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Year 2 - microbiology > Viral evasion of host immunity > Flashcards

Viral evasion of host immunity Flashcards

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Biology 101 flashcards
1
Q

what kind of pathogens are viruses?

and what does this mean for presentation via the MHC?

A
  • Viruses are intracellular pathogens
  • therefore their proteins are easy targets for processing and presentation by MHC
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2
Q

how long does cellular immune response to viral infections last?

A
  • Cellular immunity clears viral infection but is short-lived
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3
Q

why is cellular immunity an issue for internal viral proteins?

A
  • Internal viral proteins can be targets for cellular immunity via the MHC and antibody response
  • they are intracellular antigens and therefore they vary less than the surface antigens
  • therefore in order to persist they must evade cellular immunity
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4
Q

how do MHC Class I present viruses?

A
  • the foreign peptides inside the cell (eg. viral peptides) get chopped up into small peptides inside the proteasome
  • they are fed through the TAP protein into the endoplasmic reticulum
  • the tapasin protein loads them onto the MHC I molecule
  • the MHC molecule then moves to the cell membrane
  • there the viral peptide is recognized by the T cell receptors
  • the T cells are then able to kill the virus-infected cell
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5
Q

how does the Epstein Barr Virus evade antigen presentation via preventing antigen loading to TAP?

A
  • EBV expresses a protein called EBNA1
  • this cannot be cut up into smaller peptides, therefore, it can exist without being detected
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6
Q

how does the Herpes Virus evade antigen presentation via Evasion of Antigen Loading to TAP?

A
  • HSV encodes ICP47
  • this blocks access of the processed peptide to TAP protein
  • so it cant be loaded into the endoplasmic reticulum
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7
Q

how does the CMV evade antigen presentation by modulation of TAP function and Tapasin function?

A
  • CMV encodes US6 which stops ATP binding to TAP
  • this means that TAP is not able to transport peptides across the membrane
  • CMV also encodes US3 which binds to tapasin and prevents peptides being loaded onto MHC
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8
Q

how does Adenovirus E3P19K evade antigen presentation by modulation of Tapasin function?

A
  • Adenovirus E3P19K prevents recruitment of TAP to tapasin and also retains MHC in the ER so it cannot present to the T cell
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9
Q

how does Kaposi Sarcoma Herpes Virus interfere with MHC presentation at the cell surface?

A
  • Kaposi Sarcoma Herpes Virus induces polyubiquitination (this kills the protein) and internalization of MHC
  • if the MHC isn’t present at the cell surface then the virus peptides won’t be presented to T cells instead the MHC is passed onto lysosome and is degraded
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10
Q

how do viruses avoid natural killer cells by the missing self mechanism?

A
  • all normal cells display MHC on their cell membranes
  • if they don’t have MHC then they are detected and killed by natural killer cells
  • so when viruses disrupt the MHC presentation they would get killed by natural killer cells
  • Therefore to get around this viruses encode MHC analogues or upregulate MHC
  • this new viral MHC is actually useless bu it avoids the NK cells
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11
Q

what does the measles infection do to the immune system?

A
  • it is called Virus mediated Immunosuppression
  • the measles infection erases immunological memory in the child for the next 2 to 3 years
  • therefore even if the child doesn’t die of measles they might die of something else due to having limited immunity
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12
Q

why is the measles vaccine so effective?

A
  • it does not only protect against the measles virus
  • it also prevents the loss of the immune system therefore conserving immunological memory in the following 2-3 years
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13
Q

how do some viral infections use the destruction of T cells?

A
  • HIV targets CD4+ T cells, therefore, preventing an immune response
  • Ebola virus infection results in the destruction of target dendritic cells and macrophages by direct infection
  • T cells are also destroyed as a bystander response
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14
Q

how might we use knowledge of how viruses manipulate infected cells to improve medical outcomes?

using the example of HCMV and CMV?

