D19 Pathophysiology and Pharmacological Agents for Herpesvirus and CNS infection(Dr.Long)Exam
Human Herpesviruses (HHV)
replication cycle (viral
... [Show More] shedding)
Latency in sensory ganglia ( e.g., HSV-1, HSV-2, VZV)
latency in T-cells (e.g., CMV, HHV-6)
latency in B-cells( e.g., EBV, HHV-8)
I. Herpes Simplex Virus
HSV-1 (HHV-1) = cold sores
HSV-2 (HHV-2) = genital ulcers
Transmission
HSV-1 = is transmitted primarily in saliva and direct contact with herpes sores.
HSV-2= is transmitted primarily by sexual contact.
epidemiology HSV-1
recurrent herpes labials (cold sores)
after the primary HSV-1 infection, the virus will inhabit sensory ganglia in dormant form( latent herpes) and the person will be a carrier for life.
HSV-1 can be reactivated = causing the cold sores return.
HSV-2 example
genital Herpes
Pathogenesis
host cell's RNA polymerase transcribes the HSV DNA into mRNA.
Host cell translates portions of mRNA to produce:
DNA polymerase:
helps further replicate the HSV genome.
Thymidine Kinase
phosphorylates thymidine for viral DNA replication
anti-herpes drugs such as acyclovir and penciclovir are phosphorylated by this enzyme and subsequently antagonize replication of HSV DNA
gingivostomatitis
infection of the mouth and gums
herpes labialis
(I.e., fever blisters, cold sores), represent recurrent HSV-1 disease.
neonatal HSV
acquired during passage through birth canal; HSV-2 infections more common
CNS (encephalitis) herpes
Keratitis
corneal ulcers
HSV is most common cause of corneal blindness in the U.S.
encephalitis
due to HSV migration from ganglia to brain
HSV-1
major cause in children and adults
HSV-2
in infants
herpetic whitlow
painful infection of the hand.
HHV-3
varicella zoster virus
HHV-3 (Varicella Zoster Virus)
primary infection herpes varicella (chicken pox)
common in childhood
reactivated infection herpes zoster (shingles) is localized to one or few dermatomes
transmission
primary infections spread by respiratory route with latency established in ganglia neurons.
pathogenesis [Show Less]