M2 Micro 25 Ex1

Front 1

Two types of variation allow repeated infection with influenza virus

Back 1

Antigenic drift
Antigenic shift

Front 2

Antigenic drift

Back 2

1)neutralizing antibodies against hemagglutinin block binding to cells
2)mutations alter hemagglutinin epitopes so that neutralizing antibody no longer binds

Front 3

Antigenic Shift

Back 3

1)Antigeni shift occurs when RNA segments are exchanged between viral strains in a secondary host
2) No cross protective immunity to virus expressing a novel hemagluttinin

Antigenic shift (per 50-100 years) leads to pandemics (H5N1 avian flu; H1N1 swine flu)

Front 4

Latency for escaping eradication and for reactivation One common mechanism

Back 4

microbial antigens are not presented on cell-surface of latently-infected cells, and not recognized by T cells especially CTL

Front 5

Persistence and reactivation of herpes simplex virus

Back 5

HSV avoids clearance by the immune system by hiding silently in sensory neurons
Alteration of immune status can allow HSV activation
This cycle can be repeated many times
Others: Herpes zosters, EBV

Front 6

M. tuberculosis latency and tuberculosis

Back 6

Mycobacterium tuberculosis is intracellular pathogen that infects macrophages/DC and causes tuberculosis.

1/3 world population estimated is estimated to have latent M. tuberculosis infection.

Immune suppression (HIV or immune suppression drugs) cause reactivation tuberculosis.

Front 7

Resistance to immunity by manipulating the immune system

Back 7

Phagocytes engulf bacteria and destroy them by fusion with lysosome
M. tuberculosis taken up by macrophages can prevent phagosome fusion with lysosome, and instead use macrophages as their primary hosts.
This contributes to two consequences:
(1) No eradication
(2) Latent M. tuberculosis infection (1/3 world population estimated)

Front 8

Avoiding antibody responses by HIV

Back 8

Neutralizing Abs are too low and too late

Envelope is heavily glycosylated, giving minimal sites for antigenic recognition.
gp41 region has key neutralizing epitopes. However, gp41 epitopes are masked until CD4 is engaged.
High mutation rate generates escape mutants, a role of error-prone RT.

Front 9

Avoiding CTL responses by HIV

Back 9

Escape mutants emerge during early infection.
Mutation in anchor residues of eptitopes which result in no binding to MHC class I
Mutation in eptitopes that confer enhanced dissociation with MHC class I
The Tat/Rev system turbochargers HIV gene expression
Virions can be released before immune recognition