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Exam #3 > Thiele > Flashcards

Thiele Flashcards

1
Q

What are the stages of viral replication?

A
  • recognition
  • attachment
  • penetration
  • uncoating
  • transcription
  • protein synthesis
  • replication
  • assembly
  • lysis and/or release
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2
Q

Describe recognition in the process of viral replication.

A
  • through recepto-ligand interactions

- viral associated proteins (VAP) bind to specific cellular receptors

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3
Q

Describe attachment in the process of viral replication.

A
  • specific cell receptors will bind to the VAPs on the viral nucleocapsid or membrane
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4
Q

Describe penetration in the process of viral replication.

A
  • viropexis - small viruses slip through the membrane (done by chanse)
  • Membrane fusion - an F-protein allows fusion of viral membrane with cellular membrane
  • Receptor mediated endocytosis - VAP-receptor binding leads to phagocytosis of the viral particle
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5
Q

Describe uncoating in the process of viral replication.

A
  • viral RNA replicates in the cytoplasm
  • viral DNA replicates in the nucleus
  • viral genetic material released into the proper location without cover of the capsid or membrane
  • full uncoating may be done only by viral enzymes after cellular enzymes partially uncoat the viral genome
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6
Q

Define monocystronic.

A
  • each mRNA produces one specific protein
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7
Q

Define polycystronic.

A
  • each mRNA produces multiple proteins in one single chain

- individual proteins can be produced by start and stop codons or by cleavage of the large protein

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8
Q

Define monopartite.

A
  • all genes linked on a single piece of RNA or DNA
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9
Q

Define multipartite.

A
  • viral genes are distributed in several pieces of RNA or DNA making up the whole genome
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10
Q

Define polarity of the RNA strands.

A
  • Positive strands can be read like mRNA

- Negative strands can not be read like mRNA

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11
Q

What are the three phases of transcription and translation of DNA viruses?

A
  • Immediate early phase - shutting down host cell materials
  • Early phase - genome is replicated before the transcription of genes
  • Late phase - structural, capsid and glycoproteins made
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12
Q

Discuss (+) RNA viruses.

A
  • (+) RNA will act as mRNA
  • first protein produced is RNA polymerase
  • uses host ribosomes
  • produces (-) strands for template for making more (+) strands
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13
Q

Discuss (-) RNA viruses.

A
  • RNA dependent RNA polymerase accompanies genome

- polymerase then produces (+)RNA and viral capsid proteins

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14
Q

How does a retrovirus funciton/replicate?

A
  • contains a RNA-dependent DNA polymerase - produces a cDNA strand from a RNA strand
  • integrase then integrates then cDNA into the host cells DNA and new viral RNA/proteins are produced by host tools
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15
Q

What are the four processes associated with viral genetics?

A
  • recombination - genetic exchange of viral and host DNA
  • reassortment - different genes are assembled together in progeny virus
  • transcapsidation - protein capsid of one strain and genome of another are put together
  • marker rescue - helper virus stimulates can reactivate a virus via recombination
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16
Q

What are the four main time frames for a viral infection?

A
  • Early phase - time from attachment to genome replication
  • Eclipse phase - time from attachment to production of virions
  • Late phase - time from genome replication to extracellular virus detection
  • Latent period - time from attachment to extracellular detection of virus
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17
Q

What are the host and viral factors that help determine viral pathogenesis?

A
  • interaction of virus with target tissue
  • cytopathological activity of the virus
  • immune response
  • immunopathology
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18
Q

What are the three types of cytopathogenesis of viral infections?

A
  • abortive
  • lytic
  • persistent infections
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19
Q

Discuss an abortive infection.

A
  • the host stops the virus from replicating (due to temperature, inappropriate enzymes or lack of receptors)
  • virus does not have appropriate genetic material
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20
Q

Discuss a lytic infection.

A
  • morphological changes occur by destruction of the host cell or by fusion into multinucleated cells
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21
Q

What are the different methods of a lytic infection?

A
  • membrane changes
  • necrotic and degraditive changes in genome
  • inclusion bodies
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22
Q

What are the different patterns of persistent infections

A
  • chronic infections
  • Latent infections
  • recurrent infections
  • transformation
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23
Q

What are three methods of immune system escape by chronic infections?

A
  • patching - collect glycoproteins in groups
  • capping - glycoproteins move to top of host cell
  • shedding - removal of all glycoproteins so cell cannot be seen
24
Q

How do latent infections persist?

A
  • integrate into host genome

- play a hide and seek by rapid replication to states of no replication

25
Q

What are the host cells defense against viral infections?

A
  • natural barriers (innate immunity)
  • Antigen specific immune response (neutralizing/non-neutralizing antibodies)
  • Cell mediated responses
  • Interferons - activates cell mediated response and halts infections
26
Q

Name some determinants of viral disease.

A
  • nature of exposure
  • immune status
  • age
  • general health
  • viral dose
  • genetics of the virus and host
27
Q

What are the clinical stages of viral infections?

A
  • incubation period - virus gains access to cell and prduces virus
  • prodrome - non-specific symptoms (infectious)
  • disease - clinical illness
28
Q

What is transmission of virus dependent upon?

