Viral Pathogenesis - AuCoin Flashcards
What are the four cellular responses to viral infection?
- no effect
- cytopathology
- hyperplasia
- cancer
Can you have infection without symptoms?
yes
When the cell response is inclusion body formation, cell transformation, or cell dysfunction, what is the host response?
mild to severe disease
what are inclusion bodies?
nuclear or cytoplasmic aggregates of viral proteins that are stainable
T/F: most viral infections are symptomatic
false; most are subclinical
T/F: the same disease may be caused by a variety of viruses
true
T/F: the same virus may cause a variety of diseases
true
T/F: viral morphology has a correlation to disease symptoms
false
pathology is determined by host and viral factors and is influenced by patient (blank)
genetics
a virus is more (blank) if it commonly causes more severe symptoms in a patient
virulent
What are important factors to consider when looking at the steps of viral pathogenesis for making a vaccine?
- cellular recpeptor for viral entry into host
- route of infection–respiratory/GI/blood; what Abs are made at 1ry site of rep
- How is it transmitted
- Is there immune mediated cell damage
- Is the virus completely cleared or does it persist and does it SHED
why, if both measles and rhinovirus enter via the lungs, that rhinovirus has a short incubation while measles long?
rhinovirus will replicate in the lungs and cuase symptoms there, while measles may have to hitch a ride on a macrophage to get to the parotid gland to cause infection
What is the most common route of spread through the host?
blood or lymphatics
what is the presence of virus in the blood called?
viremia
Viruses may be free in the blood or associated with a specific (blank)
cell type
T/F: viruses may spread via nerves
true (like HSV and rabies)
What is the difference between primary and secondary viremia?
1ry viremia is the virus in the blood immediately after infection on its way to target tissues.
2ndry viremia is the virus reentering the blood after replicating in its target organs
What determines the pattern of systemic illness caused by a virus?
tropism, what tissues it infects
The relation between cell surface receptors and viral (blank) determines tropism
VAPs
T/F: the coded function of the cell surface receptors that bind VAPs is to solely bind to VAPs
FALSE, they just happen to have affinity for the VAPs
A lack of what would keep a virus from replicating even if it did infect a cell?
a lack of cellular transcription factors
what is the major immune response elicited with viral infection?
IFN production
What two types of cells are activated to respond to the site of viral infection?
mononuclear cells and lymphocytes
What do CTLs recognize that allow killing of virally infected cells?
viral polypeptides displayed on the cell surface
Neutralizing Abs directed against what two viral structures prevents viral infection?
capsid or glycoproteins
Secretory Ig(blank) protects against infection of viruses via the respiratory or GI tracts giving MUCOSAL IMMUNITY
IgA
How do IFNs prevent viral infection?
they interfere with viral rep via activation of NK cells and macrophages, increase recognition of infection by up-regulating Ag presentation to T cells and increase the ability of uninfected cells to resist new infection.
What systemic symptoms are associated with IFNs?
aching muscles and fever
How soon does IFN production begin post infection?
hours
IFNs are part of the (innate/adaptive) response to viral infection
innate
What is another name for IFNg?
IFN type II
IFNg is essential for defense against what types of infections?
viral, some bacterial, and some protozoal infections
IFNg activates (blank) cells and induces (blank) expression
macrophages; MHC
Dendritic cells secrete (blank)times more IFN than a similarly induced fibroblast
1000x
a cell must be (blank) for a viral infection to occur
permissive
Are ssRNA or dsDNA viruses stronger inducers of IFN synth?
ssRNA
T/F: bacterial endotoxin and dsRNA can induce IFN synth
true
when does Ab appear in response to viral infection
days after
IFNs play an important role in (specific/nonspecific) defense
nonspecific
At what day does IFN titer peak?
day 5
At what day does Ab titer begin to rise?
day 10
T/F: IFN protects the virally infected cell that produced the IFN in the first place
false
T/F: IFN itself is an antiviral agent
false
What happens once IFN binds to a cell?
activates transcription factors that translocate into the nucleus to mediate IFN-inducible GENES
What are the IFN-inducible antiviral proteins?
protein Kinase R (PKR) and Rnase L
What is the function of PKR?
dsRNA dependent protein kinase that phosphorylates and INACTIVATES eIF-2 to PREVENT CELL AND PROTEIN SYNTH
What is the function of Rnase L?
destroys ALL RNA in the cell, both viral and host
What two ways can viruses block IFN activity?
