Viral Pathogenesis Flashcards
modes of transmission
direct contact, injection, transplantation, fecal oral (+/- envelope important)
how often are we exposed to pathogen
constantly; they are everywhere though they vary based on living conditions
reasons viruses continue to persist in population
health, nutrition, genetic makeup, age, immune status
what is an outbreak
introduction of a virus into a new location which originates from a common source
how is the identification of the source of an outbreak so important
to stop the outbreak
what is an epidemic
introduction of a new strain of virus to an immunological naive population which occurs over a LARGER geographical area
what is a pandemic
worldwide epidemic
are a majority of viral disease symptomatic
no but those that target essential tissues/organs –> serious disease
symptoms and severity of viral diseases depend on what
- Patient’s ability to prevent/resolve infection
- Virulence and target tissue
- Ability to repair damage
what are some mechanisms of viral pathogenesis
- Circumvent protective barriers
- Evade immune control
- Kill cells or trigger destructive immune and inflammatory response (control infection)
- Possibly transform cells
what are some inherent barriers for host defenses
– Skin
– Mucous
– Ciliated epithelium
– Low pH
what are some induced barriers for host defenses
– Fever
– Low pH
– Humoral and cellular components
what are some non specific host defenses
– Interferon
– Complement
– Other cytokines
what are some specific host defenses
– Antibody production
– Specific immune system
when does transcription of interferons occur?
transcription only occurs after exposure to an inducer – viral infection, dsRNA – RNA viruses best
what do viruses do to our immune responses
it suppresses them
what can immune response to viral infection cause
tissue injury
example of immune response to viral infection causing tissue injury: what can circulating immune complexes lead to?
deposits —> arthritis
aka CMV
in dengue, what is the mechanism in which tissue injury happens?
hemorhagic shock syndrome: fixation of complement by circulating immune complexes –> release of products via complement cascade –> sudden increase in vascular permeability, shock, death
basic steps of viral disease
- Acquisition
- Initiation of infection at the primary site
- Incubation period (amplification, spread to secondary site maybe)
- Replication in target tissues
- Immune responses (limit AND contribute)
- Transmission
- Resolution or persistent infection
can viruses cause more than one disease
yeah
what is it called for viruses to lose their virulence
attenuation
result of viruses encoding their virulence factors
– Promoting replication, transmission
– Access and binding to target tissue
– Escape of immune system
outcomes of viral infection
1) Abortive - Failed “attempts”: no virus multiplication
2) Lytic - Cell death
3) Persisting - Infection without cell death, selection of ideal target cell subsets (Chronic – nonlytic, productive)
4) Latent-recurrent infection - Presence of virus without virus production but with potential for reactivation
difference between replication of virus during acute infection and during chronic infection via continuous productive infection
both of them after virus infects host cell –> entry and uncoating –> gene expression –> assembly and release (they have antigens for B and T cell recognition)
but in chronic a variant strand of the virus (one that was not killed) will begin the process all over again and produce variant antigens for B and T cell recognition
how is latency established
- modulation of viral gene expressions
- viral subversion of cellular apoptotic pathway
- avoidance of clearance by the immune system
- selection of cell subsets ideal for long-term maintenance of the viral genome
when does persistence occur in viral infections
when the cell is not killed - could be chronic, latent, recurrent, immortalizing, transforming
what are determinants on if a virus will be lytic or persistent
- access to target tissue
- stability
- ability to cross barriers, establish viremia, and spread
viruses apply a lot of avoidance strategies to persist. what are some of these strategies?
- viruses can alter / interfere with the processing of viral peptides by professional APCs
- can downregulate co-stimulatory and/or MHC molecules (required for T cell signaling, expansion)
- inhibit the differentiation of AP conventional dendritic cells, infect effector T and B cells directly
all of these are just ways in which the infected host’s innate or adoptive immune system is suppressed
what does the susceptibility of host cell to virus depend on?
presence of receptor for virus attachment
during what basic steps of viral disease does one see the prodrome phase?
- It could just be during acquisition
- Or it could be in acquisition, primary and/or secondary site replication
during what basic steps of viral disease does one see the symptoms of disease
at the sites of replication or at the target tissue
outcome and severity of viral infection can be due to what factors?
- virus strain, inoculum size
- health of host host response system (immune response helps determines severity, duration)
what does the target tissue of a virus determine
the predominant disease
most common site of viral infections and disease
oral and respiratory tract (upper and lower)
with primary infections spreading to other sites
how do oral and respiratory tract viral infections spread
respiratory droplets, contact, food, water, saliva
example of a respiratory tract viral infection
influenza
mechanism in which influenza occurs
aerosol inoculation of virus –> replication in respiratory tract –> desquamation of mucus secreting and ciliated cells –> influenza syndrome
desquamation of mucus secreting and ciliated cells can lead to what?
secondary bacterial infection (pneumonia), primary viral pneumonia, CNS muscle involvement
what other things add to the desquamation of mucus secreting and ciliated cells that lead to influenza
antibody, interferon induction, T cell responses
though antibody and T cell responses do lead to future protection
what are consequences of GI tract viral infection
no symptoms –> gastroenteritis, vomiting, diarrhea
Generally self limiting
what promotes GI tract viral infections
poor hygiene
GI tract viral infections has more significant effect in what population
infants
example of a GI tract viral infection
rotavirus
transmission of rotavirus
fecal matter especially in day care settings (respiratory possible)
who is at a risk for GI tract viral infections
Infants
how do you control rotavirus
hand washing and isolation
live vaccines
effects of rotavirus
from asymptomatic –> viral disease
what is rotavirus resistant to
environmental and gastrointestinal conditions
virus induced skin diseases
exanthems and hemorrhagic fevers
major classifications of viral rashes
- macules (flat colored spots)
- papules (slightly raised areas from immune response)
- nodules (larger raised areas of the skin)
- vesicular lesions (blisters likely to contain virus)
what do hemorrhagic fevers infect
endothelial cell lining of the of the vasculature, possibly compromising the structure of the blood vessel