A
  • source of the virus
  • tissue site of replication
  • ability to endure
  • enveloped or not
29
Q

What is the structure of the herpesvirus family?

A
  • linear dsDNA
  • icosahedral virus particle
  • enveloped
30
Q

What is the replication sequence of Herpesviruses?

A
  • fusion with host membrane releasing nucleocapsid into cell and delivery into nucleus
  • Immediate early, early and late phase protein production
31
Q

What are the stages of pathogenesity and immunity of the HSV 1, 2?

A
  • initiated by direct contact
  • cytopathology results in lesions
  • virus avoids Ab by cell to cell spread
  • virus establishes latentcy
  • virus reactivates due to stress
  • cell mediated immunity is required for resolution
32
Q

What are the clinical syndromes of HSV 1 and 2?

A
  • Gingivostomatitis - lesions along third trigemianal nerve
  • Eczema herpeticum - infection of open wound
  • Herpes keratoconjunctivitis - infection of eye
  • Herpetic Whitlow - infection of the finger
  • Herpes encephalitis - brain damage
  • Pharyngitis
  • Herpes Gladitorium - infection of body/trunk
  • Genital Herpes (HSV-2)
  • Neonatal Herpesvirus - frequently fatal
33
Q

How is herpes 1 and 2 diagnosed?

A
  • clinical picture (lesions in noted areas)

- Cytology (Tzanck smear, syncytia, Cowdry type A bodies)

34
Q

What are the treatments for HSV-1,2?

A
  • idoxuridine - inhibits viral DNA polymerase
  • vidarabine - analogue that forms a faulty DNA strand
  • Acyclovir - block guanosine uptake
35
Q

Discuss the characteristics of Varicella virus?

A
  • childhood exanthems
  • pock-type lesions - cover whole body and pocks at different stages
  • transmission through respiratory droplets
36
Q

Discuss the characteristics of Zoster virus.

A
  • primarily a disease of adults

- pock type lesion over a dermatomal area

37
Q

What is the pathogengenesis of the Varicella virus?

A
  • replicates in the respiratory tract
  • viremia to secondary infection site
  • replication in secondary organ
  • viremia and virus goes to skin and rash occurs
  • incubation period 10-11 days
  • contagious during rash until crusted over
38
Q

What is the pathogenesis of the Zoster virus?

A
  • re-activation of the virus occurs along the dermatomal area
39
Q

How is the Varicella-Zoster virus diagnosed?

A
  • clinical picture and recognition of outbreaks
40
Q

What is the treatment/prevention for Varicella-Zoster virus?

A
  • treat the symptoms
  • Acyclovir may shorten the course of disease
  • Zoster immune globulin - if severe
41
Q

How is the Epstein-Barr virus spread?

A
  • saliva

- blood transfusion and bone marrow

42
Q

What is the pathogenesis of EBV?

A
  • virus infects cells in oropharynx and spreads through lymphatics to infect B cells
  • virus replicates in B cells and causes Lymphoma (T cells attack B cells) then virus goes latent
43
Q

What diseases are EBV associated with?

A
  • Infectious Mononucleosis
  • Burkitt’s Lymphoma
  • Nasopharyngeal Carcinoma
  • Hairy Oral Leukoplakia
44
Q

Discuss Infections Mononucleosis

A
  • clinical triad of: sore throat, fever (high), and lymphandenopathy/hepatosplenomegally
  • Atypical T lympocytes (Downey cells) produced
  • presence of a heterophile antibody is diagnostic
45
Q

Discuss Burkitt’s Lymphoma.

A
  • B cell lymphoma that is associated with EBV and malaria

- malaria is thought to drive B cell proliferation

46
Q

Discuss Nasopharyngeal Carcinoma

A
  • B cell proliferation due to Euphorbacea plant agent with infection of EBV will = tumor
47
Q

Discuss Hairy Oral leukoplakia.

A
  • infeciton of epithelial cells of the tongue = white coat

- seen in AIDS pts

48
Q

What is the epidemiology of Cytomegalovirus?

A
  • neonates and breast fed children - crosses placenta

- sexual transmission

49
Q

What diseases are associated with cytomegalovirus?

A
  • Non-classical mononucleosis
  • Mental retardation
  • Microcephally
  • Organ transplant infection
50
Q

How is cytomegalovirus diagnosed?

A
  • cytology - owl-eye inclusion body
51
Q

What is the treatment for cytomegalovirus?

A
  • Ganciclovir - blocks quanosine uptake and stops viral DNA formation
  • Foscarnet - stops phosphorylation of nucleotides
52
Q

What are differences in Non-classical mononucleosis?

A
  • less severe sore throat

- no rise in the heterophile antibody

53
Q

What are the diseases associated with HHV-6?

A
  • Exanthem subitum (Roseola)
  • Kaposi’s sarcoma
  • Hodgkin’s disease
  • Multiple sclerosis
54
Q

What are the characteristics of Roseola infantum?

A
  • rapid onset of fever
  • rash that lasts 24-48 hours
  • lifelong latent infection in T-cells
55
Q

What is the pathogenesis of HHV-6?

A
  • needs HHV-7 as a helper virus

Exam #3 (9 decks)

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