Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Virology > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

How does the type of host influence the virus?

A

influences its viral replication and gene expression depending on whether its eukaryotic or prokaryotic

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

Where is eukaryotic genome located?

A

nucleus (nucleosomes chromatin, euchromatin)

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

eukaryotic genome encodes for proteins but a larger % does, what else does it code for?

A

RNA genes
regulatory regions
junk regions

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

where is the prokaryotic genome located?

A

cytoplasm

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

how does the prokaryotic and eukaryotic genome differ other than location?

A

pro lacks nucleosomes and is more compact

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

what does a virus need from its host?

A

1) replication of nucleic acids and viral particles (uses DNA rep. tools: DNA pol, primate, SSBPs ect.)
2) synthesis of viral proteins (transcription of viral genes to mRNA, translation of mRNA to proteins)
3) assembly and release of infectious viral particles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

function of topoisomerase:

A

relaxes super-coiled DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

function of DNA helicase:

A

unwinds double helix at replication fork

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

function of DNA primase:

A

provides starting point for DNA pol. to begin synthesis of new strand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

function of DNA polymerase:

A

synthesizes new DNA strand; also proofreads and corrects some errors

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

DNA ligase:

A

re-joins two DNA strands into double helix and joins Okaski fragments of lagging strand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

function of single-strand binding proteins (SSBP):

A

binds to separate DNA strands to keep them separated by holding them in place so each strand can be a template for new DNA synthesis

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

function of PCNA (proliferation cell nuclear antigen) sliding clamp:

A

protein complex that binds to DNA pol. and prevents the enzyme from dissociating from template DNA strand (processivity-promoting factor)

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

how does eukaryotic DNA replication get controlled, making it difficult from virus to get DNA replication done?

A
  • genome of eukaryotic. is only ever ds DNA linear
  • involves many enzymes and axhillary proteins (ability is affected by cell cycle)
  • occurs in nucleus so virus must be able to get in
  • DNA rep. is controlled by phase of cell cycle (only occurs in synthesis (S) phase)
  • if PCNA isn’t available DNA rep. apparatus doesn’t assemble properly so rep. doesn’t occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

prokaryotic DNA rep.:

A
  • ds circular or linear
  • occurs just before binary fission
  • diff. enzymes involved on rep. initiation than eukaryotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the challenges viruses face when trying to replicate in host?

A
  • euk and pro DNA rep. is under tight control
  • DNA pol does replicate ssDNA
  • Ori in euk. and pro. is diff and recognized by diff proteins (some proteins aren’t present until the cell is in DNA rep. mode)
  • cellular forms can’t rep. RNA b/c they don’t have an enzyme that makes RNA for an RNA template, virus has to bring own RNA pol.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is needed to initiate DNA replication?

A
  • proteins that recog. Ori
  • DNA template
  • DNA pol.
  • material to build DNA (nucleotides)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

in general, how can viruses replicate genome?

A
  • manipulate host cell cycle (especially if virus needs cellular enzymes like DNA pol. that’s only present during cellular DNA rep.)
  • have their own DNA pol and proteins to control viral DAN rep.
  • mechanisms/designs to ensure good genome rep.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does parvovirus do to rep. genome?

A

-uses host DNA rep. apparatus but infects young animals so cells are guaranteed to to be rep. therefore DNA rep. too

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

what do polyoma and papilloma virus do to rep. genome?

A
  • uses host DNA pol. but encodes own Ori binding proteins

- has proteins that interfere with or manipulates the host cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what do HSV, poxvirus and adenovirus so too rep. genome?

A

-encode their own DNA pol. and Ori binding proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are to features of the Ori?

A
  • AT rich

- recognition sequences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does linear viral DNA start rep.?

A
  • some pack better as linear but become circular automatically before rep.
  • other linear genomes have hairpin ends or terminal proteins at end that hold too strands together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

DNA pol. and primase don’t start lying nucleotides at the very end of the viral linear genome making the new template strand shorter, how is this problem solved?

A
  • some linear viral genomes become circular for rep. (ex. phage Lambda)
  • some linear genomes have hairpin ends
  • some have terminal proteins at their ends
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how do eukaryotic linear chromosomes rep.?

A
  • telomers (segments of junk DNA) are found at the end of each chr. segments
  • telomers are produced by telomerase that synthesizes DNA from internal RNA template
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how does Adenovirus rep. its linear DNA?

