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DWT exam 1 > virology > Flashcards

virology Flashcards

1
Q

definition of virus

A
  • Are smallest infectious particles
  • Range from 18 - 300 nm in size
  • Consist of either DNA or RNA (but not both) and proteins with or without a lipid membrane coat
  • Lack an independent metabolic system
  • Require host cells for replication: true parasites
  • Consist of an intracellular reproductive cycle, and an extracellular transmissive cycle
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2
Q

viruses vs unicellular organisms

A

Unicellular organisms:
* Protozoa, fungi, bacteria, riskettsiae, mycoplasmas, chlamydiae
* Unicellular, both DNA and RNA, binary fission

Viruses:
* Obligate intracellular, either DNA or RNA (not both)
* Two life cycles: extracellular (transmissive, inert), intracellular (reproductive)

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3
Q

unconventional viruses (subviral particles)

A

Extremely simple, replicating agents, either nucleic acid or protein
ex: viroids, virusoids, prions

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4
Q

viroids/virusoids

A

subviral particle
viroid: replicate in nucleus
virusoid: replicate in cytoplasm
mostly plant pathogens

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5
Q

prions

A
  • subviral particle
  • Proteins only, a small proteinaceous infectious particle (no nucleic acid genome).
  • High resistance to heat, UV, irradiation, chemicals
  • ex Prion diseases–Spongiform encephalitides

Prion proteins:
* Present in normal cells (PrPc)
* Abnormal, conformational aberration: amyloid formation (PrPsc)

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6
Q

virus vs prion

A
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7
Q

international committee on taxonomy of viruses naming classifications

A

Nomenclature: Orders, Families (subfamilies), genera(subgenera), species
* Order -virales example: Nidiovirales
* Family -Viridae example: Arteriviridae
–Subfamily -Virinae
* Genera -Virus, example; Arterivirus
–Subgenera
* Species Strain, example: Equine arteritis virus

order, family, genera in italics

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8
Q

how are viruses named?

A
  • describe characteristics
  • describing members of the family
  • describe site where it was first isolated
  • describe the disease it causes
  • describe the place it was discovered
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9
Q

non enveloped vs enveloped viruses building blocks

A

Non enveloped:
* Protein subunit
* Structure unit
* Capsomer
* Capsid (coat or shell)
* Nucleocapsid

enveloped:
* Building blocks of non-enveloped viruses plus Envelope: peplomer/spike, matrix proteins, lipids

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10
Q

spike/peplomer (glycoprotein)

A

important for host specificity, tissue tropism, fusion with cell membrane, infection, damages

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11
Q

enveloped viruses
epidemiology, pathogenesis, immunology

A
  • Epidemiology: short survival in environment, labile, “easier” to inactivate, often associated with seasonal diseases
  • Pathogenesis: budding through infected cells, chronic/persistent infections
  • Immunology: Glycoprotein antigens: VN, CMI, vaccine immunity
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12
Q

non enveloped virus
resistance, pathogenesis

A
  • Only nucleocapsid protein (“naked”, no envelope)
  • More resistant: longer survival in environment, not seasonal disease, difficult to inactivate
  • Pathogenesis: lytic cell infection: often associated with acute disease, less chronic
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13
Q

nuclecapsid symmetry/shape

A

Icosahedral (Cubical): efficient package: 12 vertices, 30 edges, 20 triangles
Helical: All animal helical viruses are enveloped

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14
Q

nuclecapsid symmetry types

A

Icosahedral (Cubical): efficient package: 12 vertices, 30 edges, 20 triangles
Helical: All animal helical viruses are enveloped

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15
Q

chemical composition of viruses

A

Less complex than unicelullar or multicellular organisms

  • Nucleic acid
  • Proteins
  • Carbohydrates (Glycoproteins)
  • Lipids
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16
Q

can viruses have DNA and RNA?

A

NO DNA OR RNA

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17
Q

Are viruses diploid or haploid?

A

all are haploid except retroviruses are diploid

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18
Q

which viruses are most likely to be enveloped?

A

helical

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19
Q

which viruses have generally larger genomes?

