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Virology Final > Virus Infections of the Nervous System > Flashcards

Virus Infections of the Nervous System Flashcards

1
Q

Modes of entry to CNS

A
  • neural
  • olfactory
  • hematogenous
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2
Q

Modes of entry to CNS-neural

A

2 transport pathways

  • retrograde transport along lower motor neurons in spinal cord and brain stem (HSV, rabies, polio)
  • anterograde transport via sensory axons to periphery (HSV)
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3
Q

Modes of entry to CNS-olfactory

A
  • spread intranasally acquired virus via exposed dendrites of olfactory neurons
  • subsequent spread to brain along the olfactory pathways
  • HSV, arboviruses
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4
Q

Modes of entry to CNS-Hematogenous

A
  • penetration of capillary endothelium and blood brain barrier by blood borne virus
  • HSV, polio, HIV, arbo, unconventional agents
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5
Q

Cell Targets of Neurotropic Viruses

A

Most critical targets
-neurons (neurotropic viruses-preference for neurons)-polio, rabies, encephalitic arbo
-oligodendrocytes (myelin-producing)-progressive multifocal leukoencephalopathy (PML)
Other Targets
-astrocytes, microglia

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6
Q

Viruses in Neurological Diseases

A

-acute viral infections of the CNS (poliomyelitis, rabies, west nile)
-chronic virus infections of the CNS “slow virus diseases”
-conventional virus diseases of animals
-conventional virus diseases of humans
unconventional virus diseases (Kuru and Creutzfeldt-Jakob disease-humans, scrapie (sheep) and Bovine encephalopathy (cattle) in animals)

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7
Q

Acute Viral infections of the CNS-Poliomyelitis

A

-1% of all polio infections
-invasion of CNS probably via hematogenous route
-target: neurons in anterior horn of spinal cord
vaccines-salk (killed)
-sabin (attenuated, oral vaccine)-largely effective but reversion is a risk

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8
Q

Poliomyelitis Pathogenesis

A 
ingested via food and water
small intestine-invasion and replication
mesenteric lymph nodes 
replication
blood-viruses in the blood (primary viremia)
muscle is preferred site of replication
initial antibody appearance 
CNS (invasion, rep, intraneural spread)
high levels of serum antibodies, paralysis
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9
Q

Insect borne encephalitic diseases

A
  • St.louis encephalitis, west nile encephalitis, japanese encephalitis
  • virus spread from the subcutaneous site of inoculation via Langerhans cells (skin DCs) to lymph nodes
  • viremia and rep in extraneural tissues (spleen, liver, kidneys)
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10
Q

Insect borne Viruses may enter CNS by various mechanisms

A
  1. infection or transport through the endothelium or choroid plexus epithelial cells
  2. infection of olfactory neurons and spread to olfactory bulb
  3. virus infected immune cells trafficking to CNS
  4. direct axonal retrograde transport from infected peripheral neurons
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11
Q

West Nile Virus

A
  • spread of old world flavivirus to new world
  • until 1973 restricted to Uganda
  • 1999-appeared in NY, with subsequent spread
  • 2002 epidemic
  • flu like symptoms in 20% infected humans
  • meningitis, encephalitis, poliomyelitis like symptoms in 1:150 cases
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12
Q

West Nile Virus-Transmission Cycle

A
  • birds to mosquitoes to humans
  • humans to humans via organ donation, blood transfusion
  • mosquitoes to birds
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13
Q

Disease diversity of flaviviruses

A

3 major disease types

  • hemorrhagic, encephalitic, hepatotropic (liver)
  • large differences in disease caused by small differences in genome
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14
Q

Conventional Slow Virus diseases-visna (6)

A
  • disease affecting sheep
  • slowly progressive inflammatory destruction of CNS, “wasting” disease
  • causative agent is retrovirus (lentivirus) related to HIV
  • high rate of antigenic drift in env gene
  • by late stage of disease, most cells appear to harbour virus as latent provirus
  • damage to CNS due to virus infection and cell destruction, immune mediated (macs and lymphocytes)
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15
Q

Conventional Slow Virus diseases-subactute sclerosing panencephalitis (SSPE) (6)

A
  • children and young adults
  • intellectual defects followed by loss of cortical functions
  • caused by measles
  • inclusion bodies (measles virus nucleocapsids) detected in neurons and oligodendrocytes
  • evidence for abortive infection: once measles gets into neurons + oligodendrocytes undergoes a few steps of rep, decreased expression of matrix (M), fusion (F) or hemagluttinin (H) proteins
  • damage to CNS due to virus infection and cell destruction, immune mediated
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16
Q

Conventional Slow Virus diseases-Progressive Multifocal Leukoencephalopathy (PML) (8)

A
  • disease of white matter of brain (attacks myelin producing cells)
  • requires immunodeficient individual
  • deterioration of intellect, vision, speech, muscular coordination
  • demyelination
  • intranuclear inclusions in oligodendrocytes
  • no inflammation
  • caused by polyomavirus, related to SV40, infects oligodendrocytes
  • damage to CNS due to virus infection and cell destruction
17
Q

Unconventional slow virus diseases

A
  • unconventional agents involved in “subacute spongiform encephalopathies”-brain tissue shows sponge like appearance due to vacuoles
  • amyloid plaques in brain-distinctive protein deposits in brain composed of prion protein
  • asymptomatic incubation periods lasting months/years
18
Q

Nature of Scrapie Agent

A
  • copurification of scrapie infectivity w/ 27-30 kDa protein termed prion protein (PrP)
  • PrP cross-reactive amyloid deposits found in Scrapie and CJ brain tissue
19
Q

Isoforms of PrP

A
  • normal cell isoform is PrPc-membrane bound, prominent in neurons, proteinase K sensitive
  • -hallmark of scrapie infection is presence of proteinase K-resistant form of Prp-Prpsc
  • Prpsc differs from Prp by folding
20
Q

Causes of prion disease

A
  1. Genetic
    - hereditary CJ disease usually linked to specific aa PrP mutations
    - non contagious
  2. Infectious
    - ingestion: scrapie from sheep to other animals, BSE from cattle to humans (as vCJD), Kuru among humans
    - surgical-neurosurgical procedures, growth hormone injections (pituitary gland extract)
  3. spontaneous
    - arises from spontaneous misfolding
21
Q

Model for entry and conversion of prion disease agents

A
  • harmful isoform is ingested or forms in the brain
  • seeks out normal isoform, binds and cause misfolding (in gut lumen then to neurons)
  • infectious agent able to replicate w/o the presence of DNA or RNA
22
Q

Normal function of PrP in mammals

A

Prp knockout mice differ from wild type counterparts in many functions

  • circadian rhythms
  • neuroprotection
  • synaptic function
  • lymphocyte activation
  • cell adhesion
  • stem cell renewal and proliferation
  • olfaction
  • Prp knockout mice are resistant to scrapie
23
Q

Analogies between human alzheimer’s and Prion Disease

A
  • amyloid deposits in Alzheimer’s diseased brains contain beta- amyloid protein derived from beta protein precursor
  • amyloids also assoc. w/ Huntington’s disease and Parkinson’s
24
Q

Prions as functional states of normal genes

A
  • protein polymerization as signalling mechanism
  • viral RNA binds w/ RIG-I
  • produce a tetramer
  • complexes w/ other proteins inside the cell (Ub)
  • causes aggregation of MAVS prion
  • Tc of NF-kappaB and IRF3 is induced
  • interferons are produced, which inhibit virus

Virology Final (7 decks)

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