A
  • viral DNA has no room for junk to protect ends
  • uses terminal proteins that are covalently attached to 5” ends as primers
  • terminal proteins already have the first nucleotide in place
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does Parvovirus rep. its linear DNA?

A

-hairpin ends produce temporary ds DNA that gets modified its two ss molecules later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how do viruses effect prokaryotic hosts DNA rep.?

A
  • some degrade host DNA

- lysogeny: temperate phages integrate into the hosts chr. (pro-phage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how do viruses effect eukaryotic host DNA rep.?

A
  • apoptosis: incomplete degradation of host DNA
  • tumour formation: de-repression of host DNA rep.
  • pro-virus: integration of viral genome into host genome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how does gene expression of euk. and pro. differ?

A
  • promoter structure and recognition features
  • RNA pol.
  • transcription termination
  • mRNA features
  • mRNA translation initiation features
  • regulatory mechanisms for gene expression
  • gene organization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

features of euk. promoter?

A
  • promoter has TATA box
  • RNA pol II
  • transcription factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

features of pro. promoter?

A
  • prinow box, -35 and -10

- RNA pol holoenzyme made of two parts (sigma factor and core enzyme)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the three levels that regulation of gene expression is possible?

A
  • transcriptional level (no mRNA)
  • translational level (no protein)
  • post-translational level (no protein activity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how is the euk. transcription of heterochromatin regulated?

A
  • DNA methylation

- nonacetylate histone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how is the euk. transcription of euchromatin regulated?

A
  • acetylate histones

- genes can be transcribed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

features of euk. transcription:

A
  • occurs in nucleus
  • mRNA must move to cytoplasm
  • genes are split by axons (get expressed) and introns (removed during processing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

pre-mRNA to mRNA process:

A

modifications are made before exporting to cytoplasm:

  • 5’ cap of 7-methylguanosine added
  • removal of introns/ splicing together exons (by splicosomes: proteins and RNA molecule complex)
  • addition of 3’ poly-A-tail

cap and tail protect and signal its ready for transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how does alternative splicing allow one gene to code for more than one protein?

A

-exons are joined together in different ways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the three major types of euk. RNA pol?

A

RNA pol I: catalyzes rRNA synthesis
RNA pol II: catalyzes mRNA synthesis
RNA pol III: synthesizes tRNA molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how is transcription initiated in euk?

A
  • RNA pol II needs to be aligned properly
  • TFs bind to sequence motifs in DNA to help line up RNApol
  • RNA pol II is recruited to a promoter (includes upstream regulatory enhancers, upstream elements, and TATA box)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how is euk. transcription regulated?

A

euk. gene expression is regulated by proteins that interact with elements associated with promoter region (enhancers can stimulate or decrease rate of transcription pf a gene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what segments make up the euk. core promoter?

A

BRE: TFIIB-recognition element
TATA box: binding site for several transcription elements including RNA pol II
-Inr: initiator element
DPE: downstream promoter element

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how do enhancers work?

A

transcription factors bind to them to stimulate or decrease rate of transcription of the gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

steps of euk. transcription:

A
  1. TFIID binds to TATA
  2. other TATA binding factors and pol II form pre-initiation complex
  3. TFIIE and TFIIH bind to complex to stabilize initiation complex
  4. pol II moves along template and new mRNA strand is made 5’ to 3’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

components of the signal transduction cascade:

A
  • JAK: sensor kinase located in membrane
  • STAT: response regulator in cytoplasm
  • alpha interferon: outside of cell (JAK is cell surface receptor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

steps of the signal transduction pathway:

A
  1. alpha IFN binds to JAK, JAK autophosphorylates
  2. JAK passes on phosphate group to STAT
  3. STAT migrates to nucleus and activates transcription of genes involved in interferon response
    (helps cell defend itsself from virus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

features of bacterial RNA pol.:

A
  • doesn’t edit
  • doesn’t require a primer
  • uses DNA as template
  • made of two main components (core enzyme and sigma factor)
  • diff. sigma factors designed for diff. promoters
  • transcription termination signal is recognizer. on transcribed RNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

features of bacterial transcription:

A
  • transcription and translation are simultaneous
  • ribosomes start translating mRNA before its transcription is complete
  • mRNA doesn’t need processing
  • many mRNA encode for more than one protein (polycistronic/polygenomic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what makes up bacterial RNA pol?

A

-tetrameric core and sigma factor= holoenzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

how is the transcription of genes controlled in bacteria?

