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MHD > Herpesvirus > Flashcards

Herpesvirus Flashcards

1
Q

Structure of Herpes Viruses

  1. genome
  2. envelope?
  3. What is the tegument? what is in it?
A
  1. double stranded DNA w/ capsid
  2. present with gB-gN proteins
  3. region between the capsid and the environment that contains proteins
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2
Q

Sequence of Transcription

  1. What proteins are synthesized early?
  2. What rises as these proteins are made?
  3. What proteins are synthesized late?
A
  1. DNA synthesis proteins
  2. DNA
  3. Virion proteins
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3
Q

Productive Infection

  1. What happens first?
  2. Where does viral DNA go?
  3. What happens next?
  4. What is the final step?
A
  1. Virus fuses with cell via glycoproteins on cell surface receptors
  2. goes into nucleus in its capsid, then transcribed into mRNA and more DNA is made
  3. Proteins are made in the cytoplasm and come back into the nucleus to make the capsid;
  4. virus buds off cell
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4
Q

Herpes Simplex Type 1

  1. Primary infection locations
  2. What kind of cells does it infect and kill?
  3. What does virus infect but not kill?
  4. What does it produce there?
  5. What happens in reactivation?
  6. What causes reactivation?
A
  1. cold sores, sore throat, fevery, encephalitis (rarely); less frequently found as genital infection
  2. Epithelial cells
  3. Sensory neurons
  4. Latency associated transcripts (LATs)
  5. virus travels back to epithelial cells, causing lesions and shedding
  6. Unknown
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5
Q

HSV 1

  1. How much virus is being produced in latent infection? What are the symptoms
  2. Where does virus/viral DNA reside?
  3. What happens in recurrent infection?
  4. symptoms
A
  1. none, no symptoms
  2. sensory cells of trigeminal nerve ganglion
  3. virus replicates and travels down sensory nerve fiber to infect epithelial cells around the nose and mouth
  4. milder form of primary infection
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6
Q

HSV2

  1. Primary infection
  2. Transmission
  3. Who gets it?
  4. Associated with what?
A
  1. vesicular eruptions on the genitalia
  2. sexual contact
  3. both sexes
  4. cervical carcinoma, less frequently found as herpes labialis (cold sores)
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7
Q

HSV2

  1. How much virus is produced in latent virus?
  2. Where does viral DNA reside?
  3. Where does the recurrent infection occur?
  4. Symptoms
A
  1. none
  2. sensory cells of sacral ganglion
  3. same location in genital area
  4. milder form of primary infection
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8
Q

HSV Infections

  1. What tends to cause encephalitis and meningitis?
  2. What are Whitlow’s nodules?
  3. What do Whitlow’s nodules look like?
A

1, reactivation infections

  1. nodules on hands caused by exposure to HSV at that point;
  2. bacterial infection
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9
Q

Infections Assoc w/ HSVs

  1. 1 very common infection
  2. 2 common infections
  3. 3 rare/ very rare infections
A
  1. oral herpes- usually resolves
  2. genital herpes- usually resolves; ocular herpes (more commonly in elderly)- resolution; visual impairment
  3. neonatal herpes (development impairment, death); encephalitis (neuro impairment, death); disseminated herpes (resolution or death)
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10
Q

Acyclovir

  1. Mechanism
  2. Why doesn’t it affect human cells?
  3. What does it do to duration of virus?
  4. What does it do to reactivation of virus?
A
  1. similar to GTP, is phosphorylated to acyclo GTP which is then put into extending DNA which then terminates the chain
  2. the first step is catalyzed by viral thymidine kinase, not found in human cells; inert in uninfected cells
  3. decreases duration
  4. prevents reactivation
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11
Q

Acyclovir Resistance

  1. Who tends to be infected with resistant mutants?
  2. Why these pts?
  3. 2 mutations
  4. How do you treat these pts
A
  1. Immunocompromised Pts
  2. Mutations tend to attenuate virus, so healthy immune systems can still fight infection
  3. viral thymidine kinase (drug not phosphorylated to active form)
  4. viral polymerase (no longer efficiently binds the drug)
  5. improve immune system function
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12
Q

