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Virology > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q 
Mumps:
virus type:
nucleic acid structure:
subclinical presentation?
vaccine live or killed?
transmitted via:
treatment:
viremia?
clinical symptom?
A 
paramxyovirus
-RNA
subclinical in 30%
live vaccine
transmitted via respiratory droplets
no antiviral therapy
viremia >> incubation period of 18-21
PAROTIDITIS!
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2
Q

How do you treat croup?

A

glucocorticoids administered orally

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3
Q 
Measles:
virus type;
nucleic acid structure:
subclinical presentation?
vaccine live or killed:
transmitted via:
treatment:
viremia?
clinical symptoms:
antigenic variance:
possible to eradicate? why?
A

*most contagious, more virulent
paramyxovirus
-RNA
no subclinical presentation
vaccine live
transmitted via saliva, skin, blood *infects via respiratory tract and multipies in epithelium and lymph nodes/conjunctiva
treatment: no specific treatment, but Vitamin A can help in cases of malnutrition
viremia; yes 14 day incubation
symptoms: infects ALL cells. rash, Koplik spots (white spots on mucosa of mouth), photophobia. prodromal symptoms: cold-ike, fever, red eyes
antigenic variance: no
possible to eradicate bc humans are only reservoir

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4
Q

what is the mechanism of spread of measles within cells?

A

fusion protein inserted into infected cell plasma membrane&raquo_space; multi-nucleated giant cells

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5
Q

What would happen if someone infected with measles had a tuberculosis skin test that was previously (prior to measles infection) positive?

A

the skin test would be negative. Measles causes anergy (loss of cell-mediated immunity). risk for secondary infections high

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6
Q

what causes giant-cell pneumonia?

A

measles virus combined with defective cell-mediated immmunity. occurs without apperance of rash

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7
Q

which is more important in combatting viral infections: cell -mediated immunity or antibodies?

A

cell-mediated immunity

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8
Q

JC (John Cunningham) virus

A

papovavirus,&raquo_space; Progressive Multifocal Leukoenceophalopathy (PML) in immunocompromised individuals. blindness, dementia, coma, death

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9
Q

what are the four characteristics of slow viruses?

A

long incubation, relentless course leading to death, genetic predisposition, re-emerge during immune suppression

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10
Q

What is Subacute sclerosing panencephalitis (SSPE)

A

related to early childhood infection with measles virus. intellectual deterioration, psych distrubances, slow decline. terminal paralysis w/blindness

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11
Q

characteristics of prion infections:

A

long incubation period, death, diseases confined to CNS, spongiform encephalopathy

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12
Q

5 known transmissible spongiform encephalopathies:

A
  1. KURU
  2. Creutzfeld Jacob disease
  3. variant CJD,
  4. Gerstmann-Straussler-Scheinker syndrome
  5. Fatal familial insomnia
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13
Q

Creutzfeld-Jacob Disease

A

most common human spongiform encephalopathy. linked to contaminated surgical instruments & growth hormone prepared from an undiagnosed CJD patient, also familial genetics or mutations.

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14
Q

what does iatrogenic mean?

A

caused inadvertently by physicians

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15
Q

Where does Herpes Simplex Type 1&2, EBV establish latent infection?

A

1/2: neuronal cells

EBV: monocytes

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16
Q

How does acyclovir work?

A

it is phosphorylated (in virus cells alone) by a virus-specific tyrosine kinase. It then is phosphrylated again by cellular kinases.&raquo_space; steric hindrance when incorporated into growing DNA chain, it causes chain termination

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17
Q

what is the most likely cause of a vomiting illness in a daycare?

A

norovirus

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18
Q

What is the major viral cause of congeintal abnormalities?

A

CMV. risk during 1st tri

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19
Q

keys points about Epstein Barr:

A

“kissing disease”
Herpes virus 4
can cause tumors: burkitt’s lymphoma
Mononucleosis w/ POSITIVE HETEROPHILE TEST
latent infection in B cells; transformed, latently infected B cells are hallmark of EB
no antivirals, no vaccine
recurrent disease&raquo_space;oral hairy leukoplakia

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20
Q

HHV-6 is associated with:

A

roseola rash. It can be transmitted through germline

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21
Q

HHV-8 is associated with:

A

kaposi’s sarcoma. often associated with HIV-AIDS.

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22
Q

How do Herpes viruses infect a cell?

A

linear dsDNA adsorbs to cell –> fusion to cell membrane. release of nucleocapsid to cytoplasm –> nuclear membrane & release of DNA into nucleus –> DNA becomes circular –> mRNA & proteins –> progeny nucleocapsids (NUCLEAR INCLUSION BODIES) –> glycoprotein fusion with membrane –> creation of multinucleate giants & budding out of nucleocapsids

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23
Q

what tests can be done to distinguish type 1 and type 2 herpes?

