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I & I Part II > Mechanisms of Viral Persistence > Flashcards

Mechanisms of Viral Persistence Flashcards

1
Q

Persistent Viral Infection

A
  • Chronic
  • Latent
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2
Q

3 conditions for viral persistence:

A

✷ The virus must be able to infect host cells without being cytopathic

✷ There must be mechanisms for long-term maintenance of the viral genome in the host cells

✷ The virus has to avoid detection and elimination by the host’s immune response (antigenic variation)

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3
Q

Restriction of Viral Cytolytic Effect

A

✷ Most arenaviruses replicate in animal host without any cytopathic effect

✷ HBV infects hepatocytes with little or no injury

✷ HIV is more lytic for T-cells and less cytopathic for monocytes/macrophages

✷ Infection of non-permissive Cells

  • Sensory neurons - HSV
  • B lymphocytes - EBV

✷ Evolution of Viral Variants

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4
Q

Mechanisms of Viral Genome Maintenance

A

✷ Genome integration (HIV)

✷ Genomes of EBV and some papillomaviruses are maintained as episomal circular molecules

✷ HSV as extrachromosomal (episomes) DNA

✷ Mechanisms for RNA viruses not understood

  • Low level of replication
  • Folding of RNA to provide stability
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5
Q

Avoid Elimination by Host Response

A

✷ Evasion of Host Immunity

✷ Viral Evasion Strategies

✷ Antigenic Variation

✷ Interference with the host immune system

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6
Q

Host Immunity

A

✷ Antiviral immunity

✷ Antibodies and T cells

✷ T cells see viral antigens with MHC I and II

✷ All viral proteins can be potential targets for T-cell recognition

✷ The primary mechanism employed by CD8+ T cells is killing of virus infected cells

✷ CD4+ T-cells contribute to antiviral immunity by producing antiviral cytokines

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7
Q

How does a virus evade host immunity?

A

✷ Restricted Expression of viral genes

✷ reduces lytic potential, escape host immunity

✷ Infection of Immunological Privileged Sites

✷ not readily accessible to the immune system ✷ CNS favored by viruses

✷ Two factors favor viral persistence in CNS

  • Blood brain barrier - limits lymphocyte trafficking
  • Neurons do not express MHC I or MHC II, no direct recognition by T cells

✷ Viruses can persist in kidney e.g. BK, JC, CMV

• T cells can infiltrate the kidney, but limited access to infected epithelial cells

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8
Q

Antigenic Variation

A

✷ Emergence of viral variants

  • RNA viruses undergo mutation at high frequencies
  • This can result in evasion of both T and B cell immunity
  • Viral escape from antibody recognition
  • Viral escape from T-cell recognition
  • CTL escape mutants occur in HIV, EBV, and HBV
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9
Q

Interfernece with the Immune System

A

✷ Suppression of cell surface molecules required for T-cell recognition

• down regulation of several host molecules that are necessary for T-cell recognition of virus infected cells

✷ MHC I and II

  • Adenovirus downregulates MHC I
  • CMV, HIV, and measles have been shown to interfere with MHC II expression

✷ Interference with cytokine function

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10
Q

Persistent Viral Infection of CNS

A

✷ Persistent viral infections of CNS are slow viral diseases due to protracted period between infection and the prolonged course of the illness.

✷ Involve well differentiated cells, such as lymphocytes and neuronal cells.

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11
Q

Persistent Viral Infection of CNS Conventional Viral Agents

A
  • Viruses possess nucleic acid genome and protein capsid
  • Induce immune responses
  • Replicate in cell culture system
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12
Q

Persistent Viral Infection of CNS Conventional Viral Agents - SSPE

A

Subacute Sclerosing Panencephalitis (SSPE)

  • Rare chronic measles virus infection in children produces progressive neurologic disease
  • Usually appears 2 to 10 years after measles virus infection
  • Characterized by an insidious onset of personality change
  • Caused by measles virus
  • Progressive intellectual deterioration
  • Dysfunctions of motor and autonomic neuron system
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13
Q

Persistent Viral Infection of CNS Conventional Viral Agents - Progressive Postrubella Panencephalitis

A
  • Rare degenerative neurologic disorder similar to measles
  • May be related to persistent rubella virus infection of CNS
  • Seen most often in adolescents with congenital rubella syndrome
  • Rubella virus isolated from brain tissue of the patients.
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14
Q

Persistent Viral Infection of CNS Conventional Viral Agents - PML

A
  • Caused by JC virus
  • Subacute degenerative disease of the brain
  • Primarily in adults with other chronic diseases
  • Cerebrospinal fluid (CSF) findings are normal
  • Slight increase in lymphocytes
  • Protein levels elevated
  • Characterized by the development of impaired memory, confusion and disorientation.
  • Followed by a multiplicity of neurologic symptoms
  • Death could occur 3 to 6 months after onset of symptoms
  • Incidence is on rise because of AIDS epidemic

Diagnosis:

  • JCV particles can be seen by electron microscope
  • JCV DNA sequences have been detected by PCR.