A
  • only genes recognized by specific sigma factors are translated (broad scale)
  • regulatory region on DNA (fine-tuning)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how does a repressor work?

A

binds to the operator and blocks RNA pol (ex. Lac operon repressor; a repressor of indictable genes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the regulatory regions on bacterial DNA?

A
  • promoter: recognizer. by sigma factors
  • operator: located after promoter, controlled by repressors
  • activator binding site: located before promoter, controlled by activators
  • repressors: prevents transcription
  • activators: stimulate transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how do euk. and bacterial translation initiation differ?

A
  • euk. has a 5’ cap

- bacteria has ribosome binding site called shine-dalgarno sequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what degrades ds RNA and what does it produce?

A
  • dicer

- produces siRNA and miRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is the function of siRNA?

A

-small interfering RNA interferes with expression of specific genes with comp. nucleotide sequence to regulate post-transcription

56
Q

what is the function of miRNA?

A

-regulates by binding to comp. sequence on target mRNA transcripts, results in translational repression or target degradation and gene silencing

57
Q

what was the first report of a virus and how was it described?

A
  • tobacco mosaic virus (tubular virus with DNA inside) by ivanovski and beijerinck
  • filterable agent that caused disease by multiplying in living ells and tissues
  • didnt fit Koch postulates
58
Q

what was the first discovered animal virus? human?

A
  • foot and mouth

- yellow fever

59
Q

what was the pasteur-chamberland filter?

A

-filter that could completely remove bacteria but not viruses (showed first distinctive viral characteristic)

60
Q

how was it demonstrated that viruses can attack bacteria too?

A

-d’Herelle developed use of plaques to estimate virus titer in suspension

61
Q

what is phage therapy?

A

-use of specific phages to treat bacterial infections (could be good for antibiotic resistance bacteria)

62
Q

how do phages replicate differently than bacteria

A
  • bacterial is exponential pop. growth

- virus is large pop. all at once: one step growth curve

63
Q

what was the phage school?

A
  • first training place for molecular biologists

- located in cold spring harbour

64
Q

how did EM development improve our virus knowledge in 1930’s?

A

-alllowed us to visualize the virus and get info on its structure (TMV was used)

65
Q

how did study of bacteriophages help us establish field of molecular biology?

A
  • mapped phage genes
  • elucidated phage rep. cycles
  • plaque assay
  • study of DNA rep. processes
  • study of transcription and translation
  • study of gene expression regulation
66
Q

what are some of the cellular process that were understood as a result of studying viruses?

A
  • DNA carries inherited genetic info (Hersey and Chase)
  • identification of promoters for euk. RNA pol.
  • enzymes involved in euk. cells
  • isolation of numerous cellular oncogenes (understanding that cancer is caused by their mutation/ unregulated expression)
67
Q

what do viruses lack that cellular forms have?

A
  • enzymes to produce basic components
  • enzymes to generate energy
  • ribosomes and other elements needed in protein synthesis
  • organelles and cell membranes
68
Q

what effects do viruses have on their host?

A
  • takes over hosts cell
  • host metabolism redirects to viral rep. only
  • host cell normal function is compromised
  • disease may occur
69
Q

what two things must the viral genome do in order to rep.?

A
  • direct host cell to replicate virus

- serve as template to make copies of itself for viral progeny

70
Q

how are viruses important in the biosphere?

A

-play a role in regulating release of nutrients to sustain aquatic community and maybe weather

71
Q

how could viruses affect the weather?

A

lysis of algae by a virus causes release of DMSP that gets cleaved and produces dimethyl sulphide

  • the dimethyl sulphide is oxidized into atmosphere and turned into tropospheric sulphate aerosols
  • these can act as cloud condensation nuclei and attract molecules of water
  • forming clouds
72
Q

how do viruses get into their hosts?

A
  • viruses have specific hosts because they connect to specific receptors on surface of host cell
  • key: viral anti-receptor, lock: cell receptor
73
Q

what is hemagglutination?

A
  • rapid and quantitative assay for some viruses
  • depends on ability of virus to bind to silica acid or other carbohydrate found on the surface of erythrocytes
  • cloudy tube is positive test b/c virus is bound to cells
74
Q

what are the steps of viral rep. cycle?

A
  1. the virus binds to the cell receptor
  2. entry and uncoating
  3. early gene expression
  4. early viral proteins direct rep. of viral genome
  5. late mRNA are made from newly rep. genome
  6. late viral proteins package viral genomes and assemble visions
  7. progeny visions are released from host cell
75
Q

what is the template, product, and name of DdDp?

