Human herpes virus Flashcards

1
Q

herpes virus structure

A
  • icosahedral capsid (protein nuclear capsid)
  • teguments links outer lipid bilayer and nuclear capsid
  • outer lipid bilayer has proteins which stick out, tend to be glycoproteins
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2
Q

HHP classifications

A

1) alpha
- tend to affect epidermal and neuronal cells
2) beta
- T cells and leukocytes
- slow growth
3) gamma
- primarily B lymphocytes

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3
Q

diseases caused by herpes virus

A

oropharyngeal and genital herpes
chicken pox (varicella zoster virus)
EBV causes granular fever etc

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4
Q

infection and replication of herpes virus

A

Oral epithelial cell host receptor
- viral glycoproteins bind proteoglycans binds to specific cells
- once bound, uncoats, envelope goes and nuclear capsid translocated inside the cell
- capsid goes into the nucleus, sheds coat and then enters inside DNA , human polymerase transcribes/translates viral genes
- protiens placed on viral cell surface
- build up of viral particles in the cell
Excreted into cytoplasm
- cell burts, release virus into ECM to then bind again

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5
Q

HSV

A

1
- mainly oral
infection primary hepatic gingivostomatits

2
mainly genital
reactivatio,
secodary infection herpes labials

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6
Q

what causes HSV reactivation

A

UV light
stress
illness
immunosuppression

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7
Q

HSV 1

A
now as herpetic gingivostomatitis
virus enters trigeminal sensory neurones
translocated up NS to trigeminal ganglion
remains latent until reacvated
goes to peripheral nerve entings
viral particules shed
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8
Q

clinical features of herpetic gingivostomatitis

A
drinking and eating painful (halitosis)
multiple oral vesicles
erythema
maliase
pyrexia
lympahdenopathy 

investigations include viral culture or PCR

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9
Q

PCR

A

denature DNA to singel strnas
annealing of specific primers to DNA
extension by polymerase

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10
Q

management of herpetic gingivostomatitis

A

acyclovir
fluids/soft diet
analgesics/antipyretics
local antisepctive e.g. chlorhexidine

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11
Q

how does acyclovir work

A

analogues of guanisie
more effective at phosphorylating nucleotides than human TK
ACV (False nucleotide) phosphorlayed by viral TK enzyme to ACV-P
ACV- P inhibits virus replication

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12
Q

herpes labialis features and treamtent

A

HSV 2

prodromal irritation
crusting lesions
vesicles at or near mucocutaneous junction of lips

acyclovir cream
OTC drying and antibacterial agents

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13
Q

herpetic Whitloq

A

infection of fingers from handling oral tissues of someone with active HP 1/2

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14
Q

hsv encephalitis

A

adults HSV 1
headache and gever

HSV2 neonates
skin rash lesions
CNS symptoms
repsiraotry distress

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15
Q

HHV 3

A

viracella zoster
primary infection chicken pox
secondary herpes zoster shingles

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16
Q

how does HHV3 develop

A
natural infection of nasopharynx
replication in regional lymph nodes
viral replication in host tissues
then clinical symptoms occur 
-  skin reach fever etc
17
Q

herpes zoster oral disease

A
3 phases
1)	pre herpetic neuralgia
-	
2)	rash
-	
-
3)	post herpetic neuralgia
-
18
Q

pre herpetic neuralgia herpes zoster oral disease

A
  • pain in distribution of the affected division of the trigeminal nerve
  • prior to development of rash
19
Q

rash of herpes zoster oral disease

A
  • unilateral vesicles in the distribution of a branch of the trigeminal nerve
  • ophthalmic, maximally, mandibular
  • Vesicles break down to form 1- Ulcers (mucosa), crusting lesions (skin)
20
Q

post herpetic neuralgia herpes zoster oral disease

A
  • painful burning sensation in the distribution of the affected nerve
  • effective treatment of zoster may reduce risk of neuralgia
  • treat pain with tricyclic anti depressants and neuropathic pain drugs
21
Q

treatment of herpes zoster oral disease

A

acyclovir

analgesics

22
Q

EBV infection

A

primary
- EBV replicates in oroharyngeall epotelail cells
latency in B lymphocytes

23
Q

what is EBV associated with

A

infection mononucleosis (glandular fever)
burkitts lymphoma
nasopharyngeal carinoma

24
Q

where is HSV 8 found and can cuase

A

aids pts

kaposis sarcoma