A

monoclonal antibodies or PCR

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24
Q

which three viruses have latency in sensory ganglion cells?

A

Type 1&2 herpes simplex, varicella-zoster

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25
Q

where does EB virus establish latency?

A

B lymphocytes

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26
Q

incubation period of Herpes simplex type 2:

A

1-2 weeks.

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27
Q

Herpes simplex encephalitis is most commonly associated with which type of herpes? how is it detected? treated?

A

Simplex Type 1; detected with PCR of cerebrospinal fluid ; Acyclovir

28
Q

What is herpes simplex keratitis?

A

infection of cornea & conjunctiva, presents as bilateral redness –> blindness. treat w/ topical trifluridine or systemic acyclovir

29
Q

incubation period for varicella?

A

2-3 weeks, then rash & fever

30
Q

how should immunosuppressed individuals exposed to varicella -zoster be treated?

A

passive immunity with IgG from donors with high levels of Varicella-Zoster Immune Globulin. current: treatment w/acyclovir, and (preventative) with vaccination prior to exposure

31
Q

characteristics of Shingles (Zoster)?

A

primary infection with Varicella. monocyte invasion of ganglia. dermatomally distributed lesions. recovery —> subcutaneous pain, post heretic neuralgia. treat w/acyclovir.

32
Q

Varicella-zoster vaccine is:

A

live-attenuated. recommend for children and adults. requires booster

33
Q

Cytomegalovirus:

A

3-12 week incubation period. mononucleosis w/ NEGATIVE HETEROPHILE test (contrast w/EB). congenital malformation of fetus of seropositive mother frequent. fetus makes anti-CMV IgM –> IgG once born. detect in urine. treat symptomatic neonates with Ganciclovir

34
Q

Symptoms of EB:
incubation period:
diagnostic:

A

fever, sore throat, lymphodenopathy. high quantities of cytotoxic T lymphocytes

  1. 2-3 weeks
  2. heterophile antibody induced by EB viral antigen (use sheep blood…)
35
Q

how does acyclovir work?

A

nucleotide analogue for herpes thymidine kinase. gets phosphorylated and blocks DNA synthesis (chain-termination analogue). used to treat herpes simplex and varicella-zoster.

36
Q

why can’t antivirals for herpes virus treat latent infections?

A

they target DNA replication ONLY. latent infections do not have active replication.

37
Q

triflourodine is used to treat:

it works by:

A

keratitis caused by herpes simplex. good for local infection because cells of eye do not have much active replication so it won’t affect them. acyclovir also used systemically
works by incorporating into host cell DNA and causing replication errors (which is why it can’t be used systemically).

38
Q

In addition to acyclovir, another chain termination analogue used to treat Herpes viruses is:

A

adenine arabinoside.

39
Q

Foscarnet acts by —— and can be used to treat:

A

inhibits DNA polymerase of Herpes viruses. treat CMV instead of ganciclovir, and acyclovir resistant varicella and simplex.

40
Q

characteristics of papovaviruses:

A

TUMOR VIRUSES. small (<10 genes), unenveloped icosahedral and ds(circular)DNA,

41
Q

replication strategy of papovaviruses:

A

late and early stage genes.

  1. large T-antigen expressed binds to viral DNA Origin of R, initiates replication via host cell polymerase. *large T-antigen crucial for overcoming host cell tumor suppressor genes Rb and p53.
  2. Once replication has occurred, capsid protein DNA is replicated. Capsid proteins are transcribed and begin packaging dna.
42
Q

distinction between warts and tumors in HPV infections:

A

warts: viral genome not integrated
tumor: E6 & E7 viral oncogenes integrated w/host cell DNA and highly expressed

43
Q

Adenovirus characteristics:

A

TUMOR VIRUSES (but not in humans). express E1A and E1B. E1A binds to tumor suppressors and also binds (stimulates) transcription site.

44
Q

The two Herpes viruses that are tumor viruses are:

A
  1. EB –> Burkitt’s Lymphoma, nasopharyngeal carcinoma & tumors in immunocomrpomised
  2. HHV-8 –> Kaposi’s sarcoma
45
Q

Is integration of viral DNA into host cell genome required for EB virus to cause transformation?

A

NO!

46
Q

How does EBV transform cells?

A

only possible in individuals with compromised immunity! = why malaria or HIV/AIDS & burkitt’s coincide. malaria compromises cell-mediated immunity.
expression of genes:
EBNA-2 = transcriptional activator
LMP-1 = homologue of CD40.

47
Q

How does HHV-8 result in Kaposi’s sarcoma?

A

expresses viral oncogene (G-protein coupled receptor) that induces vascular endothelial growth factor expression (a CELLULAR protein, not viral).

