Human herpes virus Flashcards
herpes virus structure
- 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
HHP classifications
1) alpha
- tend to affect epidermal and neuronal cells
2) beta
- T cells and leukocytes
- slow growth
3) gamma
- primarily B lymphocytes
diseases caused by herpes virus
oropharyngeal and genital herpes
chicken pox (varicella zoster virus)
EBV causes granular fever etc
infection and replication of herpes virus
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
HSV
1
- mainly oral
infection primary hepatic gingivostomatits
2
mainly genital
reactivatio,
secodary infection herpes labials
what causes HSV reactivation
UV light
stress
illness
immunosuppression
HSV 1
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
clinical features of herpetic gingivostomatitis
drinking and eating painful (halitosis) multiple oral vesicles erythema maliase pyrexia lympahdenopathy
investigations include viral culture or PCR
PCR
denature DNA to singel strnas
annealing of specific primers to DNA
extension by polymerase
management of herpetic gingivostomatitis
acyclovir
fluids/soft diet
analgesics/antipyretics
local antisepctive e.g. chlorhexidine
how does acyclovir work
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
herpes labialis features and treamtent
HSV 2
prodromal irritation
crusting lesions
vesicles at or near mucocutaneous junction of lips
acyclovir cream
OTC drying and antibacterial agents
herpetic Whitloq
infection of fingers from handling oral tissues of someone with active HP 1/2
hsv encephalitis
adults HSV 1
headache and gever
HSV2 neonates
skin rash lesions
CNS symptoms
repsiraotry distress
HHV 3
viracella zoster
primary infection chicken pox
secondary herpes zoster shingles
how does HHV3 develop
natural infection of nasopharynx replication in regional lymph nodes viral replication in host tissues then clinical symptoms occur - skin reach fever etc
herpes zoster oral disease
3 phases 1) pre herpetic neuralgia - 2) rash - - 3) post herpetic neuralgia -
pre herpetic neuralgia herpes zoster oral disease
- pain in distribution of the affected division of the trigeminal nerve
- prior to development of rash
rash of herpes zoster oral disease
- 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)
post herpetic neuralgia herpes zoster oral disease
- 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
treatment of herpes zoster oral disease
acyclovir
analgesics
EBV infection
primary
- EBV replicates in oroharyngeall epotelail cells
latency in B lymphocytes
what is EBV associated with
infection mononucleosis (glandular fever)
burkitts lymphoma
nasopharyngeal carinoma
where is HSV 8 found and can cuase
aids pts
kaposis sarcoma