A

helical

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20
Q

structural proteins

A

part of virion
* Capsid/nucleocapsid: protecting genome
* Envelope protein (spike, matrix, etc)
* Number: ranging from 1 to >200
* Ligands (VAPs—viral attachment protein) for cellular receptors

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21
Q

nonstructural proteins

A

enzymes, replication regulatory proteins, not part of virion
* Polymerases (transcriptases): dsDNA/dsRNA to mRNA
* Reverse transcriptase: retroviruses (from RNA to DNA)
* Integrase: integrates proviral DNA of retroviruses into host genome

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22
Q

glycoproteins

A
  • Oligosaccharides added to proteins in ER, move to Golgi complex, cell membrane, viral membrane through budding
  • Ligands, enzymes, antigens
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23
Q

viral carbohydrates

A
  • In glycoproteins, glycolipids, muco-polysaccharides
  • Most in viral membranes
  • mostly in enveloped viruses
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24
Q

endemic (enzootic)

A

Multiple, continuous transmissions, disease presence in a defined population/region/time

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25
Q

epidemic (epizootic)

A

Peaks in incidence exceeding the endemic baseline. Nature and degree of expected damage defines whether it is called epidemic (high damage) or not (low damage)

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26
Q

pandemic (panzootic)

A

worldwide epidemic

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27
Q

rate of disease

A

number of cases/population
Different diseases, different rates

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28
Q

incidence or attack rate

A

Number of cases over number of subjects over period of time (case:population ratio).
Acute, short duration diseases.
Denominator: population in a time frame: thus person-years or subject-weeks

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29
Q

prevalence

A

Insidious onset with unknown initial date.
Chronic, long duration diseases.
No time parameters, only number of cases in defined number of subject

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30
Q

parameters defining incidence in acute disease

A
  • The proportion of the population which is susceptible (S/P)
  • The proportion of the infected susceptible individuals (I/S)
  • The proportion of the diseased infected individuals(C/I)
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31
Q

case/infection ratio

A

proportion of infections resulting in clinical disease

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32
Q

case/fatality ratio

A

proportion of infections resulting in lethal disease. Varied, characteristic

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33
Q

new biotypes

A

number of new changed characteristics of a virus

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34
Q

serological studies

A

detect Antibodies
clinical disease-silent, subclinical infections.
Not informative on current infections
prospective and retrospective

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35
Q

prospective serological study

A
  • tracking events that are supposed to happen in the future
  • placebo and treatment groups
  • number of subjects depending on incidence
  • very expensive
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36
Q

retrospective serological study

A

Cost-effective
only needing limited numbers of subjects
test how prevalent a disease is

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37
Q

incubation period

A

Moment of infection to onset of clinical signs
Short? long? variable?

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38
Q

generation time

A
  • From moment of infection to first day virus shedding
  • Mostly shorter than incubation period
  • Influence in spreading disease
39
Q

period of infectivity

A
  • From first day to last day of virus shedding
  • May or may not be longer than clinical signs
  • Great influence in spreading disease
40
Q

chronic viral disease

A
  • Distinction between these time periods is difficult
  • Little correlation among disease, generation time, infectivity
41
Q

horizontal transmission

A

with or without vector, between the same or different host species
can be:
* direct contact: licking, rubbing, sexual contact (enveloped viruses)
* indirect contact: eating, bedding, needles (non enveloped viruses)
* common vehicle: water, feed
* airborne

42
Q

route of transmission for enveloped vs non enveloped viruses

A

enveloped: direct contact (dont survive as well in environment)
non enveloped: indirect contact

43
Q

vertical transmission

A

movement of virus from parents to their offspring during gestation via placenta, perinatally, colostrum, milk

ex: germline transmission: Virus integrated into genome of ovum, transcription and replication in offspring
Pass from generation to generation

44
Q

germline transmission

A

Virus integrated into genome of ovum, transcription and replication in offspring
Pass from generation to generation

45
Q

arthropod vector-borne transmission

A

can be:
* Biological vector: virus replicate, magnify in vectors, efficient transmission
* Mechanical vector: no virus replication in vectors, not efficient for transmission

46
Q

biologica vector

A

virus replicate, magnify in vectors,
efficient transmission

47
Q

mechanical vector

A

no virus replication in vectors,
not efficient for transmission

48
Q

zoonotic disease

A

Viral diseases transmissible under natural conditions from vertebrate animals to humans
ex: rabies

49
Q

what percent of human diseases are zoonotic?

