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Microbio Exam 3 Lecture 2
Terms in this set (34)
what are the three levels of tropism?
what are the four determinants of tropism?
host immune response
virus replication can be
productive or abortive in cells
may be different in cell culture vs. organism
cellular tropism +
tissue-specific antiviral responses
species tropism/host range
first two levels of tropism + overall
host immune and inflammatory responses
Receptor expression is what type of tropism determinant for influenza virus?
host range (
human to human
transmission requires that the
highly pathogenic avian H5N1 influenza viruses undergo
in the human respiratory tract due to what?
the presence of some cells with
alpha (2,3) linked sialic acids
(high doses needed)
what are the four classes of viral virulence genes?
1) affect the ability of the
virus to reproduce in vivo
2) modify the
host's defense mechanisms
virus spread in and among hosts
describe the HSV (herpes simplex virus) gene
what two enzymes does it encode in neurons?
thymidine kinase and nucleotide reductase
in neurons (non-dividing cells) needed to increase nucleotide metabolism
virus with reduced virulence
what are four ways of measuring viral virulence?
time to death
or the appearance of other symptoms
Virus-induced tissue damage
can be measured directly by examining histological sections
Median Lethal Dose:
the number of infectious particles
that will kill 50% of the infected hosts
Median Infectious Dose: the number of infectious particles that will
establish an infection in 50%
of the challenged hosts
what are several symptoms of viral infection resulting from the release of what two things?
release result in fever, malaise, aches, pains, nausea
what are the two arms of the immune response to viral infection?
innate and adaptive
for what type of viruses is it the primary basis of disease?
what are two defensive effects?
what are two destructive effects?
clinical signs and symptoms of viral disease
(e.g., fever, tissue damage, aches, pains, and nausea)
result primarily from the host's immune response to infection
price paid by the host to eliminate a viral infection
immunopathology is the primary basis of disease
caused by activated T cells, B cells, antibodies, or an excessive innate response
the consequences can be severe, even life threatening
CTL removal of infected cells
ADE (antibody dependent enhancement)
CTL mediated destruction of healthy cells
Antibody-dependent enhancement (ADE) and Dengue virus
four serotypes of dengue virus (DENV)
wide range of symptoms (inapparent infection, dengue fever, fatal dengue haemorrhagic fever (DHF) with shock)
heterotypic, non-neutralizing Ab from a primary dengue virus (DENV) infection binds to an infecting DENV particle
during a subsequent heterotypic infection but cannot neutralize the virus
Ab-virus complex attaches to the Fcγ receptors (FcγR) on circulating monocytes,
facilitating infection of cell types not infected in the absence of antibody
increased viral reproduction and higher risk of severe disease
complication for vaccine development
what are four patterns of the time course of viral infection?
, reactivating infection
acute viral infections
what event do they often cause?
what is their reproductive output?
how do the innate and adaptive immune systems respond to them?
how long is the course of disease?
High reproductive output
(many virions produced)
Breaks physical, intrinsic, innate defenses but
blocked by adaptive immunity
Short (sometimes severe) course
Rapid production of infectious virions, resolution/elimination
Memory T and B cell response against reinfection
Hard to control
When people feel ill, infection has spread to new host
Antigenic variation is advantageous in acute infections
e.g. influenza virus - high mutational rate (vaccine reformulation)
Rhinovirus - > 100 serotypes
what type of variation is advantageous in
give an example of this
Antigenic variation (Rhinovirus has 100+ serotypes)
period of infection
before symptoms are obvious
inapparent acute infections
give several examples
there are sufficient virions for what, but not what?
successful acute infection that
produces no symptoms or disease
sufficient virions are made to maintain infection in population but below the threshold of inducing symptoms in infected individual
results in rise in antiviral antibody level in otherwise healthy individual
~90% of poliovirus infections
~30% of norovirus infections
26-83% of Zika virus infections
45-86% of influenza virus infections
what is another name for it?
will there be an immune response?
infects susceptible cells/host
Replication is not completed
(e.g. essential gene not expressed)
inflammatory responses may develop, apoptosis or cytokine production may be initiated
what other type of infection does it fall under?
special type of
certain DNA viruses or retroviruses
Infected cells may exhibit altered growth properties and begin to proliferate faster than uninfected cells
what are the two types?
describe the reproductive output
what viruses are often of this type?
primary infection not cleared efficiently
(all host defenses are ineffective)
Virus produced continuously or intermittently
Ineffective intrinsic or innate immune response during primary infection
modulation of adaptive immunity for maintenance
Lower reproductive output
(few virions produced)
chronic and latent
describe the level of virions
persistent infection that is
low levels of virions
what are several characteristics?
are infectious virions detectable?
persistent infection that
lasts the life of the host
no infectious virions detectable
viral gene products promoting productive replication not made,
infected cells poorly recognized by immune system
, viral genome persists intact
reactivation results in productive infection and transmission
describe the sequence of herpes simplex 1 infection (oral herpes) AND later latent infection
what is a major factor in its spread?
what type of infection is it an example of?
infection of epithelial cells
to nucleus of trigeminal ganglia
enters the nucleus
remains as an episome in a latent state
under stress conditions, HSV‐1 reactivates
productive infection in neurons
capsids travel by anterograde transport to epithelial cells
new productive infection
31% in children aged 6-14; 49% in people aged 14-49; 80-90% in the population over 65 years
20-40% of infected people develop symptoms
healthy humans are reservoirs of herpes viruses
is a major factor in the spread
example of a latent infection
DNA molecule that replicates independently
of chromosomal DNA
inflammation in the liver
causing scarring and
describe the hepatitis C virus
how does the infection spread?
what types of drugs are used to treat it?
what percentage of patients can be cured with these drugs?
hepatotropic RNA virus
unsafe injection drug use and unsterile medical procedures
64 and 103 million people are chronically infected
direct-acting antiviral agents (DAAs)
have become available (>2011)
target three proteins involved in life cycle
Combination of two or three of these DAAs can cure >90% of patients
What needs to happen during influenza virus evolution for an avian influenza virus to become epidemic or pandemic in the human populations?
Avian influenza viruses bind to a-2,3SA preferentially, while human influenza viruses bind to a-2,6SA. Thus for an avian influenza virus to spread easily to the human population, it
must gain the ability to bind to a2,6SA
which immune barriers do persistent infections cross?
infection overcomes intrinsic, innate, and adaptive immune responses
THIS SET IS OFTEN IN FOLDERS WITH...
Microbio Exam 3 Lecture 1
Microbio Exam 3 Lecture 3
Microbio Exam 3 Lecture 4
Microbio Exam 3 Lecture 5
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