exam 1 Flashcards
What is penetration by fusion
Attachment has envelope associated with plasma membrane of the host. plasma membrane fuses to lipid envelope
2 types of penetration for enveloped viruses
entry via endosomes, fusion with plasma membrane
what is entry via endosomes
particle brought in via endocytosis
acidification to allow for fusion in entry via endosomes is created by
proton pumping
how does influenza penetrate cell
gets inside with receptor mediated endocytosis. all 8 segments of genome go striaght into the cytoplasm. endosome gets close to nuclear pore, uncoats
from a one step growth curve where protein comes up first, what type of virus is that
positive sense because the rna virus genome can be read into proteins since it looks the same as our rna
how long is the infectious cycle of polio (picornavirus)
8 hours
how long is infectious cycle of herpes virus
> 40 hours
describe what type of virus polio is
+ ssRNA
name the 8 basic steps of the infectious cycle
attachment/adsorption, penetration, uncoating, replication, genome expression, assembly, release
what is adsorption
virus develops an attachment protein that can bind to the cell receptor
tropism
ability of a virus to replicate in particular cells or tissues
what two factors control tropism
- how the virus gained entry 2. interaction of a virus attachment protein with a specific cell receptor molecule
true or false, adsorption is temperature and energy independent
true
what is the cell receptor for poliovirus
ICAM-1
why is influenza called a recycling virus
it detaches from the cell in a hydrolysis reaction which allows it to leave the cell
what are the HIV attachment proteins
gp 120 and gp 41
how is adsorption different from penetration
penetration is energy dependent
how does HIV penetrate cell
fusion with the plasma membrane
how do naked viruses usually penetrate the cell
receptor mediated endocytosis and membrane pore formation
how does polio penetrate the cell
pore formation. vp1 interacts with cell receptor, when ph is low theres a conformational change, virion enters cell
name 2 unusual ways naked viruses can penetrate the cell
-entry across plasma membrane, -direct puncture of cell membrane
purpose of uncoating
makes genome available
what happens after uncoating
degradation of the capsid and genome is transported to site where transcription and replication will occur
what two events must occur for a virus to infect a cell
- synthesis of viral nucleic acid 2. synthesis of viral protein
where to dna viruses release their genome to rely on cellular machinery for transcription
nucleus
what do + rna viruses encode and package
RdRP, does not package it
what do - rna viruses encode and package
RdRP must package it
which rna virus looks like our mrna
+ sense
example of dsDNA
hsv, adenovirus, human pap
describe how ssdna viruses create protein
reverse transcriptase creates dsDNA, dsDNA creates ssRNA intermediate, reverse transcription back in -ssDNA, dna polymerase creates + ssDNA
are +ssRNA segmented
no they are unsegmented
examples of + ssRNA viruses
poliovirus, west nile, rhinovirus
What kind of genome does -ssRNA viruses have
segmented or nonsegmented
examples of -ssRNA viruses with nonsegmented genomes
rabies, ebola
examples of -ssRNA viruses with segmented genomes
influenza
how does HIV replicate
uses dsDNA intermediate, ssRNA is reverse transcribed into dsDNA
what is assembly
components are assembled into a particle
what stage does a virus become infectious
maturation
how do enveloped viruses leave the cell
budding
how do non enveloped viruses leave the cell
lysis
when does HIV go through maturation
viral protease cleaves budding and matures after leaving cell
what happens when a virus damages a cell or kills it
cell death can cause paralysis or death or increase mucus secretion
what stage of the infectious cycle is targeted by antiviral intervention
any!
