Common Viral Pathogens - Herves Virus Flashcards
Herpes Simplex -1 (HSV)
Target cell type, latency, transmission and clinical manifestations
Target cell type: mucosal epithelium
Latency: neuronal ganglion
Transmission: close contact
Clinical manifestations: Orofacial lesions and some genital lesion Encephalitis Herpes whitlow Herpes keratitis Neonatal herpes
Herpes Simplex -2 (HSV)
Target cell type, latency, transmission and clinical manifestations
Target cell type: mucosal epithelium
Latency: neuron ganglia Transmission: close contact (usually sexually)
Clinical manifestations:
Genital lesions and some (orofacial lesions) -> encephalities, herpes whitlow, herpes ketaritis, neonatal herpes
Varicella Zoster Virus
Target cell type, latency, transmission and clinical manifestations
Target cell type: mucosal epithelium
Latency: neuron ganglia
Transmission: contact or respiratory route
Clinical manifestations: Chickenpox (varicella) and shingles (zoster)
Epstein-Barr Virus (EBV)
Target cell type, latency, transmission and clinical manifestations
Target cell type: B lymphocytes, epithelia
latency: B-lymphocytes
transmission: Saliva
clinical manifestations: Infectious mononucleosis, Burkitt’s lymphoma, in immunocompromised patients, central nervous system lymphoma
Cytomegalovirus (CMV)
Target cell type: epithelia, monocytes, lymphocytes, others
Latent cell types: monocytes, lymphocytes and others
Transmission: contact, blood, transfusions, transplantation, congenital
Clinical manifestations: infectious mononucleosis-like syndrome:
In immunocompromised retinities, pneumonia, colitis. IN new borns: congenital CMV
What kind of virus are herpes viruses
dsDNA protected by an icosahedral capsid. Nucleocapsid is further surrounded by glycoprotein rich envelope. - establishes latend infection in the host and may get reactivated later.
Herpesvirus entry/nuclear transport
Attach and bind to surface proteins ofund on host cell causing fusion of viral and host membranes. Neocleaocapsid is realeased, transported into the nucleus via cellular microtubuls where the genome enters through the nuclear pores.
Hespesvirus replication
Immediate early (IE) genes are expression prior to protein symthesis -> required for the expression of the early (E) and late (L) genes, which are synthesized de novo.
E genes encode proteins involved in DNA repocation (like DNA polymerase, etc.)
L genes encode structural proteins, such as capsid and glycoproteins.
Herpesvirus assembly and egress
Occurs in the nucleus. Capsids self-assemple and newly synthesized DNA gets packaged.
Nucleocapsids bud through nuclear membrane and acquire their glycoprotein-rick envelope as they pass through GOLGI COMPLEX.
Leaves via exocytosis or cell-lysis.
Incubation period of HSV-1 or HSV-2
2-12 days (average is 4 days)
HSV-1 and HSV-2 latent ganglions
For orofacial lesions, trigeminal ganglion
For genital lesions, sacral ganglion
Location of reoccurent HPV-1 and HPV-2
Face (orofacial)
Cornea (keratitis)
Perineum (genital herpes)
Can be reactivated by a variety of stressors
Gingivostomatitis
HSV-1 primary infection, child develops painful mouth vesciles and ulceration sof the gums,lips and tongue. Ulcers in the anterior art of the mouth. Fever. Swelling of lips/drooling. Cervical lymph node swelling
Herpatic whitlow
inocculation of HSV from oral seretions onto the fingers -> gains access into the skin via small cut.
Occupational hazard.
Eythema, swelling and grouped vesciles on an erythmatous base. Not a bacterial infection.
Mother kissing baby’s hurt finger
Genital herpes
sexually transmitted infection that is usually caused by HSV-2 (some HSV-1, 30%)
Very painful lesions that last 10-14 days
Herpes keratitis
HSV infects the cornea o the eye. More common from HSV-1. Produces dendritic lesions of the cornea, which can cause scarring and blindness.
Encephalities
can be caused by primary disease or reactivation. Can occur through blod-orne spread or neuronal transmissin of the virus. Infection of the brain is fulminant and hemorrhagic, necrotizing encephalities.
Predcilection to the temporal lobes of the brain. Altered mental status. Mortality 30% w/ treatment.
Neonatal herpes
primary inftion of the neonate that can be acquired intrauterine, peripartum or postpartum. (most during peripartum) Most caused by HSV-2 due to genital lesions.
Three forms of disease.
1) skin, eye and mucous membrane (SEM)
2. ) CNS
3. ) disseminated
disseminated is the most severe, finding vescile in neonates less than 4 weeks is a medical emergency. Herpes is high on this differential.
Herpes labialis (cold cores)
Most common symptomatic reactivation associated w/ HSV-1.
Very common and self-limited
Diagnosis of HSV infections
Gingivostomatitis and herpes labialis can be diagnosed clinically, as well as genital herpes.
Viral culture of lesions
Direct flourescent antibody staining
PCR of lesions
Treatment of HSV
Nucleoside analog drugs treat herpes, take advantage of viral enzyme thymidine kinase
aceclovir the most common. Severe HSV infections treated w/ IV acyclovir.
HSV prophylaxis
In certain paritents, oral antiviral suppressive therapy is good for frequent painful oral or genital reoccurences. Must be able to take medicine one or twice daily.
Chickenpox (varicella)
highly contagion common childhood disease. Transmitted by respiratory route or direct contact. Contagious for 102 days before the rash appears and until all blisters have formed scabs.
Incubation period. 10-21 days
Symptoms: fever, malaise… rash appears in “waves.” Lesions mature. Rash appears on face or trunk, spreads to extremities. LESIONS IN VARIOUS STAGES OF DEVELOPMENT. Itchy. Takes about 7 days for all lesions to scab.
Pathogenesis of chickenpox
virus gains enty via respiratory tract, spreads to regional lymphoid system. Replication takes place in lymph nodes in 2-4 days, and primary viremia 2-6 days after initial infection. Virus replicates in liver, spleen, and then you have a secondary viremia. Spreads to skin 14-16 days after initial exposure.
