21 - Viral Pathogenesis and Host Immune Defense (Stapleton) Flashcards
viremia
virus circulating in the blood
killing of cells by viruses
direct
indirect-host immune response kills infected cells
viral infection cellular outcomes
noncytolytic infection
cytolytic infection
transformation
abortive infection
noncytolytic viral infection
active replication, little effect on cell physiology
viral latency
cytolytic viral infection
apoptosis, necrosis, autophagy
altered cell morphology (inclusion bodies, syncytium formation)
altered cell physiology
abortive viral infection
entry of virus into cell that cannot support viral replication
transformation infection
causes cancer
DNA transformation cancer
HPV-cervical cancer
Herpes virus-burkitt’s lymphoma, HHV8
HBV-liver cancer, chronic inflammation
RNA transformation cancer
retrovirus-HIV
HCV-HCC
direct cancer formation from viruses
latent infection cause short lived cells to prolong life
disrupt host cell gene infection
indirect cancer formation from viruses
replication causes chronic inflammation
chronic inflammation causes neoplaisa
reduced immune function, and lower immune surveillance
detection of virus
not visible by light microscopy exclude bacteria, supportive care tissue, swab, blood, or exudates detect virus in cell culture viral antibody detection
molecular detection of viruses
DNA-PCR
RNA-RT-PCR
early symptoms of viral infection suggest
direct viral cytotoxicity
late symptoms of viral infection suggest
disease mediated by immune response
outbreak
community
epidemic
region
pandemic
worldwide
iceberg concept
most exposure to virus does not result in disease
severe disease and death are rare
innate immune response
first line of defense
innate immune cells recognize pathogen recognition receptor
phagocytic cells ingest and produce cytokines/chemokines
APC process antigen into peptides
peptides start effector cells to detect problem with infected cells
PRR bind what
pathogen associated molecular patterns (PAMPs)
RIG I
bind dsRNA
turn on interferon genes
steps to control viral infection
1-PRR recognize virus 2-PRR increase IFN a and b 3-cells release IFN that bind IFNa receptors 4- increase IFN stimulated genes 5-ISG inhibit replication cycle 6-IFN block virus replication
NK cells
identify cell surface changes and kill cells
monocytes/macrophages
phagocytose dying cells
remove infected cells
Type 2 IFN
IFN-y
important in adaptive immune response
made my NK and T cells
stimulates production of effector and memory T cells
adaptive immunity uses
CD4 and CD8 T cells
CD4 T cells
antigen specific response CD4T helper control intracellular pathogens respond to MHC class 2 produce lymphokines, cytokines, and chemokines to stimulate B and CD8 response
CD8 T cells
cytotoxic recognize peptides on MHC class 1 kill cells with Fas pathway and perforin produce cytokines clear most viral infections with CD8
acquired immune defense
IgM, A, G, E
neutralization
opsonization
cell lysis
memory cells
antigen specific
long lived
rapidly expand with reinfection
memory CD8
kill infected cells
memory b cells
produce antibodies
which antibody comes first
IgM then IgG
viral evasion mechanisms
elude immune detection
damage immune system
viral counter defenses
ways virus elude immune detection
antigen variation restrict gene expression reduce MHC cell surface expression infect anatomic sites poorly accessible to immune system establish immunologic tolerance
ways virus damages immune system
damage 1+ arm of immune system
immune suppression
viral counter defenses
reduce activation
express proteins that block IFN or complement
cytokine release favoring spread
cytokine that block immune response