Treatment:

  • No specific treatment for PML
  • Reducing the immunosuppression may have some clinical benefit
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15
Q

Persistent Viral Infection of CNS Conventional Viral Agents - Persistent Enterovirus Infection

A
  • •Persons with congenital or severe acquired immunodeficiency especially with agammaglobulinemia
  • Chronic CNS infection due to echovirus or enterovirus
  • Headache, confusion, lethargy, seizures and CSF pleocytosis are common manifestations.
  • Virus can be isolated from CSF, Clinical improvement by administration of human hyperimmune globulin to the infecting virus type.
  • Relapse occurs if therapy is discontinued.
  • Mainly Picornaviruses
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16
Q

Persistent Viral Infection of CNS Conventional Viral Agents - AIDS Dementia Complex

A
  • HIV causes a persistent infection of the CNS in many patients with symptomatic AIDS known as AIDS dementia complex (ADC) or HIV-associated dementia (HAD).
  • The virus does not directly infect the nerve cells, but the virus produced by perivascular macrophages and/or microglia may produce a bystander effect causing inflammation that may damage brain and spinal cord.
  • The clinical course may vary from a mild subacute illness (early stage of HIV infection) to severe progressive dementia (late stages of HIV infection).
  • HAD primarily occurs with more advanced HIV infection and symptoms include encephalitis, behavioral changes and a gradual decline in cognitive function.
  • HAD is more common is HIV infected infants than infected adults. •AIDS, reticuloendothelial malignancies, and those on immunosuppressive drugs
17
Q

Persistent Viral Infection of CNS Unconventional

Agents - Prions

A
  • Prions are small proteinaceous infectious particles
  • Small with diameters of 5-100nm
  • Produce characteristics infections and remain viable in formalinized brain tissues for many years •Resistant to ionizing radiation, boiling, autoclaving, and many common disinfectants
  • Protein molecules without genes
  • Responsible for some neurologic disorders •PrP gene found on chromosome 20
  • PrP gene is expressed as PrPc and post-translational conformational change makes it PrPsc (prion)
  • Conformational change is also the way in which prions number increase
  • Contact with PrPsc with PrPc results in a conformational change of the normal prion (PrPc ) and the formation of additional abnormal or infectious prion protein, PrPsc
  • PrPsc is responsible for transmission and infection
18
Q

Persistent Viral Infection of CNS Unconventional

Agents - Prions: 5 fatal CNS Diseases

A

✷Creutzfeldt-Jacob disease (CJD)

✷Variant CJD, Mad cow disease

✷Gerstmann-Straussler-Scheinker syndrome

✷Kuru

✷Fatal familial insomnia

19
Q

Kuru

A
  • Subacute, progressive neurologic disease of the Fore people of the Eastern Highlands of New Guinea
  • Affected adult women or children of either sex
  • Symptoms: ataxia, hyperreflexia, and spasticity leading to dementia, starvation and death
  • Pathology: changes in CNS with diffuse neuronal degeneration and spongioform changes of the cerebral cortex and basal ganglia
  • Transmission: Ingestion of organs of the deceased, mainly the soup of the brain in honor of the deceased
  • Incubation period: 60-360 months
  • Duration of illness: 3-12 months
  • Kuru has disappeared due to elimination of cannibalism from the Fore culture
20
Q

Creutzfeldt-Jacob Disease (CJD)

A
  • CJD is a progressive, fatal illness of the CNS mostly seen in the sixth and seventh decades of life
  • Clinical manifestations: change in cerebral function, usually diagnosed as psychiatric problem, forgetfulness and disorientation progress to overt dementia and changes in gait, increased tone in limbs, involuntary movement and seizures
  • Incubation period: 18 - 360 months
  • Duration of illness: 1- 55 months
  • Transmission: sporadic (85%) and familial pattern (15%)
  • Pathology: identical to kuru
21
Q

Gerstmann-Straussler-Scheinker Disease

A
  • Similar to CJD but occurs at a younger age (4th to 5th decade)
  • Cerebella ataxia and paralysis are common
  • Dementia is less often seen
  • Originally believed to be familial but also occurs sporadically
22
Q

Fatal Familial Insomnia

A
  • New familial prion disease
  • Syndrome of sleeping difficulty followed by progressive dementia
  • Occurs in patients aged 25-61 years of age
  • Duration of illness 13-25 months followed by death
  • Confirmed in experimental animals
23
Q

Bovine Spongiform Encephalopathy (BSE) (“Mad Cow Disease”) and “Variant Creutzfeldt-Jacob Disease”

A
  • BSE was identified in 1986 in the United Kingdom
  • Source of emerging epidemic was found to be a food supplement containing meat and bone meal from sheep
  • Incubation period in cattle: 2 to 8 years
  • Cows exhibited hyperesthesia, hyperflexia, muscle fasciculations, tremors and weight loss
  • Autonomic dysfunction was frequently manifested
  • BSE survives the heat of cooking and transmitted to humans consuming neural tissues or bone marrow and both are found on meats
  • More than 100 humans with variant CJD have died in the UK
  • Frequently present in young adults as psychiatric problems progressing to neurologic changes and dementia and death occurs in an average of 14 months

I & I Part II (25 decks)

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