Micro 5: Viral evasion of host immunity Flashcards Preview

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Flashcards in Micro 5: Viral evasion of host immunity Deck (57)
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How can the immune system detect viruses

Viruses are intracellular pathogens and so their proteins are easy targets for processing and presentation by MHC.


What parts of the virus is an immune response mounted against

The MHC can present all parts of the viruses, not just the outside. The antibodies will be made obviously to surface molecules But the inside of the virus can be preseted on MHC and this can trigger CD8+ T cell to kill the virally infected cell


What is more variable, internal viral proteins or surface molecles?

Internal viral proteins can be targets of cellular immunity. They tend to vary less than surface antigens.


T/F a virus can be chronic without interfering with cellular immuity

F... Viruses that persist must evade cellular immunity


Give an example of a family of viruses that evade cellular immunity

. The family of herpes viruses are the classic examples.


Outline presenation of internal peptides inside a cell

Proteins in cell chopped up by proteosome, peptides transported into the ER where they are loaded onto MHC class 1 and the b2-microglobulin is added This is then transported through the golgi apparatus and displayed on the surface of the cell The peptide being presented can then be seen by a T cell receptor on a T lymphocyte


Which cells in th ebody expresses class 1 MHC



What activates the T cell

The MHC 1, TCR, foreign peptide and CD8 is important too


How do HSV 1 prevent interfere with cellular immunity

HSV ICP47 blocks access of the processed peptide to TAP


How does EBV evade cellular immunity

EBV EBNA1 cannot be processed by the proteasome so the viral protein cannot be chopped up and put into the ER so it cannot be presented in MHC class 1 to activate T cell


What is the name of the protein that transports peptides into the ER



How does CMV evade cellular immunity

CMV US6 stops ATP binding to TAP preventing translocation .CMV US3 binds tapasin and prevent peptides being loaded to MHC (i.e. cuts off the energy to TAP so peptides can't get into the ER and thus cannot be associated with the MHC molecules and cannot be presented to the T cells)


Which molecule assists in loading the peptide onto the MHC



How can adenovirus effect cellular immnity

Adenovirus E3-19K prevents recruitment of TAP to tapasin and also retains MHC in the endoplasmic reticulum


How does the KSHV (HHV8) evade cellular immunity

KSHV kK3 protein induces polyubiquitinylation and internalization of MHC. From the internalized endosome, MHC is passed to lysosomes where it is degraded. Cannot present viral proteins to the T cell


What type of virus is the HPV

DNA virus, but with shorter genome than herpes


How does HPV evade the immune response

Both cellular and innate response Just note that because HPV has a small genome, its proteins often do diverse range of functions E6/E7 are oncogenic (interfere with cell cycle), but they are also binding to proteins involved in the interferon detection pathway (cGAS, STING etc) and the IFN-a effector pathway (innate). E7 also prevents transcription of MHC and TAP proteins E5 holds onto the MHC class 1 molecule in the ER and the golgi and prevents it from being transported to the surface (cellular)..... BUT think about the consequence of loss of MHC


What is the human response to lack of MHC on cells

This makes immune system think there is virus in the cell So loss of MHC1 activates NK cells Normal healthy cells display MHC at their surface. Cells that don’t display MHC are detected by NK cells and killed. Viruses that disrupt MHC presentation would end up being killed by NK cells.


How do viruses get around the NK response which kills them if they interfere with MHC Give an example

Viruses encode MHC analogues (CMV gpUL40) or upregulate MHC.


What are virus vaccines usually trying to achieve

An antibody response


What is antigenic drift, vs antigenic shift

Continued rapid evolution driven by antigenic pressure from the host= antigenic drift Introduction of new subtypes from animal source= antigenic shift


Give example of antigenic drift and shift

Drift: influenze antigenic drift Shift: influenza antigenic shift


What is a quasi species in relation to antigenic drift What is the difficulty for treatment

It's when HIV replicates inside you it and spits out lots of different variants of the virus (=antigenic drift) The body can't mount reponses against each subtype of the virus and contain it because of all of the different surface molecules


Outline the differences in the number of serotypes with viruses and the consequences for vaccination

There is antigenic variation existing as different genetically stable serotypes that cocirculate in humans Rhinovirus- 100s Polivoris- 3 Dengue- 4 Consequence is theat the polio and dengue viruses nit to be trivalent and quadrivalent respectively The rhnovirus it is impossible to get a vaccine to promote immunity against so many serotypes... and not worth it cos only common cold anyway


What drives influencza antigenic change



What do ABs bind on influenza

Haemagglutinin= major influenza viral spike antigen It has head and stalk domain. A trimer


Outline the conservation of haemagluttinin

There are some AAs which are highly conserved and some which are highly variable between different haemagglutinin molecules The head domain (which pokes out most into the external environment) is highly variable


Why is the head domain likely to be variable in the haemagglutinin molecule

So that the B cells don't mount an immune response to it (i.e. the AA are constantly changing so that previously formed ABs cannot bind them) =ESCAPE. This is the basis of antigenic drift


What is the head resonsible for in haemagluttinin

Binding to the cells influenza wants to infect (i.e. respiratory epithelium) The target of B cells to make antibodies against it =HA1


How much do AAs have to change within the haemagglutinin molecule in order to prevent preformed AB binding

If the haemagglutinin has only a couple of AAs change, it will escape the preformed antibodues