what enzymes does chemotherapy often target
nucleic acid polymerase, protease, integrase, neuraminidase
what step would be targeted if the antiviral targets polymerases
replication
what drugs block were tested to see if they block RdRP during transcription
Remdesivir
how does covid penetrate cell
viral host membrane fusion or endocytosis
how does covid replicate
creates a -ssRNA with RdRP, transcribes this copy into + RNA
what might chloroquine do for covid
blocks cell receptor, might stop endosomal acidification and prevent formation of clathrin complexes
how might chemotherapy affect attachment
agents block cell receptors
explain how hiv could be blocked at attachment
add extra receptor
how might chemotherapy block penetration
block low pH needed for endosome membrane fusion
how might chemotherapy block uncoating
block ion transport
how might chemotherapy block replication
take advantage of high specificity of polymerases to block reverse transcription
example of drug action that blocks replication
azt looks like thymidine and gets incorporated into RT by rna polymerase and then stops transcription
what RdRp drug is used against flu
favipiravir
what are the targets for the best drugs to treat HIV
block maturation by targeting the proteases that clips the bud
how might chemotherapy block release
a neuraminidase can block the release of viral proteins
schemes for classifying viruses
host range, tissue infected, mode of transmission. now use basic structure and molecular biology
who names viruses
international committee of taxonomy of viruses
what are the ictv properties for classifying viruses
- order 2. family 3. subfamily 4. genus
- common names
Several different criteria have been used to classify a virus. Which of the following is NOT among these criteria.
a. the type of nucleic acid that constitutes the viral genome.
b. the nature of the disease caused by the virus.
c. the metabolic activity of the virus outside of its host cell.
d. the replication strategy of the viral genome.
e. the mode of transmission of the virus.
c
why must the skin be breached in order for it to be considered a place of entry
top layers are dead so there is no virus replication in dead cells
what kind of inhibitory mechanism prevent viruses from infecting the respiratory tract
cilliated epithelium, mucus secretion, lower temepratre
why is the gi tract a difficult place of entry
hostile environment
why are the eyes an easy target for viral entry
easy to access and unprotected
examples of viruses that enter through the skin
pap virus, HSV
examples of viruses that enter through respiratory tract
rhinovirus, coranovirus, flu
viruses that infect gastrointestinal tract
rotavirus, norovirus
where do viruses most often cause symptoms
at the point of entry
define latrogenic induction
infections generated by a physician
type of virus that replicates at site of infection
localized infection
type of virus that moves to another site in the host
systemic infection
example virus of systemic infection
poliovirus, herpesvirus
what are 3 mechanisms for spread
bloodstream (viremia), nervous system, lympthatic system
how do viruses shed
usually leave through routes of entry
what does a productive infection mean
entry into permissive cells followed by virion formation
what does abortive infection mean
entry into non permissive cell, does not create virion
restringent or restrictive infection means
transiently permissive and some virus is produced
what type of infection is HSV
restringent
why are persistent infections bad
- epidemic importance
- virus reactivation
- can act as precursor for another disease
- can cause cancer
is rhinovirus persistent or non persistent and why
non persistent, gets completely cleared
example of chronic infection
hiv
example of slow infection
TSE
what does it mean when a virus is in latency
there is no infectious virus present
how does HSV latency work
HSV enters epithelial cell, then enters nerve cell, decides to just hang out there
describe the model for establishin latency
1.virion attaches and penetrates the neuronal cell
2. loss of tegument proteins on axonal transport
3. enters viral genome by uncoating and circularizes
4. does not transcribe
5. forms chromatin
6. forms latent rna
describe how hsv-1 starts as acute infection
- enters skin cell and uncoats
- genome enters nucleus
- viral mrna creates viral genome
- viral genome repackages and buds out
- goes up trigeminal ganglion
advantages of being in a neuron
- no good immune surveillance
2 non dividing
3, pathway of axon allows virus to get back to epithileal cells
what happens to t cells in aids
they all die
what kind of virus is hep b and why is it improtant
dsDNA, chronic human infection
3 conditions required for viral persistence
- infect some host cells without cytopathology
- mechanism for long term maintenance of viral genome
- must avoid detection of host defense systems
explain what it means for viral persistence to require no viral cytopathology
-infection of non permissive cells
-infection of small number of permissive cells
-infection by virus variant that are less cytopathic
explain what it means for viral persistence to require maintenance of viral genome
dna: integration into host chromosome
rna: continuous low level replication
explain what it means for viral persistence to require escape from host defense system
-limited viral gene expression to avoid detection
Which of the following are required for viral persistence?