A
  • HCMV only affects those who are immunocompromised
  • so in bone marrow transplants, the virus needs to be eliminated from bone marrow cells before they are transplanted into the immunocompromised
  • UL138 protein is produced by HCMV and it leads to loss of MRP-1 from the infected cell surface
  • MRP-1 is a transporter that transports toxic drugs out of the cell
  • the loss of the MRP-1 transporter leads to accumulation of molecules in cells infected by HCMV
  • so, for example, the toxic drug VINCRISTINE
  • the donor is treated with vincristine before transplantation to eliminate the CMV cells
  • this has improved bone marrow transplant results
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15
Q

what is Influenza Antigenic DRIFT?

A
  • continued rapid evolution driven by antigenic pressure from the host
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16
Q

what is Influenza Antigenic SHIFT?

A
  • introduction of new subtypes from an animal source
  • this is completely new to humans
17
Q

what are different genetically stable serotypes?

A
  • these viruses don’t change but there are many serotypes of them eg. rhinovirus, poliovirus, dengue
  • they co-circulate in humans
18
Q

why does the influenza vaccine get updated each year?

A
  • Because of the antigenic drift of influenza, the virus keeps looking different so the vaccine needs to be updated every year
19
Q

how many serotypes does influenza exist as?

A
  • influenza exists as four different serotypes
  • these drift year on year
20
Q

how is the serotype chosen to be put into the vaccine?

A
  • each year WHO tries to predict which influenza serotype is most likely to cause flu that year
  • but often it is not that accurate
21
Q

what is the universal flu vaccine?

A
  • doesnt actually exist
  • an ideal vaccine that protects against all types of flu
  • there are attempts to produce antibodies that attack the stalk of the virus which is always conserved
  • however antibodies do not normally act this way which is why it’s difficult
22
Q

what does the human rhinovirus cause? what is the variation in the Human rhinovirus?

A
  • Human rhinoviruses cause the common cold
  • They exist as more than 120 antigenically distinct serotypes that all circulate
  • its impossible to make a vaccine against all of them
23
Q

how is HIV able to evade antibodies?

A
  • Some viruses have glycoprotein antigens that are so heavily glycosylated so that the antibody access is hindered
  • the virus looks more like human mucin than viral antigens
  • also functionally important parts of the molecule are poorly accessible, CD4 binding site
  • so they are not able to be vaccinated against
24
Q

how might we design an HIV antibody? what is the issue?

A
  • we could genetically modify the antibody response to attack the stalk of the spike region
  • the issue is the virus keeps evolving therefore it is hard to make a vaccine that works
25
Q

how many serotypes of poliovirus?

how does the polio vaccine work?

A
  • There are three serotypes of poliovirus
  • this requires a trivalent poliovirus
  • this has resulted in one serotype being eliminated from the world
26
Q

how many serotypes does the Dengue virus have?

A
  • exists as 4 different serotypes
27
Q

what is the consequence of the antigenic variation of the dengue virus?

A
  • if you get infected by one type of serotype of dengue fever you just get a slight fever
  • if you get infected by another serotype then you might develop a hemorrhagic fever (very dangerous)
28
Q

why does this Haemorrhagic Fever happen?

A
  • if you have been infected with one serotype of dengue, you will develop antibodies against it.
  • Then if you get infected by another serotype, your antibodies will bind to but not neutralize the new serotype of dengue
  • this allows the virus to replicate more and therefore have a much greater response on the person
  • this is called antibody dependent enhancement of the current dengue serotype
29
Q

what is Dengue haemorrhagic fever ?

A
  • It causes leakage of plasma from the capillaries
  • the loss of fluid from the blood causes increased hematocrit and increased red cell count and a decrease in protein
  • therefore there is severe bruising and bleeding
  • high mortality
  • treat with IV fluids
30
Q

why is developing a vaccine for Dengue fever dangerous?

A
  • antibody-dependent enhancement
  • the vaccine might not neutralize the dengue fever and stop its replication
  • therefore it might just prevent the immune reaction to the serotype
  • , therefore, making people more susceptible to the hemorrhagic fever

Year 2 - microbiology (7 decks)

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