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March Exams > Virology > Flashcards

Virology Flashcards

0
Q

How do virus infected cancer cells differ from normal

A
  • immortalized
  • rapid proliferation
  • loss of contact inhibition
  • altered morphology
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1
Q

How to establish a link between virus and cancer

A
  • cancer prevalent in region where virus is prevalent
  • individuals with cancer have evidence of persistent infection with virus
  • cell tropism of virus is same as cell origin of tumour
  • viral nucleic acids present in tumour cells
  • incidence of cancer decreased by measures that decrease infection (vaccines)
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2
Q

How virus forces the cell to proliferate

A
  • inactivates tumour suppressor proteins
  • trans-activation of cellular genes
  • action of viral oncogenes
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3
Q

Effects of inactivation of tumour suppressor proteins

A
  • excessive proliferation
  • damaged cellular DNA is not repaired
  • cells with damaged DNA do not undergo apoptosis
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4
Q

Strains of HPV that cause cutaneous warts

A

1,2,3,4,5,8

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5
Q

Strains of HPV that cause mucosal warts

A

6,11

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6
Q

Steps in HPV induced cervical Ca

A
  • HPV infection
  • persistent HPV infection
  • cellular dysregulation
  • high grade CIN
  • invasive Ca
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7
Q

Co-carcinogens for HPV

A
  • multi parity
  • smoking
  • prolonged OC use
  • STIs
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8
Q

Co carcinogens in HCC

A
  • aflatoxins
  • iron overload
  • alcohol
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9
Q

Diseases associated with HHV8

A
  • kaposi’s sarcoma
  • primary effusion lymphomas
  • multi-centric castlemans disease
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20
Q

List viruses associated with human cancers

A
  • HPV (Ca cervix)
  • EBV (NH-lymphoma, naso-pharyngeal Ca)
  • HTLV1 (human T cell leukemia)
  • hep b and c ( HCC)
  • HHV8 (kaposi’s, body cavity lymphomas)
  • merkel cell polyomavirus (merkel cell carcinoma)
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21
Q

Clinical feature of T cell leukemia

A
  • aggressive

- tumour cells infiltrate skin and brain

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22
Q

Known human herpesviruses

A
  • herpes simplex 1 and 2
  • varicella-zoster
  • CMV
  • EBV
  • HHV6+7
  • HHV8
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23
Q

What makes a parasite successful?

A
  • high prevalence of infection

- minimal clinical disease

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24
Q

Structure of herpes virus

A

dsDNA
large and enveloped
complex genome

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25
Q

Site of infection for HSV1

A

Oral

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26
Q

Site of infection for HSV2

A

Genital

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27
Q

Mode of transmission of herpes simplex

A

-

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28
Q

Clinical features of primary HSV

A
  • most asymptomatic
  • vesicles develop 1-3 days after
  • gingivo-stomatitis
  • eczema herpeticum
  • traumatic inoculation
  • conjunctivitis
  • keratitis (dendritic ulcer)
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29
Q

What can provoke reactivation of HSV?

A
  • sunlight
  • stress
  • febrile illness
  • menstruation
  • immuno- suppression
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30
Q

Where does HSV1 go in latency?

A

Trigeminal ganglion

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31
Q

Where does HSV2 go in latency

A

Sacral ganglia

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32
Q

Rare life threatening complications if HSV

A
  • neonatal HSV infection
  • encephalitis
  • disseminated infection
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33
Q

Lab diagnosis if HSV

A
  • serology (IgG indicates exposure)
  • microscopy
  • culture from swab
  • PCR (swab, CSF, blood or biopsy)
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34
Q

Clinical features of varicella

A
  • mild febrile illness
  • generalized vesicular rash
  • centripetal distribution
  • itchy
  • heals without scarring
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35
Q

Transmission of varicella

A
  • highly infectious
  • resp secretions
  • vesicle fluid
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36
Q

Complications of varicella

A
  • secondary infection of skin lesions
  • CNS (post infectious encephalo myelitis, stroke)
  • pneumonia
  • haemorrhagic varicella
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37
Q

Problems in congenital varicella syndrome

A
  • skin scarring
  • hypoplasia of limbs
  • microphthalmia
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38
Q

Clinical feature of zoster

A
  • dermatomal vesicular eruption
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39
Q

Predictors of disease (CMV)

A
  • viral antigen detection in diseased organ

- PCR or CMV viral load in blood e

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40
Q

Symptoms of infectious mononucleosis (EBV)

A
  • fever, malaise
  • rash
  • lymphadenopathy
  • sore throat
  • HSM
  • atypical lymphocytosis
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41
Q

Lab diagnosis of EBV

A
  • mono spot (heterophile IgM antibodies)

- IgG and IgM to viral capsid antigen

42
Q

Effect of EBV of B cells

A

Immortalizes them

43
Q

Complications of latency of EBV

A
  • lympho-proliferative disorders
  • Burkitts
  • Hopkins disease
  • naso-pharyngeal Ca
44
Q

Diseases associated with HHV6a nd 7

A
  • primary infection in babies = roseola infant up (febrile illness, rash, convulsions)
  • infectious mono-nucleosis
  • immuno-compromised patients
45
Q

Transmission of HHV8

A
  • high prevalence mother to child

- low prevalence sexual

46
Q

Complications of latency (HHV8)

A
  • kaposi’s sarcoma
  • primary effusion lymphomas
  • multi-centric castlemans disease
47
Q

Definition of teratogens

A

Agent causing malformation in the developing fetus

48
Q

How can HIV mother to child transmission occur?

