Brainscape's Knowledge GenomeTM

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


See full index

Medical virology > Picornaviruses > Flashcards

Picornaviruses Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

What are picornaviruses?

A
  • positive sense ssRNA viruses that replicate in the cytoplasm
  • enteroviruses such as rhunovirus or polio
  • hepatoviruses such as hepatitis A
  • apthroviruses such as foot and mouth disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the general structure of a picornavirus?

A
  • non enveloped
  • icosahedral particle made of 60 promoters
    on the surface each made of 3/4 proteins
  • VP1, 2 and 3 form the viral capsid
  • VP4 is inside the capsid and associated with the viral RNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe picornavirus structure in terms of receptors

A
  • continuous groove acts as a binding site for cellular receptors and antibodies
  • some enteroviruses can bind to many receptors -> host trophism
  • drugs can inhibit receptor binding by filling or blocking the groove
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why weon’t receptor-blocking drugs work on all picornaviruses?

A

some such as C15a don’t have a continuous groove to block

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

Describe the genomic organisation of picornaviruses

A
  • genome encodes one polyprotein that is cleaved into multiple products
  • 5’ end has a viral protein covalently attached
  • 3’ end is polyadenylated like host mRNA
  • the 5’ UTR has an internal ribosome entry site that binds ribosomes differently to eukaryotes
  • structural proteins at the 5’ end
  • 3’ end proteins involved in replication and evasion of the host immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Briefly describe the picornavirus replication cycle

A
  • entry is poorly understood but doesnt involve afusion
  • uncoated and polyprotein is translated
  • processed by proteases
  • replication complex forms and associated with host lipid membranes to prevent its degradation
  • negative RNA strand is made + use to make more genome or for genome packing and release by cell lysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the importance of picornavirus proteins 3C and 3D?

A
  • viral protease that cleaves the polyprotein at specific amino acids
  • viral RNA-dependent RNA polymerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe polyprotein processing in picornavirus

A
  • P1 is translated and cleaves itself
  • translation occurs up until 3C which also cleaves itself and then the rest of the protein
  • cis and trans cleavage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is polyprotein processing a good drug target?

A
  • its a property specific to viruses
  • knocks out or binds to proteases to stop the production of functional proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does picornavirus turn off host protein synthesis?

A
  • 2A cleaves host mRNA 5’ caps to prevent ribosome binding
  • IRES allows binding of ribosomes in an alternative way that is not affected by the loss of 5’ caps
  • viral mRNA becomes the only mRNA available to be translated by host ribosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are enteroviruses?

A
  • a type of picornavirus
  • polio, rhinovirus
  • usually not severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does enterovirus infect and where does it shed?

A
  • infects the oropharyngeal or intestinal mucos and is shed in the faeces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the most common symptoms of rhinovirus?

A
  • febrile illness is seen but 90% of infections are asymptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does rhinovirus spread to other organs?

A

spread by viraemia to skin, muscle, brain etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is enterovirus linked with T1D?

A
  • in some, the virus infects and releases viral and beta cell antigens
  • in those genetically predisposed this can trigger T1D autoimmunity
  • IFHI gene variants can lower the risk by 50% and is involved in picornavirus recognition and interforminterferonresponsesWha
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of virus is poliovirus?

A
  • picornavirus - enterovirus
17
Q

Where does poliovirus infect and where does it spread?

A
  • infects the small intestine
  • can enter the bloodstream leading to viraemia that’s usually asymptomatic
  • but in >1% of cases the CNS is infected leading to paralysis and/or death
18
Q

How was the sabin vaccine against poliovirus produced?

A
  • live attenuated virus
  • cultured from monkeys and purified
  • blind way of making vaccines rather than targeting specific proteins
  • all have mutations in the 5’ UTR (IRES) and some in structural proteins
19
Q

What are the differences between mass vaccination (OPV) and ruotine immunisation (OPV and IPV)

A

Mass vaccination involves going to an area and vaccinating as many people as possible, it is cheaper and can lead to eradication.

Routine immunisation usually prioritises those at specific ages or circumstances and doesnt stop the virus from spreading especially when coverage in low income countries is so low

20
Q

Why is routine immunisation coverage low in many developing countries?

