Host-Pathogen Interactions Flashcards
pathogenicity
the ability of a virus to cause disease
pathogenesis
manner/mechanism of development of a disease
virulence
quantitative or relative measure of the degree of pathogenicity. depends on both the host and the virus
lethal dose 50
the dose of the virus required to cause death in 50%
infectious dose 50
the dose of the virus that will infect 50% of an experimental group of hosts/animals
ID50:LD50 ratio
ratio of the dose of a particular strain of virus that causes infection in 50% to the dose that kills 50%
the lower the ID50 and LD50…… the _______virulent
more
incubation period
from the time infected to the time where you see clinical signs
sequential steps of viral infection (5 steps)
entry of virus & primary replication; spread, tropism, & infection of target organs; virus-cell interactions; tissue & organ injury; shedding
skin defenses
keratin, low pH, fatty acids, bacterial flora, dryness
mucous membrane defenses
IgA, virucidal proteins
GI tract defenses
mucous membranes, acidity of stomach, alkalinity of intestine, lipolytic activity of bile, proteolytic activity of pancreatic enzymes, defensins, IgA, macrophages
respiratory tract defenses
mucocilliary blanket, alveolar macrophages, NALT, BALT, temperature gradient
disseminated infection
infection spreads beyond the primary site of infection
systemic infection
if a number of organs or tissues are infected
apical release of virus
facilitates virus dispersal
basolateral release
provides access to underlying tissue, facilitates systemic release
viremia
the presence of a virus in the blood. may be free in the blood or in a cell in the blood
passive viremia
direct inoculation of the virus into the blood. bite of arthropod, infected syringe
primary viremia
initial entry of virus into the blood after infection (1st time virus in the blood)
secondary viremia
virus has replicated in major organs and once more has entered the blood
active viremia
viremia following initial virus replication in host. release of virions from the initial site of replication.
virus interaction with macrophages (5 things can happen)
1- virions are phagocytosed
2- virions replicate inside macrophage, activate macrophages
3- tissue invasion (trojan horse)
4- phagocytosed and transfered to adjacent cells
5- failure to phagocytose, prolonged viremia
virus spread/interaction with endothelial cells
fenestrae (small pores), trafficking lymphocytes or monocytes, transcytosis (vesicular transport), replication in endothelial cells
neurotropic virus
viruses that can infect neural cells
neuroinvasive virus
viruses that can ender the CNS
neurovirulent virus
viruses that cause disease of nervous tissue
Herpes simplex virus (neuroinvasiveness, neurovirulence)
low neuroinvasiveness
high neurovirulence
Mumps virus (neuroinvasiveness, neurovirulence)
high neuroinvasiveness
low neurovirulence
Rabies virus (neuroinvasiveness, neurovirulence)
high neuroinvasiveness
high neurovirulence
neural spread of viruses (transport)
via axons, perineural lymphatics, endoneural space, schwann cells
retrograde spread
virus travels opposite direction of nerve impulse flow
anterograde spread
travel in the same direction as nerve impulses
centripetal movement of virus
towards the CNS/brain
centrifugal movement of virus
from the CNS to other body locations
spread of viruses to the CNS via…
olfactory routes
blood-brain barrier
acute infection
usually intensive shedding over a short period of time
persistent infection
shed at lower titers for months to years
tropism
the specificity/affinity of a virus for a particular host tissue
pantropic virus
can replicate in more than one host organ/tissue
what determines viral tropism
receptors on host cells, viral attachment proteins, viral enhancers, cell proteases, temperature, acid lability, transcriptional control of tropism, anatomic barriers, host organ response
rash
general term applied to any temporary eruption on the skin
vesicles
fluid filled cavities
ulcer
raw opening in skin due to sluffing of necrotic tissue
nodules
growths
warts
benign skin growths (papillomavirus)
papules
seen in papular stomatitis in cattle
erythema
reddening of the skin (hog cholera)
DIC (disseminated intravascular coagulation)
complication arising from viral infection of blood vessels. wide spread activation of the clotting cascade that results in the formulation of blood clots in small vessels in the body.
teratogenesis
abnormal development or arrest in development of the embryo or fetus
porencephaly
holes in the brain
BVDV in cattle
cow infected within 2-4mo after conception: calf infected with virus for life
viral-infected immunopathology
tissue injury mediated by host immune response to virus infection. the price paid by the host to clear viral infection
cytokines
broad and loose category of small proteins that are important in cell signaling. act as mediators and regulators of immune processes but also cause inflammation
monokines
cytokines produced by a mononuclear phagocytic cell
lymphokines
cytokines produced by activation lymphocytes (Th cells)
interleukins
cytokines that act as mediators between leukocytes
infectious bursal disease
virus replication causes atrophy of the bursa and a severe deficiency of B lymphocytes resulting in immunosuppression
inapparent viral infection
clinical signs an symptoms are not evident, too few cells may be infected, stimulate host immune response, possible source of virus spread
acute viral infection
short term infection, rapid clearance from the immune response
persistent viral infection
infectious virus is demonstrable continuously, whether or not there is ongoing disease
latent viral infection
infectious virus is not demonstrable except when reactivation occurs. ex. Herpesvirus
chronic viral infection
virus is continuously shed from or is present in infected tissue. ex. foot and mouth disease
slow intention
prolonged incubation period, lasting months or years
cytocidal effects
lysis & apoptosis
non-cytocidal effects
persistent infection
cell transformation effects
tumor cell formation
cytopathic/cytopathogenic effects
damage or morphological changes to host cells during virus invasion
pyknosis
degenerative condition of a cell nucleus marked by clumping of the chromosomes, hyperchromatism, and shrinking of the nucleus.
cell fusion (syncytium or polykaryon formation)
fusion of the plasma membranes of four or more cells to produce an enlarged cell with 4+ nuclei. prone to premature death
inclusion bodies
abnormal structures in a cel nucleus or cytoplasm or both, such as aggregates of proteins, having characteristic staining properties and associated with certain viral infections
negri bodies
ribonuclear proteins produced by the rabies virus
owl’s eye inclusion bodies
seen in herpesviruses
adenovirus inclusion bodies
crystalline aggregates of virions in adenovirus infections
acidophillic staining
recognize/affinity for acid dyes, such as eosin. appear pinkish upon staining
basophillic staining
recognize/affinity for basic dyes, such as hematoxylin. appear purple-blue upon staining
apoptosis
programmed cell death. a mechanism of cell suicide that the host activates as a last resort to eliminate viral factors before progeny virus production occurs
intrinsic (mitochondrial) pathway
activated as a result of increased permeability of mitochondrial membranes subsequent to cell injury, such as that associated with a viral infection
extrinsic (death receptor) pathway
activated by engagement of specific cell-membrane receptors, which are members of the TNF receptor family. thus binding of the cytokine TNF to its cellular receptor can trigger apoptosis
ADCC
1- antibody binds Ag to surface of target cell
2- Fc receptor on NK cell recognized bound Ab
3- cross-linked Fc receptors signals the NK cell to kill the target cell
4- target cell dies by apoptosis
