Virology Quiz 2 Herpesvirus Part 2

Front 1

which patients are at risk for disseminated zoster? What characterizes this condition? How can it be treated?

Back 1

immunocompromised patients; viremia with lesions outside the original dermatome; acyclovir

Front 2

infiltration of what specific cell type is characteristic of zoster?

Back 2

monocyte

Front 3

what is the theory behind the relationship between zoster and age?

Back 3

age-related decline in cell-mediated immunity

Front 4

can a zoster infection be source of a chickenpox epidemic? What characterizes the Ab against varicella-zoster in a recovered patient?

Back 4

yes; very high antiviral Ab titers

Front 5

what is the nature of the vaccine available for varicella-zoster virus?

Back 5

live-attenuated

Front 6

why is it recommended that elderly people receive the chickenpox vaccine?

Back 6

to reduce the likelihood of developing zoster

Front 7

what is characteristic of cells infected with cytomegalovirus?

Back 7

very large cells with nuclear inclusion

Front 8

which cytomegaloviral infections are usually subclinical?

Back 8

those that occur before puberty

Front 9

what is the incubation period for cytomegalovirus?

Back 9

3-12 weeks

Front 10

teenagers and adults with cytomegaloviral infections can often present with symptoms resembling which other disorder? Is the heterophile test in these patients positive or negative?

Back 10

mononucleosis; negative

Front 11

in what situation is cytomegalovirus-caused mononucleosis-like syndrome often seen?

Back 11

post blood-transfusion complication

Front 12

how is cytomegalovirus transmitted?

Back 12

via close contact through naso-pharyngeal fluid, semen, urine, and vaginal secretions

Front 13

how can mothers infect their children with cytomegalovirus? What is the likelihood of this? What symptoms do children infected in this way show?

Back 13

through breast feeding; 40%; asymptomatic

Front 14

is congenital infection with cytomegalovirus common or uncommon? What are the symptoms of the congenital disease?

Back 14

common; microcephalic mental retardation with intracerebral calcifications, neuro-sensory deafness, jaundice, enlarged liver/spleen, anemia

Front 15

how many symptomatic congenital infections of cytomegalovirus occur per year in the US?

Back 15

4000

Front 16

what is the most frequent congenital viral infection?

Back 16

cytomegalovirus

Front 17

congenital malformations from maternal cytomegaloviral infection usually result from which type of infection?

Back 17

primary maternal infection

Front 18

what is the best source of detection for neontal cytomegaloviral infections?

Back 18

urine

Front 19

which antiviral treatment is most effective at treating neonatal cytomegaloviral infections?

Back 19

gancyclovir

Front 20

what kind of vaccine is being experimented for cytomegalovirus?

Back 20

live vaccine

Front 21

in which unique situations is recurrent cytomegalocviral infection seen? What symptoms characterize this infection?

Back 21

when immune response is defective; pneumonitis and hepatitis

Front 22

what symptoms do AIDS patients with recurrent cytomegaloviral infections express?

Back 22

retinitis and gastroenteritis

Front 23

what is the current best treatment for all CMV infections?

Back 23

gancyclovir

Front 24

CMV is usually a major problem in which situation?

Back 24

organ transplantation

Front 25

which virus is the most common cause of infectious mononucleosis?

Back 25

Epstein-Barr virus

Front 26

which age groups are most prone to mononucleosis? In which group is the infection subclinical? How is it usually spread?

Back 26

teenagers and young adults; young children; kissing, via saliva

Front 27

what are the most common symptoms of mononucleosis? What is the incubation period? Which other infection can mimic this clinical presentation?

Back 27

fever, sore throat, lymphadenopathy; 4-6 weeks; HIV infection

Front 28

what characterizes the 'abnormal' lymphocyte profile in patients with mononucleosis?

Back 28

large numbers of CTLs to attack infected B cells

Front 29

which test is a good measure of mononucleosis?

Back 29

positive to heterophile antibody

Front 30

how is the heterophile Ab induced in mononucleosis infections? Does this Ab neutralize the virus?

Back 30

by EB virus Ag; no

Front 31

what is the impact of the EB virus on B cells?

Back 31

transforms them into actively dividing cells

Front 32

in which unique situation does fatal lymphoproliferative disease from EBV result?

