Lecture 7: Herpes Virus Flashcards
Human herpesviruses all have 3 phases of disease
- Primary infection
- Latency
- Reactivación
a person may never experience or notice reactivation
all human herpesviruses infect for life**
Which human herpevirus establish latency in neurons
HSV-1
HSV-2
VZV
Which human herpes virus establish latency in B lymphocytes
HHV-4 = EBV
HHV-8
Herpetic gingivostomatitis
-herpes type
-manifestations
-reactivation
HSV-1
Sores on lips, gums, tongue, cheeks (inflamed gums)
Reactivates as herpes labiales
Herpes labialis
-type of herpes
-latency where
Cold sores (fever blisters)
Reactivated from HSV-1 or HSV-2
Latency-trigeminal ganglion
HSV in immunocompromised
Can manifest as chronic, necrotic ulcers with hemorrhagic crusts
-can become bilateral
-aggressive
Genital herpes
-types of human herpes virus
-latency
Mostly due to HSV-2
Latency is established at the sacral ganglia
Neonatal herpes
-type of human herpes virus
HSV-2
-can be acquired during birth
-primary infection in 3rd trimester
Herpes diagnosis
Serology: (indirect way because measuring anti-bodies (IgM & IgG)
Elisa or western blot= differentiation between HSV-1 and HSV-2
PCR=
Differentiation between HSV-1 and HSV-2
TZANCK SMEAR shows CPE’s
CPE seen in HSV and VZV = inclusion bodies (“crowdy bodies) & syncytia
Herpes treatment and prevention
-acyclovir
-Valcyclovir
-sun avoidance
Human herpes virus-3
Also known as VZV
-genome
-capsule
-envelope
-reactivation
-genome: dsDNA
-Capsule: icosohedral
-envelope: yes
-reactivation: shingles (zoster)
VZV pathogenesis
-initial
-latency
-reactivation
-chicken Pox
-sensory neuronal cells
-shingles (herpes zoster)
Chickenpox manifestations
Maculopapular rash after 14 days post-infection
-begins in trunk-> face and extremities
Oral manifestation without scarring
Herpes zoster/shingles (VZV)
-reactivation
-manifestations
-REACTIVATION after age of 60 from chickenpox (varicela = HHV-3)
-bilateral (only on one side of the body)
-severe pain, itching, and numbness followed by bilateral rash
Herpes zoster (shingles) clinical presentation
Zoster refers to the characteristics localization of skin lesions = dermatome
Each dermatome is Innervated by a single sensory nerve
Treatment for VZV
-Chickenpox
-shingles
Chickenpox = acyclovir within 24 hours
Shingles = acyclovir within 72 hours
VZV prevention
-chickenpox
-shingles
Vaccines
Chickenpox= varivax
Shingles= shingrix (>50 y/o)
Infectious mononucleosis
-which type of Human herpes virus
-capsule
-genome
-envelope
(Kissing disease)
(Epstein-Barr virus= EBV)
-TYPE= HHV-4
-icosahedral
-dsDNA
-envelope: yes
Describe the EBV pathogenesis
(Infectious mononucleosis) and where is establishes latency
-infects B cells and epithelial cells of oropharynx
This obviously will cause your T cells to attack your infected B cells and kill them… resulting in symptoms of MONO.
-latency = memory B cells or sensory ganglion ????????? (See hong PowerPoint)
EBV manifestations
-marked fatigue- lasts for weeks (up to 6 months)
-lymphadenopathy
-hepatosplenomegaly
-enlarged tonsils can obstruct the airway
-pharyngitis
rarely reactivates
HSV-4
oral symptoms of EBV (infectious mono)
-halitosis (bad breath)
-pharyngitis with membrane formation
-petechiae on soft palate (this point was grabbed from photo)
Oral hairy leukoplakia Is caused by which herpes?
What are the manifestations?
-happens from HHV-4 (EBV) most common in immunocompromised = AIDS
-White lesions on sides of tongue (often bilateral)!
EBV is a virus of B cells linked to several forms of cancers, which are?
-gastric carcinoma
-Hodgkin’s disease
CMV
-type of HHV
-Capsule
-genome
-Envelope
-HHV-5
-icosahedral
-dsDNA
-yes
T/F: Most people become infected with CMV during their lifetime
What about the Clinical disease of CMV?
True
>90% of adults in most of the world are seropositive
-Clincial disease: generally occurs in the immunocompromised (newborns, AIDS, organ transplants)
CMV transmission
-shedding
-torch
-most common route of transmission
Shedding = bodily fluids/secretions (urine, saliva, breast milk, semen, vaginal secretions, blood)
Crosses the Placenta (TORCH)
Most common: congenital, oral, sexual, organ transplant, blood transfusion
Reactivation of CMV and its manifestations
usually occurs in context of immuno suppression
-Oral CMV ulcers = painful solitary penetrating ulcers
-CMV sialadentis = rare = painful swelling of major salivary glands, bilateral, decreased saliva, xerostomia
this makes sense since CMV establishes latency in salivary glands
CMV diagnosis
Direct microscopic observation
Looking for CPE of “OWLS EYE”
-perinuclear inclusion bodies and cytomegaly
this can be compared to the CPE of EBV which will have CPE of “Downey cells”
Diagnosing EBV
-About 10% of lymphocytes are atypical showing CPE of “Downey cells” = enlarged, mis-sharpen nuclei with increased cytoplasm
-Heterophile antibodies elevated in cases of IM patients caused by EBV
Kaposi’s sarcoma
-capsid
-genome
-envelope
Kaposi’s sarcoma = HHV-8
-dsDNA
-yes enveloped
-Kaposi’s Sarcoma often is found in associate with?
-can nonsexual transmission occur?
-found in association with HIV infection
-Nonsexual transmission can also occur mostly through organ transplant
Kaposi’s Sarcoma manifestations
-rare and malignant neoplasm of blood/blood vessels in Immunocompromised individuals
-cancer
-patches of abnormal tissue grow under the skin or mucous membranes (mouth, nose, anus)
lesions may be RED, PURPLE, BROWN, OR BLACK
Kaposi’s sarcoma oral manifestations
Aside from patches of abnormal tissue growing under the skin, they can also grow in mucosa membranes.
can occur in the absence of skin lesions
-oral manifestations (mucous membrane) occur on the hard palate or gingivae… if it happens on the soft palate then it is an advanced state of Kaposi’s sarcoma
Color = RED OR PURPLE vascular lesions