48
Q

basic characteristics of retroviruses:

what do all retroviruses encode:

A

enveloped nucleocapsid containing two identical strands of + RNA.
all (except transforming, ‘defective’ viruses causing tumors) encode Gag&raquo_space; nucleocapsid proteins; Pol&raquo_space; reverse transcriptase & integrase; Env&raquo_space; envelope glycoproteins.

49
Q

describe retroviral takeover process:

A

2 phases: extracellular = viral particle; intracellular = provirus (now exists as DNA incorporated into host cell).
replication: nucleopcapsid adsorbs to cell. in cytoplasm, RNA» DNA via reverse transcriptase. 5’ & 3’ ends duplicated (long terminal repeats). LTRs contain viral transcription elements. RNA is degraded and DNA enters nucleus to be incorporated into host cell DNA by integrase. now = provirus. All steps from here completed by host cell machinery.

50
Q

why do the viral counterparts to cellular proto-oncognes cause tumors?

A

high rates of transcription bc virus is actively replicating; elevated activity of various genes including Src

51
Q

difference between acute and non-acute transforming retroviruses:

A

acute: defective retroviral genes bc do not encode all three Gag, Pol and Env. contain protoncogene instead.
non-acute: take a long time to develop cancers. do encode Gag/Pol/Env, protooncogene inserted adjacent to viral DNA and subsequently expressed at high rates bc of viral promotor.

52
Q

Human oncogenic retroviruses are:

A

HTLV1 & 2
transmitted sexually or via breastmilk
cause T-cell leukemia

53
Q

similarities between retroviruses and Hepatitis B:

A

both use reverse transcriptase (but Retroviruses use it early, hep B late). both can be targeted by lamuvidine.

54
Q

basic characteristics of flaviviruse and toga viruses:

A

small, enveloped icosahedral +mRNA. most are transported by arthropods (arboviruses)

55
Q

what are the incubation periods for arboviruses:

A

extrinsic: in athropod. 14 days.
intrinsic: in humans. one week

56
Q

Eastern & western equine encephalitis are transmitted from arthropods to humans but not back. why? what is this called?

A

level of infectivity in humans (and horses) not typically high enough to cause viremia in arthropod. virus maintained in wilderness by birds and bugs. humans are a dead-end host

57
Q

Dengue fever

A

arbovirus; causes fever, severe headache, (hemorrhagic type&raquo_space; hemorrhage, shock, etc).
4 antigenic types. second infection w/different type causes severe form bc macrophages get infected&raquo_space; overproduction of lymphokines > increased vascular permeability.

58
Q

Yellow fever

A

similar to dengue. 1 week incubation period, infection in liver&raquo_space; jaundice. LIVE VACCINE prevents.

59
Q

the two forms of vertical transmission from mother to fetus:

A

perinatal (during birth from mother’s blood and fluid); transplacental (during development if virus crosses placental barrier)

60
Q

Characteristics of parvoviruses:

A

small, unenveloped icosahedral, linear ssDNA.

transmission via inhalation.

61
Q

Parvovirus B-19:

A

inhibits RBC production for one week&raquo_space; anemia. high risk for sickle cell anemia patients (transient aplasic crisis!) treat w/ passive immunization w/human immune globulin. primary infection subclinical w/ transient “slapped-cheek” rash&raquo_space; transient arthritis. Transplacental infection causes hydrops fetalis (severe edema of fetus)

62
Q

Rubella

A

togavirus; respiratory transmission and 18 day incubation.&raquo_space; rash and transient arthritis.&raquo_space; congenital rubella syndrome in fetus if mother infected during pregnancy&raquo_space; cataracts, heart problems, retardation. LIVE ATTENUATED vaccine.

63
Q

Rubella virus:

A

given to children to prevent infection of their mothers’ during pregnancy (herd immunity). also given to women of childbearing age who are seronegative but should avoid pregnancy for 2 months.

64
Q

How do papoviruses transform cells? Are they able to continue to be infectious if they integrate?

A

temporally regulated (early and late genes). express large T-antigen that inactivate tumor suppressor genes. These oncogenes are essential for viral replication AND tumor development (ex. E6 & E7 in HPV). UNABLE to be infectious because integration = dead-end.

65
Q

2 classes of transforming retroviruses and the major difference between them:

A

acute and non-acute: acute have a proto-oncogene replacing an essential viral gene. they are defective (cannot infect w/out helper virus) ex: Rous Sarcoma.
non-acute (non-transducing): do no have an oncogene incorporated into viral genome; instead, viral promotor incorporated next to cellular proto-oncogene. take a long time to develop tumors because require insertional activation, which is rare.

66
Q

Does measles have antigenic variation?

A

no - single piece of -RNA

Virology (3 decks)

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