A

60%

50
Q

iatrogenic transmission

A

Patient to patient transmission under veterinary care during the interactions between the vets and the animals
preventable

51
Q

nosocomial

A

transmission occurs while the animals are in hospital or clinic under the care of veterinarians
preventable

52
Q

acute infection

A
  • Rapid production of infectious viruses
  • Rapid resolution and elimination of the infection (virus clearance) by the host
  • Acute infections do not always produce disease
53
Q

persistant infection

A

Infection not cleared efficiently
Virus particles are produced for a long period of time either continuously or intermittently for months or years
can be:
* Chronic infection: persistent infections that are eventually cleared
* Latent infection: persistent infections that last the life of the host

54
Q

chronic infection

A

persistent infections that are eventually cleared

55
Q

latent infection (latency)

A
  • persistent infections that last the life of the host
  • viral genomes integrated into cellular genomes, not expressed
  • no infectious progeny
56
Q

Recrudescence

A
  • activation of latency (latent infection) due to various reasons (immunosuppression, stress, etc),
  • new infectious virus progeny causing disease flair-up
  • and new immune response
57
Q

productive infection

A

resulting in infectious progeny

58
Q

abortive infection

A

replication initiated, but not completed, limited gene expression: no infectious progeny

59
Q

restrictive infection

A

permissivity is transient (individual cells) or proportional (cell population): few virions released

60
Q

transforming infections

A
  • DNA virus or retrovirus
  • Infected cells display altered growth properties and proliferate faster
  • Integration of virus genome into host cells in some infection
  • Causing cancer in animals
61
Q

patterns of shedding

A
  • last phase of viral pathogenesis, mandatory for virus to survive in the host
  • shedding through body openings/surfaces
  • local infections = local shedding
  • systemic infections = various shedding routes
  • amount and timing of shedding defines outcome of infection
62
Q

routes of virus shedding

A
  • Skin: Not a major route, Contact, abrasions, wounds
  • Respiratory Secretions: Very important, Numerous diseases, local, systemic, Shedding occur before, during, after clinical signs
  • Saliva: Salivary gland, oral cavity (Rabies, FIV)
  • Feces: GI tract viruses, Many also without intestinal signs: polio
  • Genital secretions: Sexual activity, semen, mucus
  • Urine: Rinderpest, FMD, canine hepatitis in kidneys, Hantaviruses: mice to humans
  • Milk: Not an important route, Mammary gland replication, caprine arthritis-encephalitis
  • No shedding: Not all virus replications ends with shedding, Encephalitis (CNS), retroviruses (germ line)
63
Q

routes of virus shedding

A
  • Skin: Not a major route, Contact, abrasions, wounds
  • Respiratory Secretions: Very important, Numerous diseases, local, systemic, Shedding occur before, during, after clinical signs
  • Saliva: Salivary gland, oral cavity (Rabies, FIV)
  • Feces: GI tract viruses, Many also without intestinal signs: polio
  • Genital secretions: Sexual activity, semen, mucus
  • Urine: Rinderpest, FMD, canine hepatitis in kidneys, Hantaviruses: mice to humans
  • Milk: Not an important route, Mammary gland replication, caprine arthritis-encephalitis
  • No shedding: Not all virus replications ends with shedding, Encephalitis (CNS), retroviruses (germ line)
64
Q

host range

A

receptors on animal tissues/cells
susceptible for wide range of infections or restricted infections

65
Q

susceptibility

A

ability to become infected

66
Q

permissivity

A

ability to replicate and produce progeny viruses

67
Q

attachment

A

binding of virus attachment proteins (VAPs) on the surface of virion to the receptors on the target cell