TZP/Us

1. Mechanism of Action

A
  1. binds herpes virus helicase-primase; prevents unwinding
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13
Q

Varicella Zoster

  1. Primary infection
  2. Transmission
  3. Seasonal?
A
  1. chicken pox; systemic infection resulting in generalized pruritic vesicular rash
  2. from one infected child to another
  3. seasonal epidemics during school year (when many children are together)
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14
Q

Varicella: Clinical Features

  1. What happens first?
  2. Then what?
  3. Where does rash occur?
  4. What happens in healthy children?
  5. When is pt contagious?
A
  1. mild prodrome (fever, malaise) for 1-2 days
  2. successive crops of pruritic vesicles
  3. first on head, most concentrated on trunk
  4. mild infection
  5. From a few days before fever throughout rash;
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15
Q

Varicella

  1. Where does virus replicate?
  2. What coincides with the contagious period?
A
  1. lymph nodes

2. secondary viremia; primary viremia occurs after viral replication in lymph node

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16
Q

Varicella: Complications (5)

A
  1. Bacterial infection of lesions
  2. CNS manifestations
  3. Pneumonia (rare in children)
  4. Hospitalization in 3/1000 cases
  5. Death in 1/60,000 cases
17
Q

Varicella

  1. Who tends to get it?
  2. Who tends to have worse outcomes?
A
  1. ages 1-14

2. people older than 30

18
Q

Varicella Vaccine

  1. Type
  2. Efficacy
  3. Duration of Immunity
  4. Schedule
  5. What does immunization do?
  6. Can vaccine become latent?
A
  1. Live virus (Oka strain); may be given with MMR vaccine
  2. 95%
  3. 5 years; probably long lasting
  4. 1 dose at 12-15 mo; booster before starting school
  5. reduces incidence of most severe disease and hospitalization;
  6. yes, but it is less likely to reactivate than wild type virus
19
Q

Varicella Zoster

  1. How much virus is produced in latent infections?
  2. Where does viral DNA reside?
  3. How does virus re-infect?
  4. What is the pattern of recurrent infection? symptoms?
  5. What can happen in immune suppresssed individuals?
A
  1. none; no symptoms
  2. cells of dorsal route ganglion
  3. virus travels down sensory nerve fiber and infects epithelial cells innervated by the fiber
  4. unilateral, localized to a dermatome usually in head or upper trunk; painful vesicular eruptions
  5. severe systemic infections
20
Q
  1. What can be done to reduce incidence of herpes zoster?

2. Treatment?

A
  1. immunize the eldery; works for those that have and hadn’t it
  2. Varicella Zoster Ig- passive immunity; acyclovir not that good
21
Q

Epstein-Barr Virus (EBV)

  1. Primary infection (2 presentations)
  2. Malignant lymphoproliferative diseases (2)
A
  1. Asymptomatic, infectious mononucleosis

2. Burkitt’s lymphoma, Nasopharyngeal carcinoma

22
Q

EBV

  1. How long does infection last?
  2. How long are you contagious?
  3. Transmission?
  4. Who is at risk for infectious mono?
  5. Geography/Season?
A
  1. life-long infection
  2. life-long asymptomatic shedding of virus
  3. saliva
  4. teenagers and adults; children more likely to be asymptomatic
  5. world-wide distribution, no seasonal incidence
23
Q

EBV: Pathology

  1. What 2 cell types does virus infect?
  2. What does infection promote?
  3. Who gets severe disease?
A
  1. Epithelia and B cells in lymphatics
  2. growth of B cells;
  3. T-cell deficient pts b/c T cells kill/control B-cell outgrowth and promote latency in B cells
24
Q

EBV

  1. What are the results of invasion of epithelial cells of oropharynx? (2)
  2. What is the result of B cell proliferation
  3. What is the result of T cell activation?
  4. What happens to the liver, lymph nodes, and spleen?
A
  1. Pharyngitis and shedding of virus in saliva
  2. Heterophile antibody
  3. Aytpical lymphocytes (Downey cells)
  4. they swell
25
Q

Detection of EBV?

