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96 Cards in this Set
- Front
- Back
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Viruses within ALPHA sub-family
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HSV-1
HSV-2 VZV |
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Viruses within BETA sub-family
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CMV
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Viruses within GAMMA sub-family
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EBV
KSHV |
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Structural component unique to herpesviruses
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Tegument
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2 steps involved in Herpesvirus attachment
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Viral proteins binding GAGs of cell surface proteins
Additional binding to Herpesvirus Entry Mediator (HVE) |
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Why do herpesviruses encode enzymes involved in nucleic acid metabolism?
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Because they often infect post-mitotic (non-dividing) cells
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Where (in cell) do herpesviruses replicate?
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Nucleus
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What is the first group of genes expressed by Herpesviruses?
What do they do? |
Immediate-early genes
Primarily regulatory proteins |
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What is the second group of genes expressed by herpesviruses?
What do they do? |
Early genes
Involved in DNA metabolism and replication |
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What is the third group of genes expressed in Herpesviruses?
What do they do? |
Late genes
Involved in structure |
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These deficiencies prevent viruses from being able to replicate in neurons
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TK deletion
RR deletion Neurons do not have limited pool of DNA precursors |
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How is acyclovir first phosphorylated?
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By VIRAL thymidine kinase (TK)
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Gamma sub-family herpesviruses are tropic for what type of cells?
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Lymphoid tissue
NOTE: tissue is still mitotically active in some cases |
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EBV OriP
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EBV's origin of replication
Required for latent-phase DNA replication These are used by herpesviruses that attack dividing cells (ie gammaherpesviruses --> lymphoid cells) |
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Where do alphaherpesviruses establish latency?
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Neurons
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Where do betaherpesviruses establish latency?
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Glands
Kidneys Macrophages |
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Where do gammaherpesviruses establish latency?
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Lymphoid Tissue
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Important genomic properties of Herpesviruses
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All contain a long unique region
All contain a number of internal & terminal repeat elements In infected cells, genome is rapidly circularized |
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Is the origin of replication for KSHV and EBV viral or host dependent?
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VIRAL dependent
Virally encoded proteins tether viral genome to host's |
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Only herpesvirus that does NOT kill host cell during infection
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CMV
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Where do most herpesviruses bud through?
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Inner nuclear membrane
Herpes simplex buds through trans-Golgi membrane |
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Which herpesviruses are NON-ubiquitous
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KSHV
HSV-2 |
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Which sub-family of herpesviruses is associated w/ tumors?
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Gamma sub-family
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Only herpesvirus to have a vaccine
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VZV (live attenuated)
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What converts Acyclovir from mono- to tri-phosphate form?
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CELLULAR kinases
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What initially phosphorylates Acyclovir (to make mono- form)?
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VIRAL thymidine kinase
NOTE: this is why Acyclovir doesn't work as well w/ CMV --- CMV does NOT have TK --- |
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What initially phosphorylates Ganciclovir?
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UL97 gene product of CMV
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How is Cidofovir different from Acyclovir/Ganciclovir?
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It comes ALREADY monophosphorylated
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Do Herpesviruses integrate into host genomes?
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NO
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Things caused by HSV-1
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Skin/eye/mouth lesions
Keratoconjuctivitis Encephalitis Intrauterine or neo/perinatal infections |
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Rate of encephalitis in infected babies
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1/3
Has a poor prognosis |
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Adult seropositivity for HSV-1 approaches what?
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70 - 90%
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What causes most genital herpes?
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HSV-2
NOTE: HSV-1 causes about 10 - 15% |
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% of adults infected w/ HSV-2 by age 21
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20%
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What ganglia does HSV-1 typically travel up to?
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Trigeminal ganglia
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What ganglia does genital herpes typically travel up to?
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Sacral ganglia
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What lobe is involved in 90% of herpes encephalitis cases?
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Temporal lobe
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Prognosis for herpes encephalitis
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Untreated - 70% mortality
Treated - 19% mortality NOTE: 38% return to normal function |
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Can Acyclovir cure fever blisters and genital herpes?
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NO
Can make episodes milder, but CANNOT CURE Has NO effect on latent infection |
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What is the treatment for herpes encephalitis?
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Acyclovir
Can be effective IF given early enough |
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Route of transmission for VZV?
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Respiratory route
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Zoster
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Adult reactivation of latent VZV
10 - 20% adults experience at least one episode NOTE: almost always appears in a single dermatome |
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Treatment of Zoster
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High dose Acyclovir decreases duration and neuralgia
Needs to be given within 72 hours |
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Main route of transmission for CMV
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Close contact
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Heterophiles
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Sign of Mono
Abs that react non-specifically to various proteins |
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What type of disease(s) does CMV cause?