A
  • template: DNA
  • product: DNA
  • DNA pol used to rep. DNA
76
Q

what is the template, product, and name of DdRp?

A
  • template: DNA
  • product: RNA
  • RNA pol. used to transcribe DNA into RNA
77
Q

what is the template, product, and name of RdRp?

A
  • template: RNA
  • product: RNA
  • viral RNA replicase transcriptase
78
Q

what is the template, product, and name of RdDp?

A
  • template: RNA
  • product: DNA
  • reverse transcriptase
79
Q

how does the Baltimore classification of viruses work?

A

-classifies viruses based of the genome and the first molecule event that takes place with them upon infection

80
Q

what is the Baltimore classification of DNA?

A
  • transcription, needs genes to be expressed

- product: viral mRNA

81
Q

what is the Baltimore classification of RNA-?

A

transcription (from own RNA transcriptase)

-product: viral mRNA

82
Q

what is the Baltimore classification of RNA+?

A

translation of whole or part of viral genome (b/c it looks like the mRNA of host already)
-product: viral proteins

83
Q

what is the Baltimore classification of RNA (reverse transcription)?

A

reverse transcription of viral RNA

-product: ds DNA (goes into the genome of the infected cell)

84
Q

what is the difference between extracellular viruses and intracellular viruses?

A
  • extra: inactive, no metabolism, not undergoing rep., infectious
  • intra: virus particles/virions
85
Q

what are the taxon-specific suffixes of viruses?

A
  • order: virales
  • family: viridae
  • sub-family: virinae
  • genus: virus

all in italics

86
Q

what are the structures of a virus?

A
  • genome, protein coat (capsid), some have envelope

- nucleocapsid: genome + capsid

87
Q

what is the size range of a virus?

A
  • from 20 nm to 300 nm
88
Q

what are the two types of symmetry a viral capsid can have?

A
  • helical (rod shaped)

- icosahedral (spherical)

89
Q

how does a virus acquire an envelope?

A

-by budding from hosts membrane, the proteins found in the membrane though are encoded by the virus

90
Q

what is the definition of a disease?

A

-deviation from norm structure or function of any part of the body that affects the performance of vital functions and it usually manifests by diagnostic symptoms

91
Q

infection definition:

A

-invasion of host by microorganism resulting in the establishment and multiplication of agent

92
Q

pathogenesis definition:

A

-capability of causing disease

93
Q

virulence definition:

A

-degree of intensity of pathogenicity of an organism as indicated by fatality rates and/or ability to invade host tissues and cause disease

94
Q

definition of immunity:

A

overall general ability of a host to resist disease

95
Q

definition of immunologically naive individual:

A

-immune system has not been exposed to an agent capable of causing an immune response

96
Q

definition of herd immunity:

A

immunity that is spread in a population and prevents the establishment and spread of the infection agent

97
Q

definition of vaccination:

A

-induction of a protective immune response controlled by exposure of the individual to the antigen

98
Q

definition of epidemiology:

A

-study of factors determining the frequency and distribution of a disease caused by a pathogenic organism

99
Q

definition of epizoology:

A

study of factors determining the frequency and distribution of a disease within an animal pop.

100
Q

what factors can affect the grade of virulence and pathogenicity of a virus?

A
  • genetic ability of virus to propagate in its infected host

- physiological response of host to these factors

101
Q

how have humans had an impact on viral diseases?

A
  • human pop. into wild areas exposes to new viruses
  • social and cultural factors (sexual practice, intravenous drug use, crowded poor living conditions) allow opportunity to easily infection specific groups
  • technological advances (travelling through the globe) viruses can spread all over the world
  • economical factors (cost of medication)
102
Q

how did the AIDS EPIDEMIC spread all around the world?

A
  • originated from monkeys
  • deforestation
  • set up of mining and forestry camps with poor conditions
  • unprotected sex
  • efficient transport
  • use of blood and blood products in medicine
103
Q

what is an interferon?

A

cellular antiviral response specific to viral infection

104
Q

what is a vector?

A

organism that doesn’t necessarily suffer the disease but passes the virus from one host to another (acts as a vehicle)

105
Q

what is an arbovirus?

A

-general term indicating viruses transmitted by arthropod vectors

106
Q

what is a reservoir pop?

A

group of individuals (speeches or pop) where a particular virus is present and circulating (anyplace where the virus is maintained)

107
Q

what has the impact of viruses been on humans in the past?

