Herpes virus Flashcards
When was herpes research more popular?
the 70s
Structure of herpes viruses
-ds-DNA genome 125,000-229,000 bp
-Icosahedral symmetry of virus capsid
-162 capsomeres
-Surrounding tegument
-Envelope membrane derived from nuclear membrane by budding
How many ORFs in HSV
there are 70
multiple orfs are overlapping tho
True or false: all human herpesviruses have identical EM morpohology
true
True or false: all herpesviruses are ubiquitous infecting a majority of all hhumans
true
True or false: you can get rid of herpes viruses
false: the infection remain latent lifelong and may reactivate
How many herpes viruses exist:
-Herpes simplex virus type I (HSV1 or HHV1)
-Herpes simplex virus type II (HSV2 or HHV2)
-Varicella-zoster virus (VZV or HHV3)
-Epstein-Barr virus (EBV or HHV4)
-Cytomegalovirus (CMV or HHV5)
-Human herpesvirus 6 (HHV6)
-Human herpesvirus 7 (HHV7)
-Kaposi sarcoma-associated (KSHV or HHV8)
virus
Primary target cell, pathophysiology, site of latency and means of spread of HSV1
-Primary Target: Mucoepithelial
-Cell Pathophysiology: oral and/or genital herpes (predominatly orofacial)
-Site of latency: neuron
-Means of Spread: close contact (oral or STI)
Primary target cell, pathophysiology, site of latency and means of spread of HSV2
-Primary Target: Mucoepithelial
-Cell Pathophysiology: oral and/or genital herpes (predominatly orofacial)
-Site of latency: neuron
-Means of Spread: close contact (oral or STI)
Primary target cell, pathophysiology, site of latency and means of spread of VZV
-Primary Target: Mucoepithelial
-Cell Pathophysiology: chickenpox and shingles
-Site of latency: neuron
-Means of Spread: close contact or respiratrory
Primary target cell, pathophysiology, site of latency and means of spread of EBV
-Primary Target: B cells/epithelial cells
-Cell Pathophysiology:
infectious Mononucleosis
EBV‐associated lymphoproliferative diseases:
Burkitt’s lymphoma
EBV‐positive
Hodgkin lymphoma
Post‐transplant
lymphoproliferative
syndrome (PTLD
-Site of latency: B cells
-Means of Spread: Close contact,
transfusions, tissue transplant, and congenital transmission
Primary target cell, pathophysiology, site of latency and means of spread of CMV
-Primary Target: Monocytes and epithelial cells
-Cell Pathophysiology: infectious monocleosis like syndrome aka retinitis
-Site of latency: monocyte
-Means of Spread: saliva, urine, blood. breast milk
Primary target cell, pathophysiology, site of latency and means of spread of Roseolovirus
-Primary Target: t cells
-Cell Pathophysiology: sixth disease or roseaola infantum or exanthem subitum
-Site of latency: t cells
-Means of Spread: respiratory and close contact
Primary target cell, pathophysiology, site of latency and means of spread of KSHV
-Primary Target: lymphocytes
-Cell Pathophysiology: Kaposi’s sarcoma
Primary cavity lymphoma
-Site of latency: b cells
-Means of Spread: Close contact (sexual),
saliva?
True or false: HSV1 and HSV2 have serologically distinct membrane glycoproteins
true
True or false hsv 1 and 2 have similar m, manifestations when infecting similar sites
true
What makes hsv 1 and 2 different?
different but converging epidemiological patterns
True or false: primates can’t get infected by herpes
false they can
True or false: HSV Urogenital infection HSV1 10‐30% HSV2 70‐90%
true
True or false: Neonatal infection HSV 1 75‐85% HSV 2 15‐25%
HSV 2 75‐85% HSV1 15‐25%
MANIFESTATIONS OF HSV INFECTION
(i.e. Herpes labialis and Herpes genitalis): percentages of people
‐ 30‐100% of population infected by age 5
‐ 30‐50% of middle class children
‐ 80‐100% of poorer populations
MANIFESTATIONS OF HSV INFECTION
(i.e. Herpes labialis and Herpes genitalis):
Primary infection
‐ primary infection often asymptomatic
but may present as severe gingivostomatitis
‐ paradoxically:
‐ primary infection is most often asymptomatic
‐ but, when symptomatic, it is usually severe
MANIFESTATIONS OF HSV INFECTION
(i.e. Herpes labialis and Herpes genitalis): incubation
2-12 days
WHERE CAN HSV INFECT PEOPLE
eye, hand, or other skin sites may be infected
de novo or by autoinnoculation
What happens to people without immune compromise that get HSV
‐ usually no serious sequelae
‐ treatment is optional
where does the recurrent infection of HSV appear
same site as primary infection
where does the latency of hsv appear
in sensory ganglia
REactivations of hsv are often attributed to:
‐ concurrent infection, fever
‐ stress, menses, exposure to UV light, etc
True or false: small quantities of virus may periodically be shed asymptomatically
true
steps of hsv appearance
-clear fluid blisters
-whiteish blisters due to white blood cells
-then blisters break open
VZV: what is the difference between varicella (chickenpox) and zoster(shingles)
-Varicella
a primary infection
always disseminated
-Shingles:
a local recurrence of latent infection
true or false: when you have VZV after that you can’t get reinfected and if so why
true
all subsequent manifestations in such individuals represent reactivation of latent virus from sensory ganglia