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Mono-like disease in adolescents/adults
NOTE: this is heterophile NEGATIVE Congenital/Neonatal infections NOTE: CMV can cross the placenta Retinitis in AIDS pts. |
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% of people over 35 seropositive for CMV
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80%
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Which herpesevirus does NOT "shut off" host protein synthesis?
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CMV
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Which grows faster?
HSV-1 or CMV? |
HSV-1
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Grows in cultured human fibroblasts
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CMV
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Where does CMV set up latency?
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Macrophages
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How is cell-mediated immunity suppressed in CMV?
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Down-regulation of MHC
Inhibition of Ag presentation Inhibition of NK cells Sequestration of chemokines |
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% of births shedding CMV that exhibit developmental defects
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10%
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Developmental defects caused by CMV
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Mental Retardation
Deafness ~20% mortality |
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Herpesvirus that may be involved in atherosclerosis
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CMV
May promote growth of vascular endothelial cells |
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Hallmark microscopic sign of CMV
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Inclusion bodies
"Owl's Eye" |
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Treatment for CMV retinitis
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Foscarnet
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HHV-7 uses this as a component of its receptor
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CD4 receptor
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HHV-6 and 7 are lacking this protein
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Thymidine Kinase
Thus, not sensitive to Acyclovir |
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This virus has been linked to roseola in infants and toddlers
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HHV-6
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Another name for KSHV
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HHV-8
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Gammaherpesviruses are tropic for this cell
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B lymphocytes
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Specific type of B cell that EBV targets
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Mature, RESTING B cell
NON-dividing EBV induces such cells to enter the cell cycle |
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Cells in which EBV replication occurs most efficiently
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Epithelial cells
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Molecule via which EBV enters cells
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CD21
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% of adults seropositive for EBV
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90%
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How is EBV spread
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Via saliva
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Cells initially infected by EBV
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Oropharyngeal epithelial cells
NOTE: virus then infects B cells as they pass |
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EBV-induced B cell proliferation is usually brought under control by what?
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CTLs
NOTE: this "control" usually results in Mono |
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Incubation period of EBV
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4 - 7 weeks
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Two main periods in life when EBV is transmitted
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When young kids mouth their toys
When adolescents kiss |
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How is Mono diagnosed?
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By finding heterophile Abs, or
By finding abnormal lymphocytes |
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Monospot test
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Diagnostic test for Mono
Test for heterophile Abs, present in 70-80% of pts. Heterophile Abs agglutinate SHEEP RBCs |
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When are IgG and IgM to VCA detectable in EBV infection?
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Early, during the ACUTE phase
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When is IgG to EBV nuclear antigens (EBNA) detectable?
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LATE in convalescence of EBV infection
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Interpretation of presence of anti-VCA, but NOT anti-EBNA
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RECENT EBV infection
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Interpretation of presence of anti-VCA, AND anti-EBNA
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PAST EBV infection
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% of B cells w/ EBV Ags during acute phase of infection
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As many as 20%
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% of B cells w/ EBV Ags during convalescence of infection
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< 1%
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Potential complications of infectious Mono.
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Meningitis
Encephalitis Polyneuritis Splenic rupture Severe tonsilitis Rash (if treated w/ ampicillin) Guillan-Barre Syndrome |
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Treatment for infectious Mono.
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Primarily supportive treatment
Acyclovir stops EBV replication BUT, does NOT shorten course of the infection |
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Survivors of X-linked lymphoprolif. disease are @ increased risk for what?
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Immunoblastic lymphoma
Hypogammaglobulinemia |
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Oral hairy leukoplakia
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White, wart-like lesions on LATERAL tongue
Epithelial cells contain replicating EBV Frequently in HIV-positive pts. |
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Activation of this is implicated in Burkitt's lymphhoma
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c-myc proto-oncogene
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How does Immunoblastic B cell lymphoma differ from Burkitt's?
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Does NOT have translocation involving c-myc
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Where (in the world) is nasopharyngeal carcinoma most common?
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Southeast Asia
Southern provinces of China |
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Male:female ratio for nasopharyngeal carcinoma
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2:1
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Types of cells that KSHV typically infects
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Spindle cells
Mononuclear cells |
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"Crescent sign"
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Indicative of KSHV
Blood vessels are deformed by KS cells |
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This is directly related to risk of becoming infected with KSHV
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Number of sexual partners
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What cell is the transformed type in KSHV infections?
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Spindle cells
These secrete angiogenic and growth factors |
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What key feature of KS suggests KSHV may not be neoplastic per se?
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Lack of a histologically obvious neoplastic cell
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Current therapy for KSHV
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Systemic - chemo (DOXIL)
Local - radiation, vinblastine, cryotherapy |
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Major categories of genes encoded by KSHV (3)
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Angiogenesis promoters
Cell cycle progression inducers Anti-viral action inhibitors |
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Another name for roseola
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Exanthem subitum
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This herpesvirus MAY have a role in MS
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HHV-6
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