a. Infect some host cells without cytopathology
b. Mechanism for long term maintenance of viral genome in host cells
c. Virus must avoid detection by host defense systems
d. All of the above
d
what host changes can produce disease
age, immunity, immune supression
what viral agent changes can produce disease
survival in environment, mode of transmission, evasion of host immunity
what environment changes can produce disease
population density, climate, water
what affects severity of infection
- virus genotype
- ammount of innoculum delivered to host
- host immune competence
name some physical innate immunity
- skin
mucous
acid pH
describe the virus specificity, time frame, range of effect, and general mode of action of interferons
specificity: non specific
time frame: within minutes or hours
range of effect: localized
mode of action: induce antiviral state to affect protein synthesis
describe the virus specificity, time frame, range of effect, and general mode of action of antibodies
specificity: virus specific antiviral
timeframe: 7-10 days
range of effect: systemic
general mode: neutralize virus entry and destroy virus infected cells
describe cellular altruism
when virus infects first cell, blocks protein synthesis and stops host from makign the repressor that silences interferon formation. then it sends the interferon signal to neighboring cells.
what is considered the inducer for the interferon system
dsRNA (either enters virally like that or is an intermediate during ssRNA replication)
what receptors binds to dsRNA to send off signal for interferons
rig-I or mda5
how do you create an antiviral state
blcoking translation
what 3 pathways create the antiviral state
oligoA intiviral response, PKR, RNAse L
how does rnase L contribute to an antiviral state
kills infected cells by apoptosis and destroys viral mrna
how does pkr contribute to the antiviral state
inhibits translation by phosphorylating a kinase rgar phosphorylates the initiation factors
other examples of non specific defense
nk cells, phagocytes
how are nk cells activated
activated by interferons
examples of active evasion
adenovirus and hsv
what does active evasion do
viral protein mediates blockage
what molecule use immunosuppression as active evasion
HIV
how does HIV evade the immune response
kills t cells via apoptosis
how does ebola avoid the interferon response
virus attaches, penetrates, uncoats. dsRNA is made as replicative intermediate. this should signal interferon response, but vp35 binds to the ds rna and blocks it from rig I
how does inhibition of cytokines work for active evasion
inhibits cytokine transcription, translation, and function
how does a viroceptor block chemokines in active evasion
-competitively binds to chemokine and blocks signaling
how does vck block chemokines in active evasion
mimincs cellular cytokine and blocks cytokine receptor
how does vCkBP block chemokines in active evasion
binds to cellular chemokine to stop it from binding to receptor
2 types of passive evasion
antigenic drift (mutation accumulate to make changes in the part of rna the immune system recognized), internal sanctuaries
name several ways covid evades ifn response
blocks activation of rig-I, inhibits nfkb, blocks a lot. in neighboring cells, blocks transcription factors
what type of virus is covid
+ ssRNA
structure of covid
enveloped helical
VAP and receptor of covid
spike protein and ace2 receptor
how does covid produce a lot of proteins
ribsomal frame shifting, polyprotein, subgenomic rna
what type of virus is HIV
+ssRNA
structure of HIV
enveloped icosahedral
what type of virus is VSV
-ssRNA
what type of virus is polio
+ssRNA
structure of polio
nonenveloped icosahedral
how does polio enter the cell
pore formation
structure of HSV
enveloped icosahedral
what type of virus is flu
-ssRNA
all viruses that -ssRNA are what structure
enveloped helical
how does flu avoid the immune response
binds to reim25 and stops rig-i from starting interferon response
