Herpes Virus Flashcards
Replication of herpes virus
“The DNA becomes circular”
“Synthesis of mRNA, viral proteins, and viral DNA takes place”
Expresses DNA pol and expresses LAT RNA during latency
“Progeny nucleocapsids are assembled in the nucleus. Large arrays of nucleocapsids result in characteristic nuclear inclusion bodies”
“Enveloped infectious virions are produced by nucleocapsid budding through the nuclear membrane.”
Can cause syncitia (multinucleated cell)
Latency is clinically relevant concept (primary and recurrent have different manifestations)
Structure of herpes virus
Enveloped, icosahedral nucleocapsid with single linear dsDNA
Clinical symptoms of herpes simplex virus 1
Incubation is 1-2 weeks
Latency is had in sensory ganglion
Primary infection is subclinical, infants might get stomatitis with vesicles in the mouth
Recurrent infection is cold sores (can be activated by UV, light, emotion)
“Herpes simplex (mostly type 1) is the most common cause of sporadic (non-epidemic) encephalitis, in temporal lobe”
“When herpes simplex infects the eye it can lead to keratitis with the conjuctiva and eyelids affected as well as the cornea”
Clinical symptoms of herpes simplex virus 2
Incubation is 1-2 weeks
Latency is had in sensory ganglion
Primary infection is bilateral lesions in genitalia
Recurrent infection is unilateral lesion in genitalia
Perinatal ransmission of herpes simplex virus
Perinatal transmission (symptomatic, primary or asymptomatic) at the time of delivery -> severe disease (hepato-adrenal necrosis)
- primary is most severe - viremia without IgG
Active lesions -> C section indicated
Treatment of herpes simplex virus
Acyclovir for simplex viruses
Trifluridine for keratoconjunctivitis
Vaccine has been “spectacular failure”
Transmission of Varicella-Zoster virus
“Infection is by way of the respiratory tract with subsequent viremia”
Virions shed from skin lesions spread to others
May also shed through respiratory
Immune compromised and varicella
Primary infection can be severe/fatal - treat with IVIgG from infected individuals (VZIG) - vaccine effective - acyclovir effective Zoster/shingles can be disseminated - acyclovir
Treatment of Varicella-Zoster virus
Acyclovir
Live attenuated vaccine
- routine pediatric use -> fewer primary infections
- (also decreases natural “boosters” for elderly -> more shingles?)
- elderly as booster to prevent shingles
- requires booster
Clinical symptoms of Varicella-Zoster virus
Primary: incubation 2-3 weeks -> fever, rash
- can be severe/fatal if immunocompromised
Recurrent: shingles - unilateral, dermatomal distribution (pre-existing Ig limits spread)
- immunosuppressed may get disseminated bc no Ig
- pain -> lesions -> post-herpetic neuralgia
- more common in elderly (decreased cellular immunity)
Clinical symptoms of cytomegalovirus
Incubation 3-12 weeks
Primary infection before puberty is subclinical
Congenital syndrome is mental retardation, seizures, sensory loss, jaundice, anemia (the most common congenital viral infection now)
Recurrent infection is only when immunosuppressed, generalized infection (retinitis, colitis, pneumonitis, hepatitis, etc)
Diagnosis of cytomegalovirus
Large infected cells with nuclear inclusion
Heterophile-negative mononucleosis (infiltration of many mononuclear cells)
Transmission of cytomegalovirus
Placental (congenital)
Nasopharyngeal fluid, semen, urine, vaginal secretion
Treatment of cytomegalovirus
No vaccine
Gangciclovir - effective but very toxic (including perinatal)
Vitravene - intraocular (for retinitis)
Diagnosis of EB virus
Heterophile-positive
- heterophile-antibodies do not neutralize, just cross-react for diagnostic purpose
Also seroconvert to EB virus antigen Ab
Mononucleosis
- blood contains abnormal lympocytes (high cytotoxic T cells to fight infected B cells)
