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155 Cards in this Set
- Front
- Back
When is the best time to collect specimen for isolation of viruses?
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As early in the clinical course as possible (HSV and VZV may not be recoverable as early as 5 days post-onset of Sx)
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Which swabs are good/bad for virology specimen collection?
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Good: sterile Rayon or Dacron
Bad: calcium alginate swabs (toxic to enveloped viruses, false(+) with DFA), wooden shafts |
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What is in viral transport medium?
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Buffered saline
Stabilizers (proteins) Abx (kill fungi/bacteria) pH 7.2-7.4 |
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How many passes for each cell line?
Primary? Diploid? Heteroploid? |
Primary (PrRMK, RK) - 1-2 passes
Diploid (HDF) - 20-50 passes Heteroploid (Hep-2/A549) - infinite passes |
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VZV grows best in which cell line?
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HDF (diploid)
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Rabbit kidney (primary) is only permissive for which virus?
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HSV
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Adenovirus grows best in which cell line?
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Hep-2/A549 (heteroploid)
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CMW only grows in which cell line?
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HDF (diploid)
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Enterovirus grows best in which cell line?
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PrRMK (primary)
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Rhinovirus grows best in which cell line?
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HDF (diploid)
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Myxovirus grows best in which cell line?
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PrRMK (primary)
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RSV grows best in which cell line?
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Hep-2/A549 (heteroploid)
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What are mixed cell lines good for? (Mv1Lu + A549)
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Respiratory viruses (influenza A/B, RSV, Adenovirus, Parainflu)
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What are SUPER E-Mix cell lines good for? (BGMK + Decay Accelerating Factor)
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Detect all known Enteroviruses in single vial
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What are shell vial cultures good for?
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EARLY detection (24-48hr) of viruses (eg. CMV, HSV) vs. tube culture methods
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What is viral identification by Neutralization?
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(+)ID: neutralizing Abs prevent CPE
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What is viral identification by DFA staining?
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(+)ID: fluorescence with mAb conjugated FITC; rapid
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How do you detect Orthomyxoviruses/Paramyxoviruses in PrRMK?
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Hemadsorption (expression of hemagglutinin)
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What is viral identification by Enzyme immunoassay?
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(+)ID: enzyme-labeled antiviral Abs bind viruses and change color with substrate
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What is a good DIRECT way to test for Norwalk-like viruses (non-cultivable agents of gastroenteritis)?
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Immune EM
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What is viral Ab identification by Hemagglutination Inhibition Assay?
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Take pt serum with Abs, add virus.
Endpoint: Highest dilution of serum where hemagglutination of RBC's by the added virus occurs. 4-fold increase in titer is serum dilution of 1:80 |
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What is considered a positive Western Blot of HIV-1 Abs?
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1. gp160/120 and p24 (bobble head + core)
2. gp41 and p24 (bobble body + core) 3. gp160/120 and gp41 (bobble head + body) |
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Mnemonics for HIV-1 proteins: gp160, gp120, gp41, p24, p31
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[Mn] “160 is bobble head doll w/ 120 (head), 41 (body) spanning memb)
[Mn] “kobe is at the core of his team” [Mn] “instead of turning 31, she reversed and went to 13” |
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What is a good way to detect for TORCH titers? (pernatal infections)
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IgM Capture Assay for Detection of specific IgM Abs
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What is a simplified way to define fungi?
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Non-motile eukaryotes lacking chlorophyll
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What are some characteristics of fungi?
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PM contains ergosterol instead of choletersol.
Cell wall composed of chitin and glucans, mannans, polysaccs (no PGNs so not sensitive to PCN) Insensitive to Abx Unicellular = "Yeast" Mulicellular = "Mold" |
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The identification of fungi in the clinical lab is often based on...?
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Colony morphology.
Yeast cells, pseudohyphae (chains of elongated yeast cells) or hyphae (long filaments). For filamentous organism, the shape of the asexual sporulation body. Thermal dimorphism (mold at 25oC, yeast at 37oC) |
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Molds have what distinguishing morphological structure?
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Hyphae; structurally there are:
Septate hyphae (regular crosswalls/divisions but continuous cytoplasm). Nonseptate hyphae ("coenocytic"; no crosswalls/divisions) |
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What are the 2 functional types of hyphae in a mold?
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Vegetative hyphae - the part that holds the nutrients.
Aerial hyphae - the reproductive part (spores) |
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What is fungal dimorphism?
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Mold (25°C) vs. Yeast (37°C) form based on temperature
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What is the taxonomy of fungi based on?
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Structural features of the TELEOMORPH (sexual phase):
Zygomycota - fungi with nonseptate hyphae. Ascomycota - includes most human pathogens (septate fungi, asexual spores, myotic spores) Basidiomycota - mainly saprobes or plant pathogens. Deuteromycota - no sexual spores |
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Which antifungal drugs disrupt ergosterol?
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Amphotericin B (gold std), nystatin, azoles, allylamines
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Which antifungal drugs inhibit RNA/DNA synth?
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5-Fluorocytosine
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Which antifungal drugs inhibit mitosis?
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Griseofulvin
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Which antifungal drugs inhibit synth of glucans in cell wall?
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Echinocandins (active against Aspergillus, Candida)
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What is a dermatophyte?
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Keratinolytic fungi = use keratin as nutrient source (colonize stratum corneum).
