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
Clinical features of varicella
- mild febrile illness - generalized vesicular rash - centripetal distribution - itchy - heals without scarring
35
Transmission of varicella
- highly infectious - resp secretions - vesicle fluid
36
Complications of varicella
- secondary infection of skin lesions - CNS (post infectious encephalo myelitis, stroke) - pneumonia - haemorrhagic varicella
37
Problems in congenital varicella syndrome
- skin scarring - hypoplasia of limbs - microphthalmia
38
Clinical feature of zoster
- dermatomal vesicular eruption
39
Predictors of disease (CMV)
- viral antigen detection in diseased organ | - PCR or CMV viral load in blood e
40
Symptoms of infectious mononucleosis (EBV)
- fever, malaise - rash - lymphadenopathy - sore throat - HSM - atypical lymphocytosis
41
Lab diagnosis of EBV
- mono spot (heterophile IgM antibodies) | - IgG and IgM to viral capsid antigen
42
Effect of EBV of B cells
Immortalizes them
43
Complications of latency of EBV
- lympho-proliferative disorders - Burkitts - Hopkins disease - naso-pharyngeal Ca
44
Diseases associated with HHV6a nd 7
- primary infection in babies = roseola infant up (febrile illness, rash, convulsions) - infectious mono-nucleosis - immuno-compromised patients
45
Transmission of HHV8
- high prevalence mother to child | - low prevalence sexual
46
Complications of latency (HHV8)
- kaposi's sarcoma - primary effusion lymphomas - multi-centric castlemans disease
47
Definition of teratogens
Agent causing malformation in the developing fetus
48
How can HIV mother to child transmission occur?
- transplacentally - intrapartum - breast feeding
49
What are the two main types of tests for viruses
- serology (detects antibodies of pathogen - always blood) | - PCR (detects presence of pathogen)
50
Which antibody can cross the placenta?
IgG
51
Definition of perinatal
A week before to a week after delivery
52
Definition of neonatal
From birth to 4 weeks
53
Only which type of infections can be teratogenic?
Intrauterine
54
When does fetal immunity start to mature?
In second half of pregnancy
55
What types of organisms can cause intra-uterine infection?
- bacteria - virus - Protozoa
56
Why higher risk if primary maternal infection?
Because of lack of pre-existing maternal immunity
57
Why often persistent infection of fetus
- lack of mature immune system - clearance of infection occurs late/never - ongoing destruction after birth
58
Complications of zoster
- post hepatic neuralgia - encephalitis - myelitis - strokes
59
Treatment of HSV and VZV
Acyclovir - nucleoside analogue of guanosine - interferes with DNA polymerase
60
Suggestions for varicella PEP
- 2 doses | - 1-3 months apart
61
In which fluids is CMV shed?
- saliva - urine - breast milk - semen
62
Mode of transmission for CMV
Close contact | - also iatrogenic (blood and organ transplant)
63
Clinical syndromes of CMV
- primary infection in adulthood (infectious-mononucleosis-like) - congenital infection - immunosup pressed patients
64
Effects of congenital CMV
- well but sheds virus - delayed onset symptoms (deafness) - congenital infection syndrome
65
CMV end organ diseases
- interstitial pneumonia - retinitis - GIT ulceration - neurological disorders
66
Treatment of CMV
Ganciclovir
67
Lab diagnosis of CMV
- IgG indicates exposure | - virus detection
68
5 TORCHES
- toxo - other - rubella - CMV - herpes - syphilis
69
Effects of congenital rubella syndrome
- neurosensory deafness - cataracts, micropthalmia - PDA - microcephaly - late : type 1 diabetes
70
Why rubella so teratogenic?
- 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
Specific abnormalities of congenital CMV infection
- low birth weight - HSM - thrombocytopenia - microcephaly - chorioretinitis
72
Late presentation of congenital CMV infection
- hearing loss - subnormal IQ - behavioral problems
73
How many babies infected if primary toxo infection in pregnancy?
1/3
74
When does risk of congenital infection of toxo increase?
- later in pregnancy | - but risk of newborn clinical sign from congenital infection decreases if acquired later
75
Possible presentations of congenital toxo infection
- asymptomatic (50) - ocular involvement only (10) - sever disease (30)
76
Specific features of congenital toxo infections
- chorioretinitis - cerebral calcification - seizures
77
Late effects of congenital toxo infection
- blindness - hydrocephalus - MR
78
How many babies affected if syphilis left untreated
2/3
79
Specific features of congenital syphilis
- mucopurulent nasal discharge - vesicobullous or maculopapular rash (palms and soles) - fissures, mucosal patches - periosteitis, osteochondritis
80
Late effects of congenital syphilis
- neurological problems - deafness - optic atrophy - teeth and bone stigmata
81
Presenting features of congenital parvovirus
- fever - rash - arthritis - haematological complications (anaemia - cardiac failure - hydrops fetalis)
82
How to treat congenital parvovirus
In-utero transfusion
83
Features of congenital varicella syndrome
- maternal infection in first 20 weeks - skin scarring - limb hypoplasia - eye abnormalities
84
When is risk high for congenital herpes simplex
If primary genital herpes at time of delivery | - low if recurrent
85
Viral transcription factors of HTLV1 that activate cellular genes
- tax protein | - HBZ protein
86
4 retroviruses that infect humans
HIV 1 and 2 | HTLV 1 and 2
87
Type of cell found in T cell leukemia
Flower cell