A

storage of the vaccine is difficult in hot climates and there is year long transmission of the disease meaning many individuals will already be infected by the time the vaccinations come round

21
Q

What is poliovirus vaccinatoin like in the UK~?

A
  • inactivated vaccine used
  • 5 doses throughout childhood provides protection and stops the spread
22
Q

What are the challenges associated with the use of the OPV vaccine commonly used for mass vaccination?

A
  • virus can revert back to virulence or combine with other enteroviruses
  • can spread virus to others in places where polio has been ‘eradicated’ and in places where polio resurfaces it is shown to usually be due to vaccine dervied strains
  • has become a threat to erradication
23
Q

What progress has been ,ade in erradicating poliovirus?

A
  • type 2 declared eradicated in 2015
  • changed from a trivalent vaccine to a bivalent and type 3 was declared eradicated in 2019
  • only 1 wild type poliovirus remains
  • but now need to control the spread of virus caused by the vaccine
24
Q

What is the novel type 2 OPV?

A
  • OPV vaccine genetically engineered to stabilise mutations and improve the viral polymerase
  • to reduce mutations and reversion back to virulence
25
Q

How can vaccination be stopped?

A
  • abruptly following mass vaccination may stop the spread of vaccine derived virus
  • continued use of IPV for routine immunisation provides good covarage where mass isnt feasble and is used most countries that can afford it
26
Q

How could poliovirus re-emerge? (3)

A
  • presistence of wild type strains
  • evolution of vaccine strains
  • escape from labs
27
Q

How can poliovirus re-emergence be avoided? (4)

A
  • proper lab containment
  • disease surveillence
  • outbreak response
  • continued vaccination
28
Q

What are rhinoviruses?

A
  • picornavirus - enterovirus
  • causes 50% of common colds
  • > 100 serotypes allows for repeated infection
  • spread by respiratory secretions
29
Q

What are the symptoms of rhinovirus?

A
  • 1/3 asymptomatic
  • cold symptoms for up to a week
  • can cause chornic bronchitis in those with chornic obstructive lung disease or asthma
  • wheezing and pnemonia in children
30
Q

What are the links between rhinovirus and asthma?

A
  • study in children found that 90% of children who had severe rhinovirus before 3 developed asthma by 6
  • occurred due to respiratory tract remodelling
  • led to worsened future infection
31
Q

What is the general immune response to rhinovirus?

A
  • IgA and IgG increase after infection + give protection for several months
  • protection is only for the specific serotype that infected oyu
  • increased number of Abs against different serotypes with age
32
Q

What are the challenges of vaccines for rhinoviruses?

A
  • serotypes have little cross reactivity
  • mucosal immunity wanes faster as IgA is hard to maintain
  • inactivated vaccines can reduce virus shedding and illnessW
33
Q

What ar the challenges for antivirals against rhinovirus? (5)

A
  • where to administer - nasal mucosa?
  • compounds shown little luck in culture so far
  • drug resistence
  • when in infection to give?
  • C strains have no continuous groove !
34
Q

What is hepatitis A virus?

A

picornavirus that causes >90% of all viral hepatitisH

35
Q

How is HAV spread?

A
  • fecal oral route
  • replicates in the liver + excreted in the bile
  • can spread to and through water systems
36
Q

Why is hepatitis A virus hard to grow in culture?

A
  • replicates slowly
  • does not alter host molecular synthesis / shut down host processes
  • needs to compete for resources
37
Q

What are the clinical features of hepatitis A virus?

A
  • children more likely to be asymptomatic
  • when clinically apparent it shows liver dysfunction, jaundice, fever, fatigue
  • if noy fully cleared it can relapse within a year
  • in rare cases it can lead to liver failure and death
38
Q

What is important for prevention of hepatitis A virus?

A
  • symptoms are not distinct - doagnosis requires testing
  • personal hygiene
  • pre or post exposure passive immunoprophylaxis
  • HAV vaccine
39
Q

What is the HAV vaccine?

A
  • inactivated whole virus
  • protective Abs in over 95% and prevents liver replications and fecal shedding

Medical virology (15 decks)

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