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Virology > Enveloped/flu > Flashcards

Enveloped/flu Flashcards

0
Q

Production of enveloped virus

A

viral RNA -> protein -> Golgi -> cell membrane

virion -> membrane ->
BUDS OFF!

not lysis - cell doesn’t die immediately (vs non-enveloped)

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1
Q

Envelope

A

Lipids - from host cell membrane
Proteins - from virus genome -> specificity for receptors

Appears clear with “rods” = proteins

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2
Q

Enveloped vs non-enveloped

A

Antigens - envelope protein vs capsid protein
Envelope -
- sensitive to ether, organic solvents (-> lipids)
- unstable outside of host (dessication vs fecal oral capside crystal)
Release via budding (not fatal) vs lysis of cell

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3
Q

Structure of flu virus

A

Enveloped orthomyxo
- proteins = hemagglutinin (antigen, binds to host sialic acid)
= neuraminidase (target for antiviral)
RNA - 8 strands, (-) strand (not mRNA)
- each strand in separate helical nucleocapsid
RNA-dependent RNA polymerase

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4
Q

Classes of enveloped viruses

A 
Paramyxo
Toga
Herpes
Flavi
Orthomyxo (flu)
Rhabdo
Retro
Pox
Hepadna
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5
Q

Hemagglutination assay

A

Orthomyxoviruses contain hemagglutinin protein (HA)

  • HA binds sialic acid on RBC’s -> complex vs “button”
  • inhibited by antibody (neutralizes HA -> button)

Can assess:

  • viral concentration (dilution that still forms complex)
  • antibody concentration (dilution that prevents complex)
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6
Q

Flu antigens

A

Capsids - around RNA segments but hidden!

Hemagglutinin (HA) - necessary for adsorption (binds to sialic acid)
- can be neutralized by Ab
Neuramidinase (N) - necessary for release of new virions
(cleaves sialic acid-HA bonds)
- Ab slows spread (to other cells, people) but does not neutralize virions or prevent infection of new cells

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7
Q

Types of flu

A 
3 types (A,B,C)
 - defined by capsid protein (A,B,C)
Antigenic differences within type - HA, NA, polymerases, etc

A - most serious, epidemic q2-3 years, pandemic q10-30 years
B - less serious, epidemic q3-6 years
C - not significant

Vaccine = 2 A + B

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8
Q

Minor epidemics

A

Antigenic drift = minor mutation in existing RNA

  • usually mistake in HA gene -> conformational change
  • some existing antibodies bind (partial immunity)
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9
Q

Major pandemic

A

Antigenic shift of HA antigen (genetic reassortment)
- existing antibodies can’t neutralize -> no preexisting immunity
Sometimes N antigen also shifts
-> more severe bc N antibody can’t slow down spread

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10
Q

Diagnosis of flu

A

Rapid - fluorescent antibodies -> throat swab
Normal - seroconversion (increase in anti-HA antibodies)
Definitive - culture in eggs or tissue -> isolate

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11
Q

Flu clinical presentation

A

Aerosol spread (cough, sneeze) -> URI (can cause -> lower respiratory)
Destroys ciliated cells (can cause -> Pneumococcus pneumonia)
Inflammatory mediators -> fever, chills, H/A
Does NOT spread through viremia

Death - infant, elderly, previous lung compromise
- 1918 young adults died: strong immune response -> lung damage

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12
Q

Immunity to flu

A

Does not spread by viremia! (infects local resp tissues only)

  • > short incubation period (days)
  • > main protection is secreted IgA
  • we are better at neutralizing viremic vs local…
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13
Q

Flu vaccine

A 
Trivalent (2 A strains + 1 B)
Strains selected in anticipation of epidemic
Killed (formaldehyde) -> IM injection
 -> only induces IgG response
 - no IgA produced! sub-optimal

Also have intranasal attenuated (separate slide)

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14
Q

Attenuated flu vaccine

A 
aka FluMist
2 A strains + 2 B strains
Attenuated - can't grow at body temperature
Intranasal spray
-> IgA response! more effective!
Approved for ages 2-49
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15
Q

Flu medications

A

Oseltamivir (Tamiflu)
Zanamivir (Relenza)
Neuraminidase inhibitors - block release of new virions
- shortens symptomatic period
- must be given before or soon after infection
- active against A and B

Adamantanes = older, not recommended

  • only work against A, lots of resistance, some side effects
  • may be useful in combination, prophylactic
  • works by inhibiting polymerase
16
Q

Flu replication

A

HA binds to sialic acid -> endocytosis -> fuses ->
releases RNA strands and polymerase ->
translocate to the NUCLEUS! -> makes (+)RNA -> more (-)RNA ->
(+)mRNA (must steal 5’ cap from host transcripts) ->
translation into protein in cytoplasm

17
Q

Paramyxovirus characteristics

A

Single (-) RNA
- polymerase in virion
- no reassortment -> less antigenitic variance
Helical nucleocapsid + envelope
Replication in cytoplasm (vs flu in nucleus)

Most non-systemic respiratory

  • severe childhood -> no lifelong immunity -> subclinical adult
  • all have HA antigen (agglutination test) except RSV
18
Q

Paramyxoviruses

A

Systemic: measles, mumps

Non-systemic respiratory:
Parainfluenza (1-4)
Respiratory syncytial virus
Metapneumonia

19
Q

Croup

A

aka acute laryngeo-tracheo-bronchitis

Usu caused by parainfluenza
0-3 years (peaks at age 2)
Respiratory - dyspnea and stridor

Treat with glucocorticoids if severe

20
Q

Respiratory syncytial virus

A

Most common cause of severe lower resp in infants!
- no vaccine, no long-term immunity (IgA)

Ribavirin - treatment, mechanism unknown
Palivizumab - mAb - prevents pneumonia in high risk (premature)

Does not have HA antigen (hemagglutinin test negative)

21
Q

Coronaviruses

A

Enveloped
Helical nucleocapsid
Single +RNA

Common cold
Highly pathogenic = SARS, MERS

22
Q

SARS

A

Highly pathogenic coronavirus
2003 epidemic: China -> 8000 people -> 9% fatality
- worst in adults, older
- halted by identification and quarantine
Aerosol -> 2-10 d incubation -> dry cough/SOB -> pneumonia

23
Q

MERS

A

Highly pathogenic coronavirus

2012: Jordan, Saudi -> Europe, etc
Severe lower respiratory -> fever, cough, SOB -> 50% fatality

24
Q

Interferon system

A

Produced by infected cells (alpha, beta) and activated T (gamma)
-> production of virus inhibitory proteins in non-infected

  • induced by pattern recognition receptors (TLR, RIG, MDA) vs viral RNA
  • no viral specificity!
  • rapidly produced, very transient (vs IgM months, IgG years)
25
Q

Virus inhibitory proteins

A

Interferon -> all cells make inhibitory proteins -> activated if infected

2-5-A synthase: makes 2-5-A polynucleotide -> activates ribonuclease L -> degrades mRNA
Protein kinase R: phosphorylates IF-2 -> inactive -> no ribosome

Virology (16 decks)

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