Brainscape's Knowledge GenomeTM

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


See full index

Medical virology > Respiratory Syncytical virus > Flashcards

Respiratory Syncytical virus Flashcards

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

What is the structure of the RSV virion?

A
  • enveloped, non-segmented negative sense ssRNA
  • on the outside:
  • fusion protein (F)
  • attachment protein (G)
  • small hydrophobic protein (SH) makes an ion channel
  • RNA is wrapped in the N protein and associated with polymerase (L)and phosphoprotein(p)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does RSV enter the host cell - which receptors and proteins are used?

A
  • receptors such as TLR4 bind the G protein
  • nucleolin on the cell surface can also facilitate fusion and entry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the RSV replication cycle

A
  • in the cytoplasm
  • mRNA is produced to form viral proteins, some expressed on the viral surface, some used in replication and some to make new virus
  • antigenomes are synthesised and progeny genomes are formed that can be used to make more viral proteins or put into new virus and released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is negative sense RNA?

A

genomes are negative - act as complementary strands to mRNA that is produced by RNA dependent RNA polymerase and then read from to create viral proteins

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

How is the genome of an antisense ssRNA virus such as RSV replicated in the host cytoplasm?

A
  • during replication, mRNA is produced and polyadenylated at the end of each gene to create mRNAs for each
  • alternatively antigenomes can be produced where by the RNA polymerase ignores the stop codons of the genome and makes an enture stretch of antigenome
  • the antigenome can then be used as a template by polymerase to copy the entire genome in replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does the structure of the RSV genome allow much more transcription of 3’ early genes?

A
  • polymerase begins at the 3’ end
  • when it reaches the end of a gene a gene end signal causes a pause
  • the polymerase can either drop off and start again or continue to the next gene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is the L late gene transcribed much less frequently than the other 5’ genes?

A
  • the L transcript begins inside the M2 transcript
  • L is only transcribed when M2 is missed
  • have to miss the M2 start, catch the L start miss the M2 stop to get L transcribed so its a rare occurence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does transcription of the RSV M2 transcript make the most out of a compact genome?

A
  • codes for M2-1 and M2-2 overlap eachother
  • polymerase reaches the M2-1 stop codon, releases the M1 protein, jumps back and encodes M2-2
  • requires secondary structures on the RNA
  • M2-2 is more important in replication than transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between replication and transcription?

A
  • transcription = making the mRNA - viral proteins
  • replication = making antigenomes - genome progeny
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can be seen in cell culture where RSV virus infects cells

A
  • attaches via G fuses via F
  • complex of RNA, N P and L enter the cytoplasm
  • G+F also allow infected cells to fuse with neighbours increasing the spread
  • this leads to the formation of large syncytia where cell DNA + RNA metabolism is slowed but protein synthesis continues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does RSV evade the innate immune response?

A
  • NS1+2 subvert interferon production and signalling
  • methylation of the genome by host machinery hides it from the innate immune response
  • delaying the innate immune response gives more time for disease progression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is RSV transmitted, where does it infect?

A
  • large respiratory droplets
  • enters the nose and conjunctiva mainly
  • hands touching contaminated surfaces and then the face
  • infection initially in the upper respiratory tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does RSV progress and cause symptoms?

A
  • moves from the upper respiratory tract to the lower to the bronchioles
  • most cell death is virus-induced
  • inflammation, accumlation of cellular debrish and infiltration of immune cells can block airways especially in infants with smaller airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the epidemiology of RSV?

A
  • peaks and troughs with the climate (more time indoors)
  • infants up to 9 months are at highest risk
  • up to 2% of hospitalised infants will die of RSV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the major antigenic proteins to B cells in RSV?

A
  • F + G can have neutralising antibodies raised against them
  • these provide some protection against re-infection that doesnt last
  • T cell response has been detected in response to most viral proteins but is more direct at clearance than protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the RSV subgroups?

A
  • A + B
  • have differences in all proteins but mostly G , F and SH
  • within subgroups, there are many genotypes with further differences in G
  • this variety contributes to RSV ability to re-infect individuals
17
Q

Why was the formalin-inactivated vaccine against RSV not effective?

A
  • led to increased deaths
    -developed an antibody response that was not neutralising
  • as a result, their memory response was not effective against re-infection
  • mechanisms not fully understood but likely due to an imbalanced T cell response
18
Q

What are some of the main hurdles in RSV vaccine development?

A
  • primary target group is infants that are immunologically immature and have high levels of neutralising antibodies from their mothers that may neutralise vaccine strains
  • the virus is also able to repeatedly re-infect so a vaccine would have to be cross-reactive
  • progress on vaccines targeting the F protein has been made
19
Q

How would an F protein vaccine against RSV work?

A
  • F protein flips between a pre and post-fusion state
  • the pref-usion state has potent antibody binding sites that are highly effective at stopping infections
  • studies into stabilising F in its pre-fusion state have been promising
20
Q

What antiviral agents are available against RSV?

A
  • nucleoside analgogue that increases the error rate in the viral genome through unclear mechanisms
  • also generally inhibits RSV mRNA production
  • not great and other drugs being looked into targeting the polymerase for example
21
Q

Why might neutralising antibodies be a good option for an RSV vaccine?

A
  • maternal neutralising antibodies protect infants up to 6 weeks
  • high neutralising Ab titre decreases disease severity
  • humanised monoclonal Ab that binds F protein and prevents fusion is undergoing trials

Medical virology (15 decks)

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