68
Q

virus attachment proteins (VAPs) non enveloped vs enveloped

A

Non-enveloped: part of the capsid or a protein extending from the capsid

Enveloped virus: spike/peplomer glycoproteins on the envelope

69
Q

virus attachment proteins (VAPs) non enveloped vs enveloped

A

Non-enveloped: part of the capsid or a protein extending from the capsid

Enveloped virus: spike/peplomer glycoproteins on the envelope

70
Q

receptors

A

proteins, carbohydrates on glycoproteins or glycolipids on the cell surface
Receptors on host cells determine host range, tissue tropism

71
Q

penetration methods

A

Energy dependent, rapid
can be by:
* Translocation: non-enveloped virions
* Endocytosis: enveloped
* Fusion: some enveloped

72
Q

uncoating

A
  • Nucleocapsid is disintegrated
  • Genome freed in cytoplasm
  • Proteins disintegrate in cytoplasm
  • Following uncoating, synthesis of viral proteins by cellular metabolism
73
Q

steps of viral infection

A
  1. attachment
  2. penetration
  3. uncoating
  4. translation
  5. macromolecular synthesis
  6. assembly
  7. maturation
  8. release
74
Q

translation

A

Viral mRNA translation to viral protein is essentially the same as cellular mRNA
Posttranslational modifications to become mature protein:
* Phosphorylation (nucleic acid binding)
* Fatty acid acylation (membrane insertion)
* Glycosylation
* Proteolytic cleavage, etc

75
Q

macromolecular synthesis
DNA vs RNA viruses

A

transcription, translation, posttranslational modification, and viral genome replication
DNA viruses:
* Replicate in nucleus (except for poxvirus)
* Most use host cell’s DNA-dependent RNA polymerase II and other enzymes to transcribe viral mRNA
* Exception: poxviruses encode all enzymes in its genome

RNA viruses:
* Replicate in cytoplasm: must encode (or carry) necessary enzymes for transcription and replication in their genomes
* Exception: orthomyxoviruses, coronaviruses and retroviruses

76
Q

assembly

A

viral proteins and glycoproteins start to replace cell membrane

77
Q

maturation

A

very little/no original cell membrane left, only viral protein
budding starts

78
Q

release

A

free infections virion released

79
Q

cytopathic effect (CPE)

A

morphological changes of infected cells such as rounding, lysis, detachment, syncytia, inclusion bodies
cause:
* Direct pathological injury of the infected cells
* Side effect (altered metabolism due to virus replication)

80
Q

effect of viruses on cell metabolism

A
  • Inhibition of Cellular Transcription Mechanisms: Inhibition of transcription of cellular mRNA by cellular polymerase II enzyme
  • Inhibition of RNA Processing Pathways: virus inhibits maturation of cellular mRNA, and converts cellular pathway for virus’s own use (capping, splicing, polyadenylation, etc)
  • Inhibition of Cellular Translation: inhibit cellular mRNA translation as viral mRNAs are translated essentially the same as cellular mRNAs
  • Inhibition of Host Cell DNA Synthesis: Viruses inhibit host-cell DNA synthesis to:
    — provide nucleic acid precursors for viral genome syntheses
    — re-direct host-cell enzymes for viral DNA synthesis
81
Q

effect of viruses on cell metabolism

A
  • Inhibition of Cellular Transcription Mechanisms: Inhibition of transcription of cellular mRNA by cellular polymerase II enzyme
  • Inhibition of RNA Processing Pathways: virus inhibits maturation of cellular mRNA, and converts cellular pathway for virus’s own use (capping, splicing, polyadenylation, etc)
  • Inhibition of Cellular Translation: inhibit cellular mRNA translation as viral mRNAs are translated essentially the same as cellular mRNAs
  • Inhibition of Host Cell DNA Synthesis: Viruses inhibit host-cell DNA synthesis to:
    — provide nucleic acid precursors for viral genome syntheses
    — re-direct host-cell enzymes for viral DNA synthesis
82
Q