A
  • transplacentally
  • intrapartum
  • breast feeding
49
Q

What are the two main types of tests for viruses

A
  • serology (detects antibodies of pathogen - always blood)

- PCR (detects presence of pathogen)

50
Q

Which antibody can cross the placenta?

A

IgG

51
Q

Definition of perinatal

A

A week before to a week after delivery

52
Q

Definition of neonatal

A

From birth to 4 weeks

53
Q

Only which type of infections can be teratogenic?

A

Intrauterine

54
Q

When does fetal immunity start to mature?

A

In second half of pregnancy

55
Q

What types of organisms can cause intra-uterine infection?

A
  • bacteria
  • virus
  • Protozoa
56
Q

Why higher risk if primary maternal infection?

A

Because of lack of pre-existing maternal immunity

57
Q

Why often persistent infection of fetus

A
  • lack of mature immune system
  • clearance of infection occurs late/never
  • ongoing destruction after birth
58
Q

Complications of zoster

A
  • post hepatic neuralgia
  • encephalitis
  • myelitis
  • strokes
59
Q

Treatment of HSV and VZV

A

Acyclovir

  • nucleoside analogue of guanosine
  • interferes with DNA polymerase
60
Q

Suggestions for varicella PEP

A
  • 2 doses

- 1-3 months apart

61
Q

In which fluids is CMV shed?

A
  • saliva
  • urine
  • breast milk
  • semen
62
Q

Mode of transmission for CMV

A

Close contact

- also iatrogenic (blood and organ transplant)

63
Q

Clinical syndromes of CMV

A
  • primary infection in adulthood (infectious-mononucleosis-like)
  • congenital infection
  • immunosup pressed patients
64
Q

Effects of congenital CMV

A
  • well but sheds virus
  • delayed onset symptoms (deafness)
  • congenital infection syndrome
65
Q

CMV end organ diseases

A
  • interstitial pneumonia
  • retinitis
  • GIT ulceration
  • neurological disorders
66
Q

Treatment of CMV

A

Ganciclovir

67
Q

Lab diagnosis of CMV

A
  • IgG indicates exposure

- virus detection

68
Q

5 TORCHES

A
  • toxo
  • other
  • rubella
  • CMV
  • herpes
  • syphilis
69
Q

Effects of congenital rubella syndrome

A
  • neurosensory deafness
  • cataracts, micropthalmia
  • PDA
  • microcephaly
  • late : type 1 diabetes
70
Q

Why rubella so teratogenic?

A
  • low pathogenicity
  • slows down cell division
  • lower total cell number (small babies)
  • death of cells or slowing mitotic rate at critical stages interferes with organ development
  • organ of corti is esp vulnerable
71
Q

Specific abnormalities of congenital CMV infection

A
  • low birth weight
  • HSM
  • thrombocytopenia
  • microcephaly
  • chorioretinitis
72
Q

Late presentation of congenital CMV infection

A
  • hearing loss
  • subnormal IQ
  • behavioral problems
73
Q

How many babies infected if primary toxo infection in pregnancy?

A

1/3

74
Q

When does risk of congenital infection of toxo increase?

A
  • later in pregnancy

- but risk of newborn clinical sign from congenital infection decreases if acquired later

75
Q

Possible presentations of congenital toxo infection

A
  • asymptomatic (50)
  • ocular involvement only (10)
  • sever disease (30)
76
Q

Specific features of congenital toxo infections

A
  • chorioretinitis
  • cerebral calcification
  • seizures
77
Q

Late effects of congenital toxo infection

A
  • blindness
  • hydrocephalus
  • MR
78
Q

How many babies affected if syphilis left untreated

A

2/3

79
Q

Specific features of congenital syphilis

A
  • mucopurulent nasal discharge
  • vesicobullous or maculopapular rash (palms and soles)
  • fissures, mucosal patches
  • periosteitis, osteochondritis
80
Q

Late effects of congenital syphilis

A
  • neurological problems
  • deafness
  • optic atrophy
  • teeth and bone stigmata
81
Q

Presenting features of congenital parvovirus

A
  • fever
  • rash
  • arthritis
  • haematological complications (anaemia - cardiac failure - hydrops fetalis)
82
Q

How to treat congenital parvovirus

A

In-utero transfusion

83
Q

Features of congenital varicella syndrome

A
  • maternal infection in first 20 weeks
  • skin scarring
  • limb hypoplasia
  • eye abnormalities
84
Q

When is risk high for congenital herpes simplex

A

If primary genital herpes at time of delivery

- low if recurrent

85
Q

Viral transcription factors of HTLV1 that activate cellular genes

A
  • tax protein

- HBZ protein

86
Q

4 retroviruses that infect humans

A

HIV 1 and 2

HTLV 1 and 2

87
Q

Type of cell found in T cell leukemia

A

Flower cell

March Exams (14 decks)

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