Chapter 9 Flashcards
Infection
presence or growth of a pathogen in the body
Viral infection
presence or growth of a pathogenic virus in the body
Theoretically, require one virion
Practically, require minimum infectious dose
Acute infection
Rapid onset, lasts for a short time
Persistent infection
lasts for a long time
Cytocidal infection
Cell death
To establish infection, a virus must
- Gain access to a permissive cell
2. Overcome host defense
Permissive cells
Have receptors for virus to bind
Have all requirements for viral replication
Permit viral replication inside
Interferon
protein produced by cell in response to viral infection
• α-, β-, and γ-
α-, β- interferon
produced by virus infected cell to protect nearby cells
bind to interferon receptor -> trigger anti-viral activity
γ- interferon
produced by T and NK cells to activate T cell-mediated immunity
Stimulate antigen-presenting, phagocytes, NK cells
NK cell
present throughout body, but mainly in blood
• recognize surface change of virus-infected cells
• Bind and kill them by releasing perforin or inducing apoptosis
• Release γ-interferon
Perforin
A pore-forming protein
Produced by killer cells of immune system
-> a channel in cell membrane of target cell-> cell death
APOBEC3 proteins
enzymes induce lethal mutation: dC->dU during reverse transcription -> interfere with replication of retroviruses
Lymphocytes
Key cell in specific(adaptive) immunity
B-cells and T-cells
B- cells
develope in bone marrow -> antibody-mediated immunity
T-cells
matured in thymus -> cell mediated immunity
Helper T cells (TH, CD4)
Cytotoxic T Cells (TC, CD8)
Antibodies
- Glycoproteins contain antigen binding sites
- Ig (immunoglobulins) IgG, IgM, IgA, IgE, IgD
- Produced by plasma cells derived from B cell
- Bind specific Ag on virion on infected cells
Outcomes of antibody binding to virus antigen
- Neutralization: block virus -> lose infectivity
- Increase phagocytosis: Fc region binds Fc receptor on phagocyte -> destroy virus
- Active complement -> cell lysis
Helper T cells
(TH, CD4)
Stimulate other immune cells by secreting cytokines
Cytotoxic T cells
(TC, CD8): “killer T cell”
Kill infected cells by releasing perforin or by inducing apoptosis
How T cell recognizes cell
Te cell receptor recognizes Antigen presented Major Histocompatability Complex class I of infect cell
RNA silencing
Post transcriptional gene silencing or RNA interference
• Induced by dsRNA
• Destroy sequence specific mRNA (a part of its sequence is the same as a part of inducing ds RNA)
• Dicer: cellular enzyme cleaves dsRNA
• siRNA: small interfering dsRNA (21-25 bp)
• RNA-induced silencing complex
• Activated RISC
o (+) RNA fragment is removed
o (-) RNA bind to mRNA w/ complement sequence
• mRNA cleaved in that region by RISC protein
Apoptosis
Programmed cell death in animal cell
A series of genetically programmed events leading to cell death
Bacteria have similar mechanism to protect bacterial population
Outcomes of virus-infected cell
Productive infection
Non-productive infection( no progeny virions produced)
Productive infection
Produce progeny virus
Cell death or
persistent infection: long term
Latent infection
persistent but not productive Viral genome maintained in infected cell Integrate into cell genome Or persist as multiple copies of circular genomes may be activated by induction
Abortive infection
Incomplete virus replication
Genome not persisted in infected cell
Causes of abortive infection
Non-permissive cell
Defective virus
Host defense
Abortive infection may also kill host cell
Disease
abnormal state of the body resulted from infection, chemical, physical or genetic effects
Symptom
subjective change in the body, felt by a patient as a result of disease
Sign
objective changes, observable detectable
Incubation Period
time between viral entry and appearance of syptoms
Viremia
virus present in bloodstream
Subclinical Infection
asymptomatic
Carrier
infected but asymptomatic
Disease in animal/humans
Infection may not cause disease
Not all viruses are pathogens
Some viruses are pathogenic only under certain conditions
8 Stages in Viral Pathogenesis (animal/human)
- Entry into host cell
- Primary virus multiplication
- Spread through host
- Host immune responses
- Secondary viral multiplication
- Cell/tissue injury
- Transmission
- Resolution, persistence, or death
Cell or tissue tropism
the tendency of a virus to favor replication in a specific type of cells or tissues
Fates of virus-infected host
Fate is determined by virus factors, host factors, and environment
Recovery
Persistent Infection
Death(cytocidal infection)
Recovery
clearance of virus; or become carrier
Persistent Infection
Chronic: virus always detectable
Latent: dormant, but viral genome is in host cell
Slow: very long incubation period
