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MD2- Neuroscience Block > Viruses affecting the CNS > Flashcards

Flashcards in Viruses affecting the CNS Deck (38):

Neurotropic virus?

capable of REPLICATING in nerve cells


Neuroinvasive virus?

capable of entering or infecting the CNS


Neurovirulent virus?

capable of causing disease within the nervous system



infection of the meninges surrounding the brain and spinal cord



an infection of the brain itself



an infection of the spinal cord



both brain and spinal cord infection


primary viral encephalitis/acute viral encephalitis

direct viral infection of the spinal cord and brain. can be focal or diffuse.


secondary encephalitis, aka post-infectious encephalitis

results from complications of a current viral infection that spreads to the brain, usually via the blood


main causative pathogen of viral meningitis?

enteroviruses (enter the body via mouth). also caused by mumps, varicella zoster, influenza, HIV and herpes simplex type II (genital herpes)


main causative pathogen of viral encephalitis?

herpes simplex virus type I and II. rabies virus, arbo viruses (insect-borne viruses), and enteroviruses


how does viral meningitis typically present in patients?

neck stiffness, headache, fever, with or without vomiting and/or photophobia


main causative pathogen of viral encephalitis?

herpes simplex virus type I and II. rabies virus, arbo viruses (insect-borne viruses), and enteroviruses.

(mumps encephalitis may also involve the brain parenchyma, but usually mild).


how does viral meningitis typically present in patients?

neck stiffness, headache, fever, with or without vomiting and/or photophobia


how does viral encephalitis present in patients?

presents like meningitis with neck stiffness, headache and fever. but also develops personality and behavioral changes, seizures, partial paralysis, hallucinations, altered levels of consciousness -->ultimately coma and death


what are the common causative agents behind post-infectious encephalomyelitis?

may occur in the wake of measles, chickenpox, rubella, or mumps.
The virus is not present, but inflammation and demyelination is evident.
Possible to be autoimmune in nature.


Guillain Barre syndrome pathogenesis?

-acute inflammatory demyelinating disease following infection with viruses such as EBV, CMV, HIV
-results in partial or total paralysis, but with total regain of function in 75% of cases


Reye's syndrome pathogenesis?

post-infection with influenza or chickenpox.
CEREBRAL OEDEMA, but not inflammation.
NB: Associated with administration of aspirin during initial fever.


chronic demyelinating disease features?

Very rare. exemplified by Sub-acute sclerosing panencephalitis (SSPE), a late sequel to measles infection.


AIDS encephalopathy (AIDS dementia complex)

once HIV infection leads to immunodeficiency, the HIV becomes neurovirulent.
50% of patients develop progressive dementia.


how do viruses exploit the PNS to breach the BBB and infect the CNS?

Nerve cells do not have MHC class I receptors! uncoated nucleocapsids or whole virions can travel passively along the axon or dendrites from the peripheral tissues into the CNS.

ex. rabies virus, yellow fever virus, herpes simplex type I and II


where do neurotropic viruses replicate?

body of the nerve (soma) b/c this is where protein synthesis takes place.

released progeny can then cross the synaptic junction.


how might viruses reach the CNS via the blood? examples of viruses?

once already in the blood, viruses might reach the CNS (brain) via a meningeal blood vessel.

poliovirus, mumps, measels, coxsackie, and HIV (in monocytes)


describe structure of rabies virus?

Rabies is a bullet-shaped, negative-stranded RNA virus, with helical capsid and an envelope.


describe life cycle and pathogenicity of rabies virus

Highly neurovirulent and highly neuroinvasive.
Obligatory neurotropic virus.

1. virus enters muscle via bite of rabid animal.
2. replicates in myocytes of striated muscle
3.enters PNS nerve ending, carried via axoplasmic flow to spinal cord (8-20mm/day)
4.virus travels along neural process and replicates in CNS.
5.travels from CNS along peripheral nerves to the salivary gland
6.replicates in salivary acinar cells, virus is discharged in saliva

**70-day Cycle


structure of herpes simplex virus type I and II? (varicella zoster virus)

Linear dsDNA genome, icosohedral, sorrounded by envelope.

Obligatory neurotropic virus.

Low neuroinvasiveness. High neurovirulence.


life cycle and pathogenicity of Herpes Simplex type 1 and 2

HSV-1 enters body through contact with infected saliva, primary infections involve mouth and/or throat.

HSV-2 enters through mucous membrane of genital region.

A) 15% of cases:
Follow primary disease route, enters adjacent nerve endings to enter sensory nerve ganglia (trigeminal for HSV-1, or sacral for HSV-2).
Remains a latent infection until a stressor event reactivates virus, migrates along axon, leading to localized multiplication and disease recurrence at trigeminal or sacral nerve endings.
In rare cases, it may enter blood and distant organs, causing severe sporadic encephalitis (infected neurons and glia in the temporal lobe). 70% case fatality rate.

B) 85% of cases:
Undergo local replication in regional lymph nodes, and infection eventually gets cleared. In rare cases, virus can also enter blood from lymph nodes and cause severe sporadic encephalitis.


majority of fatality's of HSV-1 and HSV-2 related severe sporadic encephalitis are primary cases or reactivated cases?

Reactivated cases.


how is the HSV viral genome maintained in latency?

20% people harbour latent genome in ganglia.
Genome is maintained as an episome (circular piece of DNA) coated with histones.
They express a latency activated mRNA transcript (LAT's).

CD8+ T cells may be responsible for keeping genome in dormant state.


which conditions does varicella zoster cause?

chicken pox (varicella) and shingles (zoster)


describe pathogenesis of chickenpox (varicella)

-viral infection of conjuctiva/and or mucosa of URT.

-replication in regional lymph nodes.
-->primary viremia in blood stream.

-further viral replication in liver and spleen
-->secondary viremia

-infection of skin, and appearance of vesicular rash.
-->scratching of rash releases virus into the air.



describe pathogenesis of shingles (herpes zoster )

following primary infection with chickenpox (varicella), virus may travel to dorsal root ganglion and remain latent.
-->reactivation causes herpes zoster vesicles following a dermatome path.

**Tx with Acyclovir ASAP*


describe the structure of poliovirus?

Poliovirus is a + stranded RNA virus with an icosahedral capsid and no envelope.

Member of Enterovirus genus of the Picornavirus family (small RNA viruses).


pathogenisis of poliovirus?

Low Neuroinvasiveness and High Neurovirulence.
NOT an obligatory neurotropic virus. Cytocidal, kills cells it replicates in.

1. virus ingested from water/food contaminated with feces
2.reaches GALT (gut associated lymphoid tissue). invades tonsils and peyers patches.
3. replicates in regional lymph nodes
4.enters blood stream, causes plasma viremia
5.crosses BBB
6.replicates in anterior horn cells of spinal cord, causes cell lysis
7.reaches gut, excreted in feces

**targeting of ventral horn motor cells causes paralysis
**if CNS is targeted, total paralysis may occur in a matter of hours





T/F in polio infection, lower limbs are more frequently affected than upper limbs?

TRUE. "Acute flaccid paralysis."


in which polio cases is the mortality rate greatest?

when virus affects brain stem motor neurons, impacting breathing centres.


how do coxsackie virus type A and B, and echoviruses spread?

via fecal/oral route.
circulate in the blood to target organs.
-->Brain (encephalitis, paralysis)
-->Meninges (meningitis)
-->Skin (hand, foot, mouth disease)
-->Muscle (myocarditis, endocarditis, pleurodynia)