Introduction Flashcards

(31 cards)

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
Adsorption
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
Polio replication
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
Patterns of pathogenesis
- 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
Patterns of infection
Acute - occurs then clears Persistent - virus and/or infection not clears - inc latent and slow May be asymptomatic (aka subclinical, inapparent, silent)
29
Incubation period
Length of time between infection and symptoms | Defined by symptoms - may have detectable antigen or antibodies
30
Window period
Infection without detectable antigen or antibodies | Depends on sensitivity of tests (higher sensitivity can shorten but not eliminate)
31
Eclipse period
Time between phagocytosis of virus and release of new virions Defined on cellular vs organism basis