  1. What are heterophile antibodies?
  2. What test detects them?
  3. What other test may be used to
A
  1. Diverse antibodies made by B cells activated by EBV
  2. Monospot test, can give false (-) in children
  3. Antibody to EBV VCA; IgM/IgG to viral capsid Ag
26
Q

EBV: Course of Infection

  1. High levels of what early on?
  2. What Ag is found early on?
  3. What Ag is found later?
  4. How long do the Ag and Ab last?
A
  1. BOTH IgM and IgG to capsid antigen
  2. early antigen
  3. EB nuclear antigen
  4. Anti-VCA IgM and IgG last for years/life; Anti-EBNA last for years/life
27
Q

EBV Clinical Syndromes (5)

A
  1. Infectious Mononucleosis
  2. Post-trasnplant Lymphoproliferative disorder (PTLD- transplant frm EBV+ to EBV -
  3. Hairy Oral Leukoplakia (w/ AIDS)
  4. African Burkitt’s Lymphoma (malaria is cofactor)
  5. Nasopharyngeal carcinoma (esp in China)
28
Q

Cytomegalovirus (CMV)

  1. Primary infection (2)
  2. What happens in immunocompetent carriers?
  3. What happens in immunocompromised carriers?
A
  1. asymptomatic; can be serious in fetal/neonatal time
  2. asymptomatic shedding
  3. serious complications
29
Q

CMV

  1. Causes lifelong what?
  2. How is it transmitted?
  3. Who is at highest risk for symptomatic and recurrent disease?
A
  1. asymptomatic shedding of virus
  2. blood, secretions (including breast milk and semen)
  3. babies and immunosuppresssed
30
Q

CMV

  1. What cells does it infect?
  2. Where does it become latent?
  3. What allows recurrence?
  4. When does the potential for CMV to be in cervical secretions increase?
  5. What disease presentation is common in immunosuppressed individuals?
A
  1. epithelium
  2. T cells, macrophages, and other cells
  3. suppression of cell-mediated immunity
  4. third trimester of pregnancy
  5. pneumonia
31
Q

CMV:

  1. What can babies have with a CMV infection?
  2. What disease can CMV be confused with?
A
  1. can be fatal, usually results in long lasting sequelae

2. EBV

32
Q

Lab Tests for CMV

  1. What does Ag Detection find?
  2. What does Serology find?
  3. What does cytology/histology find?
  4. Where are samples taken from?
A
  1. early antigens by immunofluorescence
  2. CMV specific IgM and IgG
  3. “owl eye” inclusion body
  4. urine, saliva, blood, bronchoalveolar lavage, tissue biopsies
33
Q

CMV: Treatment

  1. What can be used?
  2. Problem/ Side effect
A
  1. Ganciclovir

2. bone marrow toxicity

34
Q

Roseola

  1. Which herpes viruses?
  2. What is the first symptom?
  3. What develops next?
  4. What cell type resolves the infection?
  5. Long term
A
  1. HHV-6 and HHV-7
  2. rapid onset of high fever
  3. Generalized rash 24-48 hrs later
  4. T cells
  5. recovery w/o complications
35
Q

Roseola

  1. How many have been exposed by age 5?
  2. How common is it?
  3. Diagnostic Tests
  4. Therapy
  5. Does virus become latent?
A
  1. > 95% seropositive
  2. major cause of visits to ER, febrile seizures, and hospitalization
  3. no rapid test
  4. none
  5. yes, but it remains latent
36
Q

Kaposi’s Sarcoma

  1. Who clasically gets it?
  2. Four types
  3. Who is it especially common in?
A
  1. elderly men of Mediterranean or Eastern European descent
  2. Classical, African(endemic), iatrogenic (post-transplant), AIDS-related (epidemic)
  3. AIDS pts
37
Q

Kaposi’s Sarcoma

  1. What does it look like grossly?
  2. Under microscope?
  3. How is it transmitted?
  4. What resolves the infection?
A
  1. large purple spots
  2. spindle-shaped tumor cells w/ neovascularization and inflammatory infiltrate
  3. sexually transmitted disease (HHV-8)
  4. T-cells
38
Q

Kaposi’s Sarcoma

  1. How can it be activated?
  2. How can it be treated in HIV pts?
A
  1. immunosuppression

2. use of ani-retroviral drugs

MHD (17 decks)

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