A
  • used as biological weapons (small pox)
  • influenza pandemics killed millions (Spanish flu)
  • agriculture (could wipe out several seasons of food)
108
Q

what are the hypotheses of virus origin?

A
  • viral forms may have evolved parallel to cellular forms
  • viruses de-evolved from cellular forms
  • retro-transposons may have give origin to some
109
Q

what self-replicating pathogens are smaller than viruses? 🦠

A
  • defective virus particles
  • viroids
  • prions
110
Q

what is the first line of defence against a virus

A

-cellular

111
Q

what are the two types of responses vertebrates have to a virus?

A
  1. host immune response

2. intrinsic cellular response (rapid pathogen recognition)

112
Q

how are pathogens recognized by the host cell?

A

-by detecting microbial molecular features that are different from their own (MAMPs: microbe associated microbial patterns recognized by PRRs: pattern recognition receptors)

113
Q

what are the steps of detection and response that the host goes through?

A
  1. PRRs bind to viral component
  2. the detection triggers a signal transduction cascade
  3. many molecules produced are inflammatory mediators that coordinate elimination of pathogen and infected cells
    (cytokines that communicate to other cells, interferon-stimulated genes that tell other cells of the virus so they can prepare)
114
Q

what does an interferon need to be activated?

A

NF-kappa beta and IRF-3/IRF-7

115
Q

what does a cytokine need to be activated?

A

NF-kappa beta

116
Q

what is the order, family, and genus of HSV-1?

A

order: Herpesvirales
family: Herpesviridae
genus: simplexvirus

117
Q

what does HSV-1 genome look like?

A

-linear, ds DNA (120-230 kilobase pairs)

118
Q

what is unique about the DNA of HSV-1?

A

-it has 2 unique sequences called UL and US on the long and short segments respectively and are held together by inverted repeats

119
Q

how bid is the diameter of HSV-1’s envelope?

A

-200nm

120
Q

what is the shape of HSV-1’s capsid?

A

-T=16 icosahedral (spherical) capsid

121
Q

why can HSV-1 structure be considered complex?

A

-includes a tegument that makes up the space between the capsid and the envelope that contains many of its important proteins

122
Q

how many ORF’s are found in the genome of HSV?

A

84, most found in the UL and US sequences

123
Q

what does ICP4 do in HSV?

A

important in viral rep. as a transcriptional activator

124
Q

what does ICP0 do in HSV?

A

-degrades ND10 and inhibits IFN-gamma signals (both host defences)

125
Q

what is the function of the LAT region for HSV?

A

-needed for virus to reactivate after latency

126
Q

what is the function of gamma ICP34.5 in HSV?

A

-fights against hosts response after DNA synthesis

127
Q

other than humans, what are the hosts for HSV?

A

-mammals, birds, reptiles, fish, frogs, and bivalves

128
Q

how is HSV-1 most commonly spread?

A

-oral-to-oral contact

129
Q

what issues are caused by HSV in humans?

A
  • when the virus is replicating its DNA in the epithelial cells, its killing them creating lesions on the skin of the host
  • brain or eye infection
130
Q

where does HSV become latent?

A

-in the neuronal cell body

131
Q

what are some medications that lessen the effects of HSV?

A

acyclovir, famciclovir, and valacyclovir

132
Q

how does HSV enter host cells?

A
  • attaching to mucosal epithelial cells by glycoprotein receptors gB and gC that bind to hosts heparan sulphate proteoglycans
  • then gD on virions envelope binds to pectin 1 receptor
133
Q

how does HSV vision get to the nucleus of the cell?

A

-dyenein motors

134
Q

how does viral rep. occur for HSV?

A
  1. DNA get circularized and uses host’s RNA pol II
  2. alpha genes are encoded first that regulate expression of other genes
  3. beta genes are transcribed next and allow viral DNA to replicate by coding for DNA pol.
  4. DNA rep. occurs by a rolling circle mechanism that produces concatemers
    - gamma genes are transcribed which code for structural proteins and capsid assembly
135
Q

how does HSV acquire an envelope?

A

-by budding from host cell membrane

136
Q

how does HSV leave the cell?

A

-exocytosis machismo of host (vesicle pathway)

137
Q

how does HSV achieve latency?

A

-virions infect nerve-endings and travel to axonal termini of sensory neutrons then to sensory ganglia by retrograde axonal transport

Virology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions