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Virology > Test 1 - Host-Pathogen Interactions (8) > Flashcards

Test 1 - Host-Pathogen Interactions (8) Flashcards

1
Q

_______ refers to the ability of a Virus to cause Disease in Host (i.e., harm the host).

The Virus which causes Disease is called a ________.

________ is the manner/mechanism of development of a Disease.

A

Pathogenicity

Pathogen

Pathogenesis

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2
Q

The term ________ is used as a quantitative or relative measure of the degree of pathogenicity of the infecting virus.

If a virus is avirulent this means that…

A

Virulence

Avirulent = not harmful to the host

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3
Q

TRUE/FALSE.

Virulence is an absolute property of a virus.

A

FALSE.

It depends on many variables

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4
Q

What are factors of virulence related to the virus?

A
  • Virus strain (Genetic Makeup of the Virus/Strain Variation)
  • Portal of entry of Virus in Host
  • Tropism to Host Organs
  • Dose of Infection
  • Immuno evasion
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5
Q

What are virulence properties related to the host?

A
  • Host Species
  • Host Immunity
  • Expression of Critical Receptors
  • Host Physiological factors (Nutrition status, Age, Hormonal Factors, Stage of Cell Differentiation)
  • Interferons, Other Inhibitors
  • Fever
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6
Q

Define LD50

A

Lethal dose 50 (LD50): The dose of the virus required to cause death in 50% of animals

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7
Q

Define ID50

A

The dose of virus that will infect 50% of an experimental group of hosts/animals.

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8
Q

What is the ID50:LD50 ratio?

A

Ratio of the dose of a particular strain of virus that causes infection in 50% of individuals [infectious dose 50 (ID 50 )] to the dose that kills 50% of individuals (LD 50).

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9
Q

TRUE/FALSE.

The higher the ID50 and LD50, the more virulent the organism.

A

FALSE.

The lower these values are, the more virulent it is.

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10
Q

What are some other ways of assessing degree of virulence?

A
  • Degree of Severity of illness (Clinical signs): measured as the porportion of infections that are fatal or by the survival time until death.
  • Incubation Period
  • Degree of Severity, location, and distribution of gross, histologic, and/or ultrastructural lesions in affected animals.
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11
Q

What are some defenses found on the skin to combat viruses?

A
  • Dense layer of keratin
  • Low pH
  • Presence of fatty acids
  • Bacterial flora
  • Components of innate and adaptive immunity
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12
Q

What are some routes of entry through the skin via transcutaneous injection?

A
  • Bite of arthropod
  • Bite of an infected animal
  • Contaminated objects (e.g. needles)
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13
Q

What are some defenses found on the mucous membranes?

A

IgA antibodies

Virucidal proteins

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14
Q

What are some defenses found in the GI tract?

A
  • Mucous membrane of oral cavity and esophagus
  • Acidity of the stomach
  • Alkalinity of the intestine
  • Layer of mucous covering the gut
  • Lipolytic activity of bile
  • Proteolytic activity of pancreatic enyzymes
  • Defensins (host defense peptides)
  • IgA
  • Scavenging macrophages
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15
Q

What are defenses in the respiratory tract against viruses?

A
  • Mucociliary blanket
  • Alveolar macrophages
  • NALT (nasal associated lymphoid tissue)
  • BALT (Bronchus-associated lymphoid tissue)
  • Temperature gradient
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16
Q

TRUE/FALSE.

Spread of viruses on epithelial surfaces may result in spread to adjacent subepithelial tissues.

A

FALSE.

It may produce localized infections but it may or may not spread to subepithelial tissues.

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17
Q

After traversing the epithelium, what are ways that facilitate the virus reaching the epithelium?

A
  • Inflammatory response to virus infection and/or destruction of the epithelium
  • Transcytosis
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18
Q

What is a disseminated infection?
Systemic infection?

A

Disseminated Infection: Infection spreads beyond the primary site of infection.

Systemic Infection: If a number of organs or tissues are infected.

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19
Q

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

A

Apical release

basolateral release

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20
Q

What do viruses have access to in subepithelial tissues?

A

Lymphatics, phagocytes and tissue fluids.

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21
Q

What is viremia?

What are the different types?

A

The presence of a virus in the blood. Virus may be free in blood or in a cell, such as lymphocytes.

  • Primary viremia: Initial entry of virus into the blood after infection
  • Secondary viremia: virus has replicated in major organs and once more entered circulation
  • Passive viremia: direct inoculation of virus in blood. Bite of arthropods or contamimnated syringe.
  • Active viremia: following initial virus replication in host. Release of virions from the inital site of replication, such as lymphatics or epithelium of intestine to the bloodstream.
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22
Q

What determines the length of viremia?

A

Short duration viremia: free in plasma (e.g. parovirus)

Prolonged viremia: cell associated viruses - multiply in macrophages or lymphocytes.

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23
Q

What are the different ways a virus may interact with a macrophage?

A
  • Macrophages may fail to phagocytose host cells containing virions. Prolonged Viremia
  • Virions may be phagocytosed & transferred passively to adjacent cells, where replication begins
  • Tissue invasion via carriage of virus inside monocytes/macrophages that emigrate through the walls of small blood vessels (Trojan Horse)
  • Virions may be phagocytosed and destroyed
  • Virons may be phagocytosed by macrophages and then replicate within them. This will lead to an activated macrophage, and lead to inflammatory and vasoactive mediators
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24
Q

What are the different vascular endothelial cell interactions and how may a virus enter an organ?

A
  1. Fenestrae (pore)
  2. Traficking lymphocyte or monocyte (trojan horse)
  3. Transcytosis (vesicular transport of macromolecules from one side of a cell to the other)
  4. Replication in endothelial cells (infection of the luminal aspect of the cell and release from the basal aspect.
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25
Q

How can viruses be cleared from the bloodstream?

A
  • Mononuclear phagocytes in the spleen, liver, bone marrow
  • Antibody clearance
  • Complement-mediated clearance (classic & alternate)
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26
Q

Define a neurotrpic virus.

A

Viruses that can infect neural cells. Infection may occur by neural or hematogenous spread.

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27
Q

Define a neuroinvasive virus.

A

Viruses that enter the central nervous system (spinal cord and brain) after infection of a peripheral site.

28
Q

Define a neurovirulent virus.

A

Viruses that cause disease of nervous tissue, manifested by neurological symptoms and often death.

29
Q

What are the different ways a virus may spread through the CNS?

A
  • Transport of virus within axons
  • Transport of virus in perineural lymphatics
  • Transport of virus in the endoneural space
  • Transport of viruses via infected Schwann cells
30
Q

What are the different types of neural spread?

A

Retrograde Spread:

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.

Anterograde Spread:

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

31
Q

What kind of movement through the CNS can viruses have?

A

Centripetal movement of virus:

Towards the CNS/Brain

Centrifugal movement:

From CNS, within peripheral nerves, to other locations in body.

32
Q

Explain how viruses can evade the Blood-Brain Barrier.

A
  1. Increasing permeability of endothelial cells through the secretion of TNF (tumor necrosis factor).
  2. Breakdown of endothelial cell juntions through Matrix-metalloproteinase (MMP)
  3. Trojan horse (trafficked by monocytes)
33
Q

Compare and contrast Localized vs Systemic acute infections for the following categories:

  • Site of pathology
  • Incubation period
  • Viremia
  • Duration of immunity
  • Secretory IgA
A
34
Q

_______ of infectious virions is crucial to the maintenance of infection in populations.

What is critical to transmission?

A

Shedding

Critical to virus transmission:

The amount of virus shed in an excretion or secretion is important in relation to disease transmission.

35
Q

TRUE/FALSE.

Viruses have a preferential site of shedding and typicalling have one route from which they are shed.

A

FALSE.

Some viruses are shed from a variety of sites and several sites

.

36
Q

Describe the differences in shedding patterns between acute and persistent infections.

A

Acute infection

usually intensive shedding over short time period.

Persistent infections

can be shed at lower titers for months to years.

37
Q

What is tropism? What are some determinants?

A

The specificity/Affinity of a virus for a particular host tissue

Determinants:

  • Receptors on Host Cell
  • Viral attachment proteins
  • Viral enhancers: Gene activators that increase the efficiency of transcription of viral or cellular genes, facilitating Virus Replication.
  • Cellular protease requirement
  • Temperature of replicatio
  • Acid lability and protease digestion
  • Transcriptional control of tropism
  • Anatomic barriers
  • Host organ response to infection
38
Q

What are pantropic viruses?

A

Viruses that can Replicate in more than one host Organ/Tissue

39
Q

What is a rash? what is an example of a virus that causes one?

A
  • A general term applied to any temporary eruption on the skin
  • A rash usually is a shade of red. Varies with the disease in question
  • Ex: Lyme disease causes a bulls eye rash
40
Q

Describe an ulcer.

A

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

41
Q

Describe a nodule/Tumor.

A

Palpable, solid elevated mass. Nodules may have distinct borders. Tumors extend deep into the dermis.

42
Q

Define Warts.

A

Benign (not cancerous) skin growths that appear when a virus infects the top layer of skin.

43
Q

What are papules?

A

Solid elevations without fluid with sharp borders.

44
Q

What is erythema?

A

Reddening of skin, consequence of system viral infections (endothelial injury in blood vessels throught the body, including those of the subcutaneous tissue.

45
Q

How may a virus cause injury to the GI tract?

A
46
Q

How may injury to the respiratory tract manifest?

A
  • Loss of ciliary activity
  • Loss of integrity of the lining mucus layer
  • Multifocal destruction of epithelium
  • Inflammation
  • Exudation
  • Influx of inflammatory cells
  • Obstruction of air passages
  • Hypoxia and respiratory distress
  • Secondary bacterial infection
47
Q

What are some ways that injury to the CNS may manifest?

A

Lytic infections by togaviruses, flaviviruses, herpesviruses, may lead to encephalitis or encephalomyelitis characterized by neuronal necrosis, phagocytosis of neurons (neurophagia) and perivascular infiltration of inflammatory cells (perivascular cuffing).

Other: Progressive demyelination, neuronal vacuolation

48
Q

How may damage to the endothelium manifest?

A
  • Petechial (pinpoint) and ecchymotic (larger, ill-defined) hemorrhages
  • Disseminated intravascular coagulation [DIC]
  • Edema
  • Infarction
  • Ischemic necrosis
49
Q
A
50
Q

Describe disseminated intravascular coagulation (DIC).

A
  • Complication arising from Viral Infection of Blood Vessels.
  • Widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body.
  • Some of these clots can clog the vessels and cut off blood supply to organs such as the liver, brain, or kidneys.
  • Lack of blood flow can damage the organ and it may stop working properly, often resulting in Ischemia and Necrosis.
  • Over time, the clotting proteins in your blood are consumed or “used up.” When this happens, severe bleeding can occur from various sites.
51
Q

What is teratogenesis?

A

This is the abnormal development or arrests in development of the embryo or fetus. May result in death or malformations during the antenatal period. Susceptibility to teratogens varies with the species and stage of development, decreasing with fetal age.

52
Q
A
53
Q

What is virus-induced immunopathology?

A
  • Tissue injury mediated by host immune response to Virus infection. It is the price paid by the host to clear a viral infection.
  • Depends on the delicate balance between the protective and destructive effects of the host immune response to viruses.
  • Immunopathology is often the cause of damage with viruses that are relatively non-cytolytic and persistent, i.e. infected cells are not immediately destroyed and immune response becomes chronic.
  • If the immune response clears the infection by destroying a small number of virus-infected cells, the host survives with minimal symptoms and no permanent damage.
  • On the other hand, if a large number of cells are infected before immune induction, the same immune mediated destruction can cause severe or fatal pathological consequences
54
Q

What are the types of immunopathologies that can occur?

A
  • Tissue damage mediated by hypersensitivity reactions
  • Autoimmune diseases, eg, moon blindness in a horse
  • Inflammation-mediated tissue damage, eg, fibrosis
  • Immunodeficiency disorders
55
Q

What role can T cells have in immunopathology?

A

T cells, for example, can directly destroy virus-infected cells or release cytokines, such as tumor necrosis factor (TNF), that damage cells.

  • There may be Cytotoxic cell mediated lysis/killing of infected host cells. With some non-cytopathic virus infections, such as HCV and HBV, destruction of infected cells by CD8+ effector T cells is the main cause of damage to the liver.
  • There may be 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.
  • CD4+ cells elaborate far more cytokines than CD8+ cells and also activate other non-specific effector cells, such as neutrophils.
56
Q

What is the role of innate immunity in immunopathology?

A
  • Invading viruses and replicative intermediates can be recognized by innate immune receptors expressed either at the host cell surface or within cells, e.g. Toll-like receptors (TLRs).
  • 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 inflammation.
  • Injury can also be mediated by free radicals, such as Nitric oxide and Superoxide. Normally, they inhibit viral replication. But when produced in abundance, cause celldamage.
57
Q

How can toxicity from antibody responses lead to immunopathology?

A
  • This occurs when antibody binds to an infected cell, activates complement and causes an inflammatory reaction.
  • Alternatively, antibody mediated inflammatory reactions involve toxicity following:
    • Engagement of IgG with Fc receptors on inflammatory cells, which causes inflammatory mediator release.
    • Following deposition of viral antigen–antibody complexes in capillary beds, leading to activation of the complement cascade. (results in vasculitis and edema). E.g. FIP
58
Q

What can result from infection and damage to mononuclear phagocytes?

A

This can protect an invading virus from phagocytic removal. Moreover, these infected cells may exhibit aberrant behavior, resulting in a cascade of events that are detrimental to the host.

59
Q

List the different types of viral infections.

A
  1. Inapparent Infections
  2. Acute Infections (short term)
  3. Persistent Infection
  4. Latent infection
  5. Chronic infection
  6. Slow Infection
60
Q

Define an Inapparent Infection.

A
  • Clinical signs and symptoms are not evident
  • Too few cells may be infected
  • Stimulate host immune response
  • Possible source of virus spread
61
Q

What is an acute infection?

A

Short clinical course and rapid clearance from host immune response.

62
Q

What is a persistent infection?

Why are they important

A

Persistent infections, in which infectious virus is demonstrable continuously, whether or not there is ongoing disease. Disease may develop late, often with an immunopathologic or neoplastic basis, or in other instances, there may be no manifestation of clinical signs. The pathogen is not cleared efficiently by the adaptive immune response. They are important because:

  • Recrudescent episodes of disease in the individual host
  • Immunopathology
  • Survival of virus in host and continuous shedding
63
Q

What is a latent/persistent infection?

A

Latent infections, in which infectious virus is not demonstrable except when reactivation occurs. Reactivation is often stimulated by immunosuppression and/or by the action of a cytokine or hormone.

Viral latency may be maintained by:

  • Restricted expression of genes that prevents the expression of proteins which, otherwise, would have killed the infected cells.
  • Virus genome maintained indefinitely in cell by integration of viral nucleic acid into host cell DNA, or by carriage of viral nucleic acid in episomal form. Example: Infectious Bovine Rhinotracheitis
64
Q

Define a chronic infection.

A

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

  • Established if host immunity is unable to clear virus from acute infection.
  • Not all chronic infection may start as acute infection.

Example: Foot and Mouth Disease in Cattle

65
Q

Define a slow infection (persistent).

A
  • Prolonged incubation period, lasting months or years.
  • Quantities of infectious virus gradually increase during a very long preclinical phase
  • Slow progressive lethal disease.

Virology (13 decks)

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