Lecture 8: infection and vaccines
1) What is communicable disease? How can we get rid of them
2) What causes damage to the host cell most of the time? How can you prevent this damage?
3) Immune response to VIRUS: how does a virus enter the cell? Do they want to kill their host? What
kind of response is produced during virus production?
4) When we get a virusinfected cell, what does this cell release? And what happen after this?
5) Explain the humeral and cell mediated immune response against virus?
6) How can virus inhibited humeral immunity effect?
7) How can virus inhibit inflammatory effect?
8) How can virus inhibit antigen presentation or processing?
9) How can virus cause immunesupression?
10) Influenza virus: what are the two key viral glycolpeptides? Where do we see the most antigenic
variation in different type of HINI virus?
11) What is the reason for the different H1N1 virus? What is the process called?
12) Second reason why H1N1 or other virus changes and it is when two different virus combine
together what happens?
13) What is an original antigenic sin?
14)5 ways antibody mediated mechanism work to kill outside bacteria?
15) Explain how the immune system fights the intracellular bacteria like TB?
16)If bacteria are persistent in that it is always present what does the body do?
17) What is the prime mechanism through which the body fights the immune system? Which is the
mechanism through which fungus is destroyed? What are some ways fungi has found ways to escape
18)Why is it bad idea to take antimicrobial or antifungal medication?
19) Between Th1 and Th2 what are the role of each in fighting off fungi?
20) Leishmaniasis: where does it lice? What two syndrome does it produce? What type of response is
very effective against this?
21)Malaria: caused by what? Life cyclyes moves through what? What does it evade the immune
22)Helmith: a worm that enters host through intestine and is extracellular: how does the body fight it?
what is the best response out of these? How does the worm try to evade this?
23)Trypanosome: why is called sleeping sickness? Why are their waves of different types of these that
evade the immune system?
24) Why might vaccines reemerge?
25) What is the difference btw passive and active immunity?
26)Vaccines: Live attenuated vaccines that are weakening. What are the pros and cons?
27)Vaccines: killed or inactivated vaccines. What are the pros and cons?
28)Subunit vaccines: what are they? Pros and cons?
29)Recombinant vector vaccines: what are they? Pros and cons?
30) What are DNA vaccines? Pros and cons?
31) Conjugate and multivalent (i.e. Ag coupled to something else) why are they used?
32)Can linking different antigen be done to stimulate CTL? What are ISCOMs?
33) What are adjuvants? When is t used? benefits? Lecture 8: infection and vaccines
1) Any disease that can be transferred It can be dealt with very easily by using vaccines
2) Most damage is due to your own immune response. To prevent that from happening we want a
balance between pathogen elimination (inflammation response) and preventing harm to the hos.
3) Surface receptor endocytosis. No they don’t want to kill their host They trigger both humeral and
cell mediated response.
4) IFN β and IFN α are produced. Once this is produced we began producing resistance to viral
replication (no protein production), increase MHC I expression (CTL killing now), and activate DC,
NK, macrophages to kill virus infected cell.
5) Humoral: antibodies are released such as IgA (blocking binding to host cell), IgG, IgM also do the
same and enchances phagocytosis, opsonization, agglutination of virus particles and they also
activate the complement pathways to kill a irus. Cell mediated: NK▯ADCC killing. CTL direct
apoptosis and the TNF λ released by TH and TC cells direct antiviral effect.
6) Use virally encoded Fc receptor (no killing), complement receptor ( no complement effect) and
virally encoded complement proteins ( that inhibits other remaining complement receptors)
7) Viral encoded: chemokine’s receptor, viral encoded soluble cytokines receptor homologs (such as
for IL1, Interferon ϒ, and TNF) so its blocks the effects of these cytokines, also inhibition of
adhesion molecules ( LFA3 and ICAM1) so nothing bind to this cell and using viral encoded TLR
so no NFκB is not produced and thus no inflammatory response is elicited by Il1/bacteria
8) Blocking of antigen presentation: inhibit MHC I expression, inhibit peptide transporter like TAP.
9) It can also suppress and immune response by producing IL10 which reduce TH1 response and
reduces Interferon ϒ prod.
10)Hemagglutinin (HA1) allows attachment of virus to cells Neuraminidase (N) helps new virus
escape from host cells. It is in these region we see the most variation which leads to different H1N1
strains being produced.
11) It is called Antigenic drift which occurs