Introduction Flashcards

1
Q

Virion

A

Extracellular virus particle
Inc nucleic acid and protein coat (and sometimes lipoprotein membrane envelope)
Size: 20-300 nm

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2
Q

Common features of viruses

A

Obligatory intracellular growth (virion = vehicle)
Replication - via synthesis in host vs binary fission
Contain one kind of nucleic acid (RNA or DNA)

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3
Q

Eclipse period

A

Virion undetectable within hours after initial infection of cell
- virion disintegrates -> releases nucleic acid (=”eclipse”) -> subsequently assembled into new virions

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4
Q

Baltimore classification

A
Via type of genome and type of replication
ex:
dsDNA (Adeno, Herpes, Pox)
ssDNA (Parvo)
\+ssRNA (Picorna, Toga) - "+" is mRNA
-ssRNA (Orthomyxo, Rhabdo) - "-" is nRNA/template
ssRNA-RT (Retro)
dsDNA-RT (Hepadna)
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5
Q

Steps of viral replication cycle

A
Asorption
Penetration
Uncoating -> eclipse period
Synthesis
Assembly -> ends eclipse
Maturation (usu involves enzyme)
Release
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6
Q

Requirements for viral growth

A

Cell:
- machinery (ribosomes, tRNA), ATP, precursors (nucleotides, amino acids), various enzymes, transport pathways (lysis, vesicle, etc)
Virus:
- genes for virion
- non-virion genes -> replication enzymes, manipulation of host cell

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7
Q

Susceptible vs permissive

A

Describe host cell infectability
Susceptible
- presence of host cell surface receptor (adsorption and entry)
Permissive - can virus replicate after entry
- innate cellular defenses can be overcome
- machinery for replication cycle (synthesis, transport)

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8
Q

Viral challenges

A
  • must encounter host cells
  • must evade physical defenses (skin, mucous, etc)
  • must overcome defense mechanisms (intrinsic, innate, adaptive)
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9
Q

Protein coat structure

A

Symmetrical
Identical capsomeres

Helical
Icosahedral (like geodesic dome)
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10
Q

Nucleocapsid

A

= nucleic acid + capsomer protein coat

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11
Q

Enveloped viruses

A

Lipoprotein membrane around nucleocapsid

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12
Q

Viral antigens

A

Only proteins!
Unenveloped nucleocapsid -> capsomer
Enveloped -> envelope proteins

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13
Q

Detection methods

A
Detection - clinical methods
 - cytopathic or transforming effect
 - inclusion bodies
 - plaques
 - syncytia
Cultivation is slow, labor intensive, still doesn't provide specific identity
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14
Q

Cytopathic effect

A

Viral infection -> change in size, shape, motility, attachment
-> lysis
Visualize with light microscopy as infection spreads

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15
Q

Transforming viruses

A

Abnormal proliferation -> piles or mountains from single layer culture
- aka tumor viruses

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16
Q

Inclusion bodies

A

Sites of viral replication
Requires histologic staining
Location may be characteristic (cytoplasm vs nuclear)

17
Q

Plaque formation

A

Zone of dead cells from cytopathic virus

PFU = plaque forming unit = only quantitative method for measuring virions in sample

18
Q

Syncytia

A

Virus envelope includes “fusion” protein ->
large multinucleated cell

Ex RSV

19
Q

Viral identification

A

Usually relies on detection of virion:antibody match

  • neutralization
  • complement fixation
  • hemagglutination (not all viruses)
  • fluorescent antibody
  • radioimmunoassay, ELISA, etc
20
Q

Diagnosis of viral disease

A

Antibodies
- isolate virus -> interaction with known antisera (Ig)
- Seroconversion - acute (prior) vs convalescent antibody levels
= may have “window period” - active infection but not seropositive (Hep B, HIV)
Rapid - presence of viral components
- protein antigens (via antibody)
- nucleic acid (via PCR) - works during window period

21
Q

Neutralization

A

Tight binding of antibody:virion surface

  • high affinity, essentially irreversible dt repeating epitopes
  • > can’t adhere/enter cells
    • doesn’t impact intracellular multiplication
    • ex local IgA in resp or GI
  • > also use for diagnosis (fewer PFUs)
    • only works for infectious virions
22
Q

Simple nucleocapsid viruses

A
All icosahedral
Stable in env't (don't require direct contact for transmission)
RNA -> assembled in cytoplasm
DNA -> assembled in nucleus
 (enveloped are different...)
23
Q

Host range

A

Species that can be infected
Determined by adsorption (cell receptors)
Ex - polio -> humans and higher primates

24
Q

Tissuetropism

A

Range of tissue that can be infected

25
Q

Adsorption

A

Virions bind to receptor protein
Highly specific
Determines host range and tissuetropism

Can be bypassed experimentally (ex polio RNA -> chicken cell -> synthesis of virions)

26
Q

Polio replication

A

RNA-dependent RNA polymerase (no DNA, not inhibited by DNA-> RNA block via actinomycin)
Cytoplasm
Inhibits host synthesis

mRNA (+ strand) -> large protein -> cleavage -> capsomer and enzymes (inc polymerase)

  • > complementary (-) strand = template -> synthesis of new + strand
  • >
    • strand + capsomers -> new virions
27
Q

Patterns of pathogenesis

A
  • growth in cells at site (no illness) -> viremia
    • incubation weeks/months
    • immunity reliable, decades/life
  • growth at site -> illness (mucosal)
  • incubation days
  • immunity via IgA, less effective, 3-10 years
  • less severe illnes
  • growth at site -> neural spread (rabies)
28
Q

Patterns of infection

A

Acute - occurs then clears
Persistent - virus and/or infection not clears
- inc latent and slow

May be asymptomatic (aka subclinical, inapparent, silent)

29
Q

Incubation period

A

Length of time between infection and symptoms

Defined by symptoms - may have detectable antigen or antibodies

30
Q

Window period

A

Infection without detectable antigen or antibodies

Depends on sensitivity of tests (higher sensitivity can shorten but not eliminate)

31
Q

Eclipse period

A

Time between phagocytosis of virus and release of new virions
Defined on cellular vs organism basis