea pigs in lab, mice need adaptation (infected baby mice – finetuning virus, infect other mice with this strain)
  • Macrophage, Kupffer, DC infected, travel to lymphe node, liver and spleen, rest of body
  • Also sexually transmittable (reservoir)
48
Q

How ebola infects same cells in different mammels

A

mimic ligands.

49
Q

Filoviral entry

A

gps on virions interact with attachment factors, taken up by micropinocytosis

50
Q

Controleren of ebola muteert

A
  • Infecteren baby mice met ebola, grown up, infected and ill, isolate again and sequence (or infect adult mice and sequence)
  • Sequencen mensen – mutatie in mensen die later geinfecteerd zijn. Beter in infecteren dan toen het nog leek op bat ebola
51
Q

Arbo virus survival

A

RNAi
antimicrobial pathways
dicer expression
Human innate immunity enhances virus infection after bite! Use very general receptors

52
Q

dengue

A

Enveloped (+)ssRNA virus, flavivirus
well adapted
no receptor, binds many receptors

53
Q

chikungunya

A

Enveloped (+)ssRNA virus family Togaviridae: Alphavirus,

54
Q

why is translation challenging in CHIKV –

A

pattern of nucleotides, degenerate (multiple codes for same amino acid). How does organism select right codon. Interplay of codon usage between virus and host. Some are preferred over others. Virus can not produce proteins properly in host

55
Q

hiv1

A

A-rich genome with codon use very different from
humans
* HIV infection alters the tRNA pool in infected cells
* Low abundant tRNA’s with anticodons for rare human
codons are present at higher levels at later stages of
infection
* Codon usage of HIV-1 early genes is similar to that of
highly expressed host genes, but codon usage of HIV-1
late genes was better adapted to the selectively
enriched tRNA pool

56
Q

why do virusses not adapt their nucleotide composition

A

Reduction of CpG dinucleotides in RNA genomes could, for
instance, avoid recognition by ZAP, a molecule of the
innate immune system
But:
 Nt composition could be important for packaging of viral
genomes, to set them apart from human mRNA
 Suboptimal translation might be a regulatory mechanism
 Activation of innate immunity could be beneficial, since
many viruses use immune pathways or activated
immune cells for infection

57
Q

Pegivirus

A

hepatitis G only

58
Q

Replication HCV

A

Replicates via RNA dependent RNA polymerase without proofreading, high genetic diversity

59
Q

Egypt shift in disease

A
  • from schistosomiasis to hcv by treatment schistosomiasis with unsterile needles
    presence hcv also endemic due to traditional practices
60
Q

Outcome hcv

A
  • Acute infection is mild/asymptomatic
  • 20/25% infection is resolved
  • 755-80% chronic infection with cirrhosis, carcinoma (HCC)
61
Q

Chronic hepatitis C treatment goal and outcomes

A
  • Goal is sustained virological response (without breakthrough or relapse)
  • Unclear if infection is really cleared when levels are below detection level, because breakthrough (during therapy) or relapse (after therapy) is possible
  • Non response is worse
62
Q

Chronic hepatitis C treatment medicine

A
  • IFNalpha/pegIFN – around 6% sustained virological response, lots of side effects
  • Ribavirin (guanoside analogue) – bit more effective, blocking RNA synthesis
  • Direct acting antivirals DAA that target protease/polymerase. Extremely expensive
63
Q

DAA (direct acting antivirals)

A

direct acting antivirals that target viral proteins block action. Very effective but resistance, therefore combination necessary, very epensive

64
Q

HTA (host targeting agents)

A

parts of the host cell that are needed for virus can be blocked.

65
Q

Benefits of HTA;

A

not variable and thus very conserved, broad pan genotypic antiviral activity, high barrier to resistance, might act in synergistic manner with DAAs and shorten therapy.

66
Q

Viral escape DAA vs HTA

A
  • DAA AANVULLEN
  • HTA – block cellular vectors. Most viruses much more sensitive to these agents
67
Q

miRNA122

A

liver specific. For differentiation, cholesterol, fatty acid, tumor suppressor, host factor for HCV. Promotes HCV RNA stability, protects RNA from exoribonuclease

68
Q

RG101

A

inhibitor miR122. Preventing binding HCV, prevent replication. Treatment, majority has rebound tho – 5 RACE PCR (primer, poly C tail, poly G tail weer andere kant op afschrijven) revealed mutation miRNA binding site

69
Q

HBV how infectious

A

50-100x more infectious than HIV. Sexually and vertically transmitted

70
Q

HBV genome

A

smallest of all viruses. Circular with overlapping reading frames, alternative start codons and splicing and folding of proteins. E antigen – proteolytic cleavage and altered conformation of core protein

71
Q

HBV forms cccDNA –

A

very stable DNA that stays in the nucleus and acts like an extra chromosome

72
Q

HBV disease outcome

A
  • 95% clears infection. Cytotoxic T clears
  • 5% chronic, swelling of the liver. However 95% infants will have chronic infection.
73
Q

Chronic HBV viral load etc

A

high viral load, detectable, no liver damage (normal ALT)

74
Q

Immune active phase HBV

A

HBV specific T cells kill infected liver cells resulting in liver damage

75
Q

Low replicative phase HBV

A

loss of HBeAg, presence of anti HBeAb
will eventually lead to tumors and death

76
Q

Chronic hbv treatment

A
  • Interferon – will suppress, a lot of side effects
  • Nucleoside analogue – interfere with polymerase (reverse transcriptase). Suppress de novo virus and cccDNA. But you will have to take medication for life
77
Q

Nucleoside analogue how it works

A

for hbv
translation blocked

78
Q

HBx protein of HBV identification –

A

accessory protein, function unknown. First identify transcriptional restrict ion factor degraded by hbx. But unstable, degrades target after binding. Fusion protein hbx will bind but not degrade. Hbx induces degration of talin1. Hbx inhibitor can stop transcription hbv

79
Q

Transcription assay hbx

A

One plasmid with luciferase and hpv promotor in front and another plasmid with hbx. More hbx more luciferase, more transcription

80
Q

how to determine point of introduction of a pathogen

A

Cohort study can be set up to investigate

81
Q

Virus specific factors

A
  • Virus replication in two mammalian species or bird/mammal or insect/mammal/bird
  • Immune systems to counteract
  • Receptors or uptake mechanisms to infect
  • Host proteins to replicate
  • Codon usage for gene expression efficiency
  • Body temperature for enzyme kinetics

advanced medical microbiology (4 decks)

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