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Virology > Host Pathogen Interaction > Flashcards

Host Pathogen Interaction Flashcards

1
Q

Pathogenicity

A

Ability of virus to cause disease in hose (harm it)

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2
Q

Pathogen

A

virus which causes disease

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3
Q

Pathogenesis

A

manner/mechanism of development of a disease

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4
Q

Virulence

A

quantitative or relative measure of the degree of pathogenicity of the infective virus
Not an absolute property of a virus- depends on many variables

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5
Q

Avirulent

A

not virulent (not harmful to host)

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6
Q

Lethal dose 50

A

LD50
Dose of virus required to cause death in 50% of animals
Lower is more virulent

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7
Q

Infectious dose 50

A

ID50
Dose of virus that will infect 50% of an experimental group of hosts/animals
Lower is more virulent

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8
Q

Routes of entry into host

A

Skin
Mucous membranes
GI tract
Respiratory tract

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9
Q

Skin defenses

A 
Dense outer layer of keratin
Low pH
Presence of fatty acids
Bacterial Flora
Dryness
Components of innate and Adaptive immunity (migratory dendritic cells: Langerhans cells)
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10
Q

Transcutaneous injection

A

Bite of arthropods
Bite of infected animal
Contaminated objects

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11
Q

Mucous membranes defenses

A

IgA

virucidal proteins

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12
Q

GI tract defenses

A

Mucous membrane of oral cavity and esophagus
Acidity of the stomach
Alkalinity of intestine
Layer of mucus covering the gut
Lipolytic activity of bile
Proteolytic activity of pancreatic enzymes
Defensins (host defense peptides) with antiviral activity
IgA
Scavenging Macrophages

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13
Q

Respiratory tract defenses

A 
Mucociliary blanket
Alveolar macrophages
NALT
BALT
Temperature gradient (33-37) (nasal passages- alveoli)
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14
Q

Disseminated infection

A

Infection spreads beyond the primary site of infection

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15
Q

Systemic infection

A

If a number of organs or tissues are infected

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16
Q

Virus spread in host

A

Directional shedding of viruses from the infected epithelium is critical to subepithelial spread
Apical release facilitates virus dispersal, whilst basolateral release provides access to underlying tissues, facilitating systemic spread

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17
Q

Viremia

A

Presence of a virus in the blood

Virus may be free in blood or in a cell, such as lymphocytes

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18
Q

Primary viremia

A

Initial entry of virus into blood after infection

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19
Q

Secondary viremia

A

Virus has replicated in major organs and once more entered circulation

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20
Q

Passive viremia

A

Direct inoculation of virus in blood.
Bite of arthropods or contaminated syringe
No initial replication elsewhere in host before

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21
Q

Active viremia

A

Viremia following initial virus replication in host.

Release of virions from the initial site of replication, such as lymphatics or epithelium of intestine, to blood stream

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22
Q

Neurotropic virus

A

Virus that can infect neural cells

Infection may occur by neural or hematogenous spread

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23
Q

Neuroinvasive virus

A

Virus that can enter the CNS (spinal cord and brain) after infection of a peripheral site

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24
Q

Neurovirulent virus

A

Virus that causes disease of nervous tissue, manifested by neurological symptoms and often death

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25
Q

Herpes

A

Low neuroinvasiveness bc it always enters PNS but rarely enters CNS
high neurovirulence bc severe when in CNS

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26
Q

Retrograde spread

A

Travel opposite direction of nerve impulse flow

Invades axon terminals and then spread to Dendrite or cell body, and then cross synapse to reach next axon terminal

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27
Q

Anterograde spread

A

Travel in direction of nerve impulse flow
Virus invades dendrites or cell bodies and then spread to axon terminals, then cross synaptic contacts to invade dendrite of next neuron

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28
Q

Neural spread of virus through:

A

Olfactory route

Blood Brain Barrier

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29
Q

Acute infection

A

Usually intensive shedding over short period of time

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30
Q

Persistent infection

A

Can be shed at low titers for months to years

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31
Q

Tropism

A

Specificity/affinity of a virus for a particular host tissue

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32
Q

Pantropic viruses

A

Can replicate in more than one host organ/tissue

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33
Q

Vesicles

A

Fluid filled sacs/elevations of skin

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34
Q

Ulcers

A

Opening in the skin causes by sloughing of necrotic tissue, extending past the epidermis

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35
Q

Nodule/tumor

A

Palpable, solid, elevated mass
Nodules with distinct borders
Tumors extending deep into dermis

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36
Q

Warts

A

Benign skin growths that appear when virus infects top layer of skin

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37
Q

Papule

A

Solid elevations without fluid with sharp borders

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38
Q

Erythema

A

Reddening of skin, consequence of systemic viral infections (endothelial injury in blood vessels throughout body, including those of the subcutaneous tissues)

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39
Q

Injury to GI tract

A

Ingestion
Hematogenous spread, systemic infection

Destruction of enterocytes due to viral replication, hypersecretion
Gastrointestinal disease, malabsorption, diarrhea
Pronounced dehydration, acidosis, hemoconcentration

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40
Q

Injury to Respiratory tract

A 
Loss of ciliary activity
Loss of integrity of lining mucus layer
Multifocal destruction of epithelium
Inflammation
Exudation
Influx of inflammatory cells 
Obstruction of air passages
Hypoxia and respiratory distress
Secondary bacterial infection
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41
Q

Injury to CNS

A

Encephalitis or encephalomyelitis
Characterized by neuronal necrosis, phagocytosis of neurons (neuronophagia) and perivascular infiltrations of inflammatory cells (perivascular cuffing)
Progressive demyelination- canine distemper
Neuronal vacuolation- prion disease

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42
Q

Damage to endothelium

A

Hemorrhages
Petechiae
Ecchymoses

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43
Q

Disseminated intravascular coagulation

A

Clots form in small blood vessels throughout body
organs do not get blood
organ failure
Later stages, raw material for clot exhausted due to over use
no clot formation in later stages
hemorrhages throughout body

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44
Q

Teratogenesis

A

Abnormal development or arrests in development of embryo or fetus
May result in death or malformations during the antenatal period

45
Q

Virus induced immunopathology

A

Tissue injury mediated by host immune response to virus infection
Price paid by host to clear a viral infection
Depends on the delicate balance between the protective and destructive effects of the host immune response to viruses

46
Q

Immunopathology

A

Tissue damage mediated by hypersensitivity reactions
Autoimmune diseases (moon blindness in horse)
Inflammation- mediated tissue damage (fibrosis)
Immunodeficiency disorders

47
Q

Roll of T cells

A

Cytotoxic cell mediated lysis/killing of infected host cells
Release of cytokines from T cells (CD4+ and CD8+) and other cells that cause inflammation and tissue damage that becomes chronic against persistent virus infections

48
Q

Toll like receptors TLRs

A

Persistent activation of these receptors of innate host cells by viruses causes production of pro-inflammatory cytokines and interferons, as well as signals that recruit and activate cells involved in inflammationIn

49
Q

Injury

A

Can also be mediated by free radicals
Like Nitric oxide
Superoxide

50
Q

Toxicity from antibody responses

A

Antibody responses to viruses may also contribute to tissue damage

51
Q

Immunosuppression

A

Infectious bursal disease: Virus replication causes atrophy of the bursa and a severe deficiency of B lymphocytes, resulting in immuno suppression
As a result, infected birds become susceptible to other pathogens

52
Q

Inapparent infections

A

Clinical signs and symptoms are not evident
Too few cells may be infected
Stimulate host immune response
Possible source of virus spread

53
Q

Acute infection

A

Short term infection
Short clinical course
Rapid clearance from host immune response

54
Q

Latent infection

A

Persistent infection
Infectious virus not demonstrable except when reactivation occurs
Reactivation is often stimulated by immunosuppression and or by the action of a cytokine or hormone

55
Q

Chronic infection

A

Persistent infection
Acute infection followed by chronic infection in which the virus is continuously shed from or is present in infected tissue

56
Q

Slow infection

A

Persistent infection
Prolonged incubation period, lasting months or years
Slow progressive lethal disease

57
Q

Effects of viruses on host cells

A

Cytocidal (cell death- lysis, apoptosis)
Non-cytocidal (persistent infection)
Cell transformation (tumor cells)

58
Q

Cytopathic effect

A

Damage or morphological changes to host cells during virus invasion
Cytopathogenic effect

59
Q

Cell fusion

A

Syncytium or polykaryon formation
Involved fusion of the plasma membranes of four or more cells to produce an enlarged cell with four or more nuclei.
Prone to premature cell death
Result from the fusion of an infected cell with neighboring infected or uninfected cells

60
Q

Inclusion bodies in host cell during viral infection

A

Abnormal structure in a cell nucleus or cytoplasm or both
Like aggregates of proteins, having characteristic staining properties and associated with certain viral infections
Help to identify certain viral infection

61
Q

Inclusion bodies can be:

A

Accumulation of viral components
Resultant from degenerative changes in cell
Crystalline aggregates of virions