they can block IFN expression or IFN induced signal transduction
virally encoded immunomodulatory proteins inhiibit (blank) function
MHC
T/F: viruses may inhibit general cytokine activity
true
Viruses mutate and change antigenic proteins to (blank)
evade the immune system
T/F: most viral infections are self-limiting
true
(blank) infections give no overt sign of their presence
subclinical
A replicating virus that is continuously detectable at low levels a is (blank) infection
chronic or persistent
What does it mean when an infection is latent?
virus is in a hidden form and no new virus is being made
Intermittent flare ups of clinical disease happen in (blank) patients with a chronic infection
immunocompromised
HSV 1 primarily infects the mouth while HSV2 infects the (blank)
genitals
Why do generalized skin rashes develop as a result of viral infections?
the virus spreads to the skin from the blood stream following rep at a different site
Does polio first replicate at the sight of infection or at its target location?
site of infection
How does a virus gain access to the CNS?
replication within cerebral endothelial cells
What are the two ways that viruses can gain access to the CNS?
rep in cerebral endothelial cells or via neuronal transport with initial uptake at sensory nerve endings
pathologic reaction may include CNS cell necrosis, inflammation, and phagocytosis by (blank cells)`
glial cells
What cells, when infected, will loosen the tight junctions between the cerebral endothelial cells?
glial cells
What is the most common route of viral infection?
infection of the respiratory tract via inhalation of aerosolized droplets
What are the host defenses against respiratory tract infections?
mucus, ciliary action, lymphoid cells , alveolar macrophages and secretory IgA
Do all viruses that enter in the lung as a primary site remain in the lung?>
No, some travel to develop other symptoms, like chicken pox
How are GI viruses spread?
contaminated food or fecal oral route
What types of viruses normally cause GI infections and why?
NAKED CAPSID; they are exposed to harsh elements like acid, bile salts, and proteolytic enzymes
rota virus and Norwalk virus both cause (blank)
GE
Is the incubation period of Gi viruses short or long?
short
Do maternal viral infections result in fetal viremia?
NO
T/F: Maternal-fetal viremia is a serious danger to the fetus
true
What two viruses are resonsible for congenital defects?
Rubella and HCMV
Deafness, eye abnormalities, and congenital heart disease are defects caused by (blank) virus
Rubella
What is the LEADING cause of infectious deafness?
HCMV
What virus causes deafness, learning disabilities, and mental retardation?
HCMV
T/F: antiviral agents work by inhibiting cellular responses to viral infection
false; they inhibit viral functions within the cell but not the cellular functions themselves
What are the stages of infection that are targets for antivirals?
attachment of virus to host cells uncoating of the viral genome viral nucleic acid synthesis translation of viral proteins release of progeny virus
What are the four general classes of antivirals?
- Nucleoside analog
- Reverse transcriptase inhibitor
- Protease inhibitor
- Fusion inhibitor
How do nucleoside analogs work?
Incorporate a terminal nucleoside in the viral Pol
How do RT-inhibitors work?
bind to RT to disrupt enzyme catalytic site
How do protease inhibitors work?
inhibits viral proteiase that is required at the late stage of HIV rep cycle
How do fusion inhibitors work?
Prevent viral and cell membrane fusion in ENTRY of HIV into cells
What is the most cost effective method of preventing serious viral infections
IMMUNIZATION
What are the targets of viral vaccines?
viral glycoproteins
T/F: viral immunity is also conferred via Abs to viral core proteins and non-structural proteins (like riboproteins)
FALSE
Viruses that infect the mucosa require what Ig class?
IgA; influenza
Viruses that have a viremic spread are controlled with what Ig class?
IgG; polio, hepatitis A/B, varicella
Cell mediated immunity is used against systemic infections to control the (blank)
latent state; herpesvirus
Multiple viral (blanks) can complicate the dev of a vaccine
serotypes; rhinovirus OR rapidly mutating viruses (HIV)
Attenuated live vaccines antigenically overlap with (blank) viruses
wild-type
How do you make an attenuated virus?
cell passage in animals or cell culture
After being vaccinated, where do you want the vaccine to induce an Ab response and resistance?
at the portal of entry
Do live viruses or killed viruses give longer immunity?
live viruses
Do live or killed viruses give more effective protection?
live
what types of Ig are produced by killed viruses?
IgG
What types of Ig are produced by live viruses?
IgG and IgA
Do killed viruses produce mucosal immunity?
NO, no IgA!!
Compare cell mediated immunity in killed vs live viruses>?
killed= poor live= good
Are heat killed or live viruses stable at room temp?
heat killed
T/F: live virus vaccines can be given in combos
true
T/F: antibody response to each component of these vaccines is comparable with antibody response to the individual vaccines administered separately
ture
