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96 Cards in this Set

  • Front
  • Back
Viruses within ALPHA sub-family
Viruses within BETA sub-family
Viruses within GAMMA sub-family
Structural component unique to herpesviruses
2 steps involved in Herpesvirus attachment
Viral proteins binding GAGs of cell surface proteins
Additional binding to Herpesvirus Entry Mediator (HVE)
Why do herpesviruses encode enzymes involved in nucleic acid metabolism?
Because they often infect post-mitotic (non-dividing) cells
Where (in cell) do herpesviruses replicate?
What is the first group of genes expressed by Herpesviruses?

What do they do?
Immediate-early genes

Primarily regulatory proteins
What is the second group of genes expressed by herpesviruses?

What do they do?
Early genes

Involved in DNA metabolism and replication
What is the third group of genes expressed in Herpesviruses?

What do they do?
Late genes

Involved in structure
These deficiencies prevent viruses from being able to replicate in neurons
TK deletion
RR deletion

Neurons do not have limited pool of DNA precursors
How is acyclovir first phosphorylated?
By VIRAL thymidine kinase (TK)
Gamma sub-family herpesviruses are tropic for what type of cells?
Lymphoid tissue

NOTE: tissue is still mitotically active in some cases
EBV's origin of replication

Required for latent-phase DNA replication
These are used by herpesviruses that attack dividing cells
(ie gammaherpesviruses --> lymphoid cells)
Where do alphaherpesviruses establish latency?
Where do betaherpesviruses establish latency?
Where do gammaherpesviruses establish latency?
Lymphoid Tissue
Important genomic properties of Herpesviruses
All contain a long unique region
All contain a number of internal & terminal repeat elements
In infected cells, genome is rapidly circularized
Is the origin of replication for KSHV and EBV viral or host dependent?
VIRAL dependent

Virally encoded proteins tether viral genome to host's
Only herpesvirus that does NOT kill host cell during infection
Where do most herpesviruses bud through?
Inner nuclear membrane

Herpes simplex buds through trans-Golgi membrane
Which herpesviruses are NON-ubiquitous
Which sub-family of herpesviruses is associated w/ tumors?
Gamma sub-family
Only herpesvirus to have a vaccine
VZV (live attenuated)
What converts Acyclovir from mono- to tri-phosphate form?
CELLULAR kinases
What initially phosphorylates Acyclovir (to make mono- form)?
VIRAL thymidine kinase

NOTE: this is why Acyclovir doesn't work as well w/ CMV
--- CMV does NOT have TK ---
What initially phosphorylates Ganciclovir?
UL97 gene product of CMV
How is Cidofovir different from Acyclovir/Ganciclovir?
It comes ALREADY monophosphorylated
Do Herpesviruses integrate into host genomes?
Things caused by HSV-1
Skin/eye/mouth lesions
Intrauterine or neo/perinatal infections
Rate of encephalitis in infected babies
Has a poor prognosis
Adult seropositivity for HSV-1 approaches what?
70 - 90%
What causes most genital herpes?

NOTE: HSV-1 causes about 10 - 15%
% of adults infected w/ HSV-2 by age 21
What ganglia does HSV-1 typically travel up to?
Trigeminal ganglia
What ganglia does genital herpes typically travel up to?
Sacral ganglia
What lobe is involved in 90% of herpes encephalitis cases?
Temporal lobe
Prognosis for herpes encephalitis
Untreated - 70% mortality
Treated - 19% mortality

NOTE: 38% return to normal function
Can Acyclovir cure fever blisters and genital herpes?
Can make episodes milder, but CANNOT CURE

Has NO effect on latent infection
What is the treatment for herpes encephalitis?
Can be effective IF given early enough
Route of transmission for VZV?
Respiratory route
Adult reactivation of latent VZV

10 - 20% adults experience at least one episode

NOTE: almost always appears in a single dermatome
Treatment of Zoster
High dose Acyclovir decreases duration and neuralgia

Needs to be given within 72 hours
Main route of transmission for CMV
Close contact
Sign of Mono

Abs that react non-specifically to various proteins
What type of disease(s) does CMV cause?
Mono-like disease in adolescents/adults
NOTE: this is heterophile NEGATIVE

Congenital/Neonatal infections
NOTE: CMV can cross the placenta

Retinitis in AIDS pts.
% of people over 35 seropositive for CMV
Which herpesevirus does NOT "shut off" host protein synthesis?
Which grows faster?