Back 32

patients with a mutation which blocks cell mediated immune response to EB virus

Front 33

what happens to Ab against EBV and heterophile Ab as mononucleosis progresses?

Back 33

EBV Ab increases; heterophile Ab rapidly disappears

Front 34

during an acute EBV infection, what type of cells can be cultured during the acute disease to show infection?

Back 34

B lymphocytes

Front 35

where is EBV produced in patients with mononucleosis?

Back 35

in B cells of the oropharynx

Front 36

does the production of EBV in infected patients stop immediately following the end of the disease?

Back 36

no, it may continue for months after

Front 37

what is oral hairy leucoplakia? In which patients is this common? What characterizes this?

Back 37

disease seen from recurrent infection of EBV; with immunocompromised patients; whitish patches on tongue or buccal mucosa

Front 38

what characterizes infection with human herpes virus 6? Is this infection local or systemic?

Back 38

fever, with sometimes a rash in infants; systemic

Front 39

human herpes virus 8 is a probable cause of which disease?

Back 39

Kaposi's sarcoma

Front 40

which 2 diseases result from EBV infections in immunocompromised patients?

Back 40

oral hairy leucoplakia and B cell tumors

Front 41

why is selective chemical inhibition of viruses difficult?

Back 41

because they rely on host cells for most biochemical processes

Front 42

which viruses have more potential targets for drug therapy?

Back 42

viruses with larger genomes

Front 43

what do antivirals for herpesviruses do? How do they help latant infection?

Back 43

inhibit viral replication; they do NOT

Front 44

what is the source of most thymidylic acid in cells?

Back 44

de novo synthesis from glucose and certain amino acids

Front 45

do herpes viruses have the gene for their own thymidine kinase?

Back 45

yes

Front 46

why is an antiviral against thymidine kinase effective only against infected cells? How is the virus inhibited in infected cells?

Back 46

because cells infected with herpesvirus have more thymidine kinase activity than do uninfected cells; thymidine analogues

Front 47

when are thymidine analogue antivirals toxic?

Back 47

when they are given systemically

Front 48

which is more specific, the host thymidine kinase or that of the virus?

Back 48

the host

Front 49

which type of antiviral is acyclovir an example of?

Back 49

thymidine analogue

Front 50

how does acyclovir work in vivo?

Back 50

acyclovir is phosphorylated nu the herpes viral thymidine kinase and is then converted by host cell enzymes to the triphosphate, which is incorporated into DNA and blocks further incorporation of nucleotides

Front 51

what is the best antiviral for VZV and HSV infections? For CMV infections?

Back 51

acyclovir; gancyclovir

Front 52

what is the effect of the nucleotide form of trifluridine on the host cell?

Back 52

causes lethal DNA synthesis errors and inhibits thymidylic acid synthetase of the host cell

Front 53

for which viral infection is triflurodine useful? Where is it applied?

Back 53

recurrent keratitis; to the eye

Front 54

why are cells of the cornea not affected by triflurodine?

Back 54

cells of cornea have a very small amount of DNA synthesis and thus are not affected by the drug

Front 55

other than triflurodine, what is used to treat keratitis?

Back 55

systemic acyclovir

Front 56

why can trifluridine not be used for systemic infections?

Back 56

because some tissues have a rapid rate of DNA synthesis and a high thymidine kinase activity and thus are sensitive to trifluridine

Front 57

what do antivirals adenine arabinoside and foscarnet inhibit?

Back 57

viral DNA polymerase (preferentially)

Front 58

what is the antiviral adenine arabinoside an analogue of?

Back 58

deoxyadenosine

Front 59

what occurs when adenine arabinoside triphosphate is incorporated into viral DNA by the viral-DNA polymerase?

Back 59

it blocks further DNA synthesis

Front 60

in which diseases has adenine arabinoside been proven useful?

Back 60

herpes simplex encephalitis and in immunosuppressed patients with zoster

Front 61

the antiviral foscarnet is an analogue of which molecule? Which molecule does it inhibit?

Back 61

pyrophosphate; herpesvirus DNA polymerase

Front 62

for which other antiviral is foscarnet an alternative?

Back 62

gancyclovir