Intracytoplasmic or intranuclear or both
single or multiple
large or small
round or irregular in shape
Eosinophilic/acidophilic or basophilic
62
Q

Acidophilic staining

A

Affinity for acid dyes- stains pink

63
Q

Basophilic staining

A

affinity for basic dyes- stains blue

64
Q

General mechanisms of virus induced cell injury and death

A

Inhibition of host-cell nucleic acid synthesis
Inhibition of host cell RNA transcription (mRNA production and processing)
Inhibition of host cell protein synthesis

Some viruses cause lysosomes to release their hydrolytic enzymes, which then destroy the host cell

Interference with cellular membrane function

65
Q

Apoptosis

A

Process of programmed cell death
Mechanism of cell suicide that host activates as last resort to eliminate viral factories before progeny virus production complete
Different from lysis

66
Q

Lysis

A

Viral replication complete

Host cell destroyed and new virions released (burst out)

67
Q

Apoptotic pathways

A

Activation of host cell ccaspase enzymes mediate death of the cell
Once activated, caspases are responsible for degradation of the cell’s own DNA and proteins
Mitochondrial pathway
Death receptor pathway

68
Q

Intrinsic (mitochondrial) pathway

A

Mitochondrial pathway is activated as a result of increased permeability of mitochondrial membranes subsequent to cell injury, such as that associated with a viral infection

69
Q

Extrinsic (death receptor) pathway

A

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

70
Q

T cells- apoptosis

A

Cytotoxic T lymphocytes and NK cells can also initiate apoptosis of virus-infected target cell, utilizing preformed mediators such as perforin and granzyme that directly activate caspases in target cell

71
Q

Antibody dependent cell mediated cytotoxicity resulting from surface membrane fusion of enveloped viruses

A

Viral glycoproteins are retained on cell surface and since these are antigenic the cell can become a target of the immune system of the host

Ab binds Ag on surface of target cell
Fc receptors on NK cell recognize bound antibody
Cross-linking of Fc receptors signals the NK cell to kill the target cell
Target cell dies by apoptosis

72
Q

Cell transformation

A

Changing of normal cell into cancer cell

73
Q

Neoplasia

A

descriptive term
abnormal tissue overgrowth that may be either localized or disseminated
Process that leads to the formation of neoplasms

74
Q

Oncology

A

Study of neoplasia and neoplasms

75
Q

Benign neoplasm

A

Growth produced by abnormal cell proliferation that remains localized and does not invade adjacent tissue

76
Q

Malignant neoplasn

A

Locally invasive and may also be spread to other parts of body (metastasis)

77
Q

Oncogenic viruses

A

Viruses that cause or give rise to tumors

78
Q

Metastasis

A

Spread of cancer cells from the part of the body where it started (primary site) to other parts of the body

79
Q

Proto-oncogenes

A

Encode proteins that function in normal cell growth and differentiation

80
Q

Tumore suppressor genes

A

Plays a role in keeping cell division in check
Encodes proteins that regulates and inhibits uncontrolled growth
Rb and P53

81
Q

Oncogenes

A

Mutated forms of proto-oncogenes or aberrantly expressed proto-oncogenes

82
Q

Rb: Retinoblastoma protein

A

Important tumor suppressor gene/protein
Blocks E2F and keeps cell division in check
E2F facilitates cell division

83
Q

P53

A

Tumor suppressor gene/protein
Prevents cells with damaged DNA from entering into cell division
Tries to mediate repairing of the damage host cell DNA
If damaged DNA cannot be repaired, p53 mediates apoptosis of cell with damaged DNA

84
Q

Tumor/oncogenic viruses

A

Viruses that causes cancer
Oncogenic viruses generally have DNA genome or generate DNA provirus after infection (retrovirus)
In permissive cells: can replicate successfully- no cancer
In non-permissive- cannot replicate, integrates into host DNA and causes cancer

85
Q

Oncogenic DNA viruses

A

DNA tumor viruses interact with cells in one of two ways:
1. productive infection in permissive cell, in which the virus completes its replication cycle, resulting in cell lysis (no cancer)
2. Non-productive infection in non-permissive cell, in which virus transforms cell without completing replication cycle (cancer)
During non-productive, viral genome or a truncated version os it is integrated into cell DNA; alternatively complete genome persists as an autonomously replicating plasmid

86
Q

Oncogenic RNA viruses

A

Acutely transforming retroviruses
These steal the proto-oncogene from the infected host cell DNA,
Then virus converts proto-oncogene into oncogene (cancer causing gene)

87
Q

Slow/chronic transforming retrovirus

A

Oncogenic RNA virus
Virus genome gets inserted into regulator (enhancer) gene of host cell DNA
As result of insertion, regulatory gene cannot function properly
No control on proto-oncogene of host DNA
Excessive cell division or cancer as result

88
Q

Expression of tumor antigens

A

FOCMA: feline oncoronavirus membrane-associated antigen

89
Q

Host immune response

A

Innate immunity
Adaptive immunity
Passive immunity

90
Q

Innate Immunity

A

Innate immune defenses exhibit neither antigen specificity nor memory
Provide critical line of first defense against viral infections because:
-constantly present
-operational immediately after infection
-only immune defense available for first few days after infection

91
Q

Natural killer cells

A

Mediate death of virus infected cells via apoptosis

92
Q

Cellular pattern recognition receptors

A

Cells at portals of virus entry possess surface receptors (pattern recognition receptors (PRR)) that recognize specific pathogen-associated molecular patterns (PAMPs)
One class of PRRs are the toll-like receptors (TLRs)
-phagocytosis
-chemotaxis
-inflammatory mediators
-interferons

93
Q

Interferons

A

Group of cytokines that are secreted by somatic cells in response to viral infections and to other stimuli
Possess potent antiviral, immunomodulating and anti-cancer properties
Show no virus specificity
RNA viruses are stronger inducers of interferon than DNA viruses
Being glycoproteins, they are orally inactive, and should be administered via injection
3 types:

94
Q

Interferon-1

A

IFN a and B
Inhibit virus replication in host cells
Activate NK cells to kill infected cells
Increase expression of MHC-1 molecules and antigen presentation
Stimulate differentiation of monocytes into dendritic cells
Maturation of dendritic cells
Stimulated memory T cell proliferation

95
Q

IFN-a

A

Leukocyte interferon

Produced in large quantities by plasmacytoid dendritic cells

96
Q

IFN-B

A

Fibroblast interferon.

Secreted by virus infected fibroblast

97
Q

Interferon Type II

A

IFN-y- most immunoregulatory

Produced by antigen stimulated T cells and NK cells

98
Q

Interferon Type III

A

At least 3: IFN-L1, L2, L3
Recently discovered
Expressed in response to viral infections and activation of TLR
Primarily functions as immunoregulator

99
Q

Adaptive Immunity

A

Includes humoral and cellular components
Humoral- mediated by antibodies released from B lymphocytes
Cellular-medicated by T lymphocytes
Antigen specific, so that these responses take time (several days) to develop, and this type of immunity is mediated by lymphocytes that possess surface receptors that are specific to each pathogen
Stimulated long-term memory after infection
Internal viral antigens usually elicit protective cell mediated immune response
Surface antigens elicit protective humoral and CMI responses

100
Q

Antibody mediated Immunity (Humoral)

A

Antibodies may be directed against viral proteins on free virions (capsid or envelope), or against viral proteins expressed on surface of infected cells

101
Q

Antiviral effects of antibodies- Virus neutralization

A

Neutralizing antibodies prevent virus attachment and entry into host cell, bind to viral capsid or host envelope

102
Q

Antiviral effects of antibodies- Opsonization

A

Coating of virions with antibodies

Antibody coated virion is recognized and phagocytosed by macrophages, and sometimes by neutrophils

103
Q

Antiviral effects of antibodies-

A

Clumping of viruses- immunocomplex formation
Activation of complement system
Antibody-dependent cell mediated cytotoxicity

104
Q

Cell mediated immunity

A

CD4+ helper T cells + microbial antigen in phagocyte

  • activation of macrophages
  • inflammation
  • stimulation of B lymphocytes

CD8+ cytotoxic T cells + infected cell containing microbial antigen
-Killing of infected cells

105
Q

Evasion of immune system- antigenic plasticity

A

Rapid changed in the structure of viral antigens
May be result of mutation, reassortment, recombination
Due to change in Ag structure, virus may become resistant to immunity generated by previous infection

106
Q

Evasion of immune system- antigenic multiplicity

A

Antigenic variants with little or no cross-reactivity

107
Q

Evasion of immune system- Negative cytokine regulation

A

Virokines- some viruses synthesize proteins with are homologs of cytokines/interferons
Viroceptors- some viruses encode proteins that are homologous to the receptors for cytokines. Competitive antagonist

108
Q

Evasion of immune system-

A 
Down regulation of MHC class 1 pathway
Inhibition of complement activation 
Evasion of neutralizing antibodies
Latency
Cell-to-cell spread of viruses
Inhibition of apoptosis

Virology (28 decks)

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