Viral infections

Question 1

Latency
mechanism and example

Answer 1

MECHANISM: hiding from immune system via little to no expression/replication

initial entry associated with replication and immune response -> ablation of immune response but virus stays latent and its genome in non-replicative mode

HSV: retrograde transport to dorsal root ganglion -> presistance, re-activation stimulus leads to anterograde axonal spread and epithelial lesions

Question 2

low titer replication
mechanisms

Answer 2

continous replication on low level -> smoldering infection
detectable immune response without clearance

• immunological privileged sites
• intracellular bridges
• suppression of MHCI
• ADE
• Impaired CTLs
• antigenic variation

Question 3

infection of immunoogical privileged sites

Answer 3

mechanism of persistance - low level replication

important tissues, not easily replicated
limited immune repsonse prevents clearance

e.g. Brain –> BBB hinders migration, low MHCI expression
e.g. kidney –> maybe crossing of basment membrane not possible

Question 4

infection via intracellular bridges

Answer 4

mechanism of persistance - low level replication
spread without exposure to extracellular space and the containing immune mechanisms

Question 5

suppression of MHCI

Answer 5

mechanism of persistance - low level replication
in comparison of immunological privileged sites where MHCI downregulation is physiological
this is virus-induced
lowers susceptibility to CTL attack

Question 6

ADE of infections

Answer 6

mechanism of persistance - low level replication

formation of infectous immune complexes
internalization via FcgR by macrophages

dependent on Ab titer -> sub-neutralization levels required

Question 7

impaired CTLs

Answer 7

mechanism of persistance - low level replication

CTL impairment via Treg or deficiency in effector molecules
e.g. HIV-CTLs conatin only low levels of perforin

Question 8

antigenic variations

Answer 8

mechanism of persistance - low level replication

• escap form Ab neutralization: via different capsular polysaccharides (S. pneumococcus) or recombination abilities (Trypanosomae)
• CTL escape: selective pressure favors selection of escape mutants
• antigenic drift: point mutations in surface-genes, usual slight cross-immunity possible
• antigenic shift: reassortment and exchange of genes between strains in secondary host, only in Influenza A

Question 9

upper tract infections

Answer 9

common cold: many pathogens, bad cross-immunity

pharyngitis: mostly viral vie RV, Cov or Inf, bacterial via S. pyogenes

Question 10

lower tract infections

Answer 10

BROCHITIS
acute: mostly viral or M. pneum, pertussis

chronic COPD

Question 11

Diagnosis of viral infections

Answer 11

pathogen detection: full virus less common and time-intensive
viral components standard method (ELISA, PCR)

antbody detection less for diagnosis more retrospective (titer CMV check for pragnancy)

Question 12

Innate immune response to viral infection

Answer 12

NK cells -> eradication
IFNa and IFNb -> block viral replication
antiviral enzymes -> induced by IFNa/b, PKR, 2’5’ oligo A synthase, Mx proteins

IFN induced by TLR, RLR via IRF, by TLR, NLR and STING via NFkB

Question 13

Adaptive immune reponse against viruses

Answer 13

neutralizing Ab
B cells
TH1 cells
CTLs
TH2 cells -> activate B cells