effect of viruses on cell structure

A
  • Membrane fusion of neighboring cells: leading to the formation of syncytia, a characteristic CPE for several enveloped viruses
  • Changing the permeability of the cell plasma membrane: leading to increased influx of various ions, toxins causing cell lysis
  • Disruption of cytoskeletal fiber systems, microfilaments and microtubules: causing rounding of cells, a frequent type of CPE
  • Cytoskeletal components incorporated into infected cell structures either in cytoplasm (vaccinia or rabies virus Negri body) or in the cytoplasm and nucleus as inclusion bodies
83
Q

skin entry into host

A

Natural barrier: epidermis (outer layer contains keratinized dead cells of stratum corneum)
Penetration/loss of barrier: cut, insect bites, abrasions, etc
Local infection, or systemic spread
Examples:
* HERPESVIRUS
* PAPILLOMAVIRUS
* POXVIRUS

84
Q

ways a virus can enter host

A
  • Respiratory tract
  • GI tract
  • Conjunctiva
  • Genitourinary tract
  • Skin (epidermis)
85
Q

respiratory tract entry into host

A

Barriers:
* Mucus, mucociliary movement, neutrophils, macrophages
* IgA, CMI
* Droplet size, air currents, humidity, temperature (cold)

Many viruses (local or systemic infections), examples:
* ADENOVIRUSES
* CORONAVIRUSES
* HERPESVIRUSES
* CALICIVIRUSES
* ORTHOMYXOVIRUSES
* PARAMYXOVIRUSES
* PICORNAVIRUSES

86
Q

respiratory tract entry into host

A

Barriers:
* Mucus, mucociliary movement, neutrophils, macrophages
* IgA, CMI
* Droplet size, air currents, humidity, temperature (cold)

Many viruses (local or systemic infections), examples:
* ADENOVIRUSES
* CORONAVIRUSES
* HERPESVIRUSES
* CALICIVIRUSES
* ORTHOMYXOVIRUSES
* PARAMYXOVIRUSES
* PICORNAVIRUSES

87
Q

GI tract entry into host

A

Barriers:
* Low pH, proteases, bile salts, mucus, IgA, CMI
* Enzymatic enhancement

Many viruses, local or systemic infections, examples:
* ADENOVIRIDAE
* CALICIVIRIDAE
* CORONAVIRIDAE
* PICORNAVIRIDAE
* REOVIRIDAE
* TOROVIRIAE
* NON ENVELOPED (survive harsh environment)

88
Q

GI tract entry into host

A

Barriers:
* Low pH, proteases, bile salts, mucus, IgA, CMI
* Enzymatic enhancement

Many viruses, local or systemic infections, examples:
* ADENOVIRIDAE
* CALICIVIRIDAE
* CORONAVIRIDAE
* PICORNAVIRIDAE
* REOVIRIDAE
* TOROVIRIAE
* NON ENVELOPED (survive harsh environment)

89
Q

genitourinary tract entry into host

A

Barriers: mucus, IgA, CMI
Examples:
* Papillomaviruses
* Herpesvoruses
* Togaviruses

90
Q

conjunctiva entry into host

A

Barriers: tear, IgA, IgG
Not a major route of transmission
Examples:
* Herpesviridae
* Adenoviridae

91
Q

viremia (hematogenous spread)

A
  • Vascular system: major pathway, systemic spread
  • Entry site: limited replication
  • Primary viremia: spread to distant organs (major replication sites)
  • Secondary viremia: major clinical signs
  • high viremia = virulence

most efficient way to spread a virus systemically

92
Q

lymphatic spread

A
  • less important than viremia, less effective
  • Primary replication: epithelial cells, vascular system
  • Spread: lymphatic vessels to other tissues
93
Q

neural spread

A

Factors influencing the spread via CNS:
* primary replication site
* viremia (titer and length)
* duration of nerve tissue exposure, etc

Transport speed: 2 - 16 mm/day along the nerve axons (slow)
Ex: Rabies, polioviruses, herpesviruses, arboviruses
Different pathways may spread same virus to the same target organ

DWT exam 1 (13 decks)

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