HSV-1 or CMV?
Grows in cultured human fibroblasts
Where does CMV set up latency?
How is cell-mediated immunity suppressed in CMV?
Down-regulation of MHC
Inhibition of Ag presentation
Inhibition of NK cells
Sequestration of chemokines
% of births shedding CMV that exhibit developmental defects
Developmental defects caused by CMV
Mental Retardation

~20% mortality
Herpesvirus that may be involved in atherosclerosis

May promote growth of vascular endothelial cells
Hallmark microscopic sign of CMV
Inclusion bodies
"Owl's Eye"
Treatment for CMV retinitis
HHV-7 uses this as a component of its receptor
CD4 receptor
HHV-6 and 7 are lacking this protein
Thymidine Kinase

Thus, not sensitive to Acyclovir
This virus has been linked to roseola in infants and toddlers
Another name for KSHV
Gammaherpesviruses are tropic for this cell
B lymphocytes
Specific type of B cell that EBV targets
Mature, RESTING B cell

EBV induces such cells to enter the cell cycle
Cells in which EBV replication occurs most efficiently
Epithelial cells
Molecule via which EBV enters cells
% of adults seropositive for EBV
How is EBV spread
Via saliva
Cells initially infected by EBV
Oropharyngeal epithelial cells

NOTE: virus then infects B cells as they pass
EBV-induced B cell proliferation is usually brought under control by what?

NOTE: this "control" usually results in Mono
Incubation period of EBV
4 - 7 weeks
Two main periods in life when EBV is transmitted
When young kids mouth their toys
When adolescents kiss
How is Mono diagnosed?
By finding heterophile Abs, or
By finding abnormal lymphocytes
Monospot test
Diagnostic test for Mono

Test for heterophile Abs, present in 70-80% of pts.
Heterophile Abs agglutinate SHEEP RBCs
When are IgG and IgM to VCA detectable in EBV infection?
Early, during the ACUTE phase
When is IgG to EBV nuclear antigens (EBNA) detectable?
LATE in convalescence of EBV infection
Interpretation of presence of anti-VCA, but NOT anti-EBNA
RECENT EBV infection
Interpretation of presence of anti-VCA, AND anti-EBNA
PAST EBV infection
% of B cells w/ EBV Ags during acute phase of infection
As many as 20%
% of B cells w/ EBV Ags during convalescence of infection
< 1%
Potential complications of infectious Mono.
Splenic rupture
Severe tonsilitis
Rash (if treated w/ ampicillin)

Guillan-Barre Syndrome
Treatment for infectious Mono.
Primarily supportive treatment

Acyclovir stops EBV replication
BUT, does NOT shorten course of the infection
Survivors of X-linked lymphoprolif. disease are @ increased risk for what?
Immunoblastic lymphoma
Oral hairy leukoplakia
White, wart-like lesions on LATERAL tongue
Epithelial cells contain replicating EBV

Frequently in HIV-positive pts.
Activation of this is implicated in Burkitt's lymphhoma
c-myc proto-oncogene
How does Immunoblastic B cell lymphoma differ from Burkitt's?
Does NOT have translocation involving c-myc
Where (in the world) is nasopharyngeal carcinoma most common?
Southeast Asia
Southern provinces of China
Male:female ratio for nasopharyngeal carcinoma
Types of cells that KSHV typically infects
Spindle cells
Mononuclear cells
"Crescent sign"
Indicative of KSHV
Blood vessels are deformed by KS cells
This is directly related to risk of becoming infected with KSHV
Number of sexual partners
What cell is the transformed type in KSHV infections?
Spindle cells

These secrete angiogenic and growth factors
What key feature of KS suggests KSHV may not be neoplastic per se?
Lack of a histologically obvious neoplastic cell
Current therapy for KSHV
Systemic - chemo (DOXIL)

Local - radiation, vinblastine, cryotherapy
Major categories of genes encoded by KSHV (3)
Angiogenesis promoters
Cell cycle progression inducers
Anti-viral action inhibitors
Another name for roseola
Exanthem subitum
This herpesvirus MAY have a role in MS