Eg. orgs that cause Tinea |
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What does dematiaceous mean?
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"Dark-colored fungi"
eg. Chromoblastomycosis eg. Phaeohyphomycosis Stain with Fontana-Masson Stain for Melanin. |
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What are the superficial (cutaenous) mycoses?
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Piedra
Pityriasis versicolor (Tinea versicolor) Dermatophytes (Tinea) Onychomycosis (nails) Tx: topical antifungals |
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What is Piedra?
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Superficial/cutaneous fungal infxn: Hair shaft
Caused by: Piedraia hortae (black) - scalp Trichosporon beigelii(white) - beard |
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What is Pityriasis (Tinea) versicolor?
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Superficial/cutaneous fungal infxn: Epidermis (chest/back)
Caused by: Malassezia spp. - dimorphic, lipophilic, linked to dandruff Malassezia furfur - life-threatening enteric infxn in neonates |
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What is Tinea (ringworm)?
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Superficial/cutaneous fungal infxn: Keratinized tissues
Caused by: Dermatophytes: Trichophyton tonsurans mc fungal infx in peds |
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What is Onychomycosis
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Superficial/cutaneous fungal infxn: Nails
Caused by: Candida and Dermatophytes |
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What are the subQ mycoses?
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Mycetoma (Eumycetoma)
Chromoblastomycosis Sporotrichosis Lobomycosis Rhinosporidiosis |
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What is Eumycetoma?
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SubQ fungal infxn:
Chronic granulomatous infxn, swelling, deformity, sinus drainage, bone destruction Caused by: saprophytic fungi (Pseudoallescheria boydii) Tx: surgical debridement/amputation |
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What is Chromoblastomycosis?
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SubQ fungal infxn:
Cauliflower lesions on lower extremities of agricultural men Caused by: Dematiaceous fungi Tx: cryosurgery, topical antifungs |
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What is Sporotrichosis?
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SubQ fungal infxn: mc cutaneous myocosis in US → spreads to subQ.
"Rose gardener's Disease" Follows lymphatics (lymphocutaneous lesions) Caused by: Sporothrix schenckii in immunocompr (DIMORPHIC) Tx: azoles |
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What are the dimorphic fungi?
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Blastomyces dermatitidis,
Histoplasma capsulatum, Coccidioides immitis, Paracoccidioides brasiliensis, Penicillium marneffei, Sporothrix schenckii |
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What is Lobomycosis?
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SubQ fungal infxn:
Keloidal lesion, granulomatous inflammatory tissue Caused by: Loboa loboi Tx: excision |
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What is Rhinosporidiosis?
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SubQ fungal infxn: mucous memb (nose/eye/ear/larynx)
Chronic granulomatous infxn Caused by: Rhinosporidium seeberi (protozoa) Tx: excision |
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What is Phaeohyphomycosis?
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Dematiaceous fungi infxn that can be superficial, cutaneous, subcutaneous or systemic (immunocompr).
eg. darkly pigmented fungal structures in brain bx |
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What are the systemic OPPORTUNISTIC fungi?
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Candida spp.
Aspergillus fumigatus Cryptococcus neoformans Pneumocystis carinii (jiroveci) Penicillium marneffei |
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What are the systemic PRIMARY fungi?
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Blastomyces dermatitidis
Histoplasma capsulatum Coccidioides immitis Paracoccidioides brasiliensis |
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Currently, opportunitis fungi infxns are increasing in number, why?
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New susceptibilities: HIV, transplants, cancer
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Candida spp?
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OPPORTUNISTIC systemic fungal infxn: part of nl flora,
Leads to: 1. Muco-cutaneous candidiasis (from nl flora) 2. Disseminated candidiasis (from catheters, wounds→biofilms) |
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Aspergillus fumigatus?
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OPPORTUNISTIC systemic fungal infxn:
Can grow at high temps (50°C). Leads to: 1. ABPA, Allergic BronchoPulmonary Asperogillosis (IgE-mediated asthma with immune complex deposition) 2. Invasive fungal ball, lung hemorrhage High mortality |
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Cryptococcus neoformans?
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OPPORTUNISTIC systemic fungal infxn:
Pigeon droppings AIDS-defining illness Leads to: Meningocephalitis (mc presentation) Hallmark: India ink (halo) stain of CSF from its capsule |
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Pneumocystis carinii (jiroveci)?
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OPPORTUNISTIC systemic fungal infxn:
AIDS-defining illness Usu colonizes lung at birth but cleared in immunocompetent |
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Penicillium marneffei?
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OPPORTUNISTIC systemic fungal infxn: (DIMORPHIC)
Soluble red pigment diffuses into agar |
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Blastomyces dermatitidis?
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PRIMARY systemic fungal infxn: (DIMORPHIC)
"Chicago Disease" Diffuse pneumonitis and ARDS Culture @ 30°C Can convert to yeast form in body = unsusceptible to macrophages and not contagious |
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Histoplasma capsulatum
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PRIMARY systemic fungal infxn: (DIMORPHIC)
Bat guano Prevents phago-lysosomal fusion in host cells (lives in macs) Influenza-like illness, resembles TB (cavitations) Oral lesions |
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Coccidioides immitis?
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PRIMARY systemic fungal infxn: (DIMORPHIC)
Arthroconidia easily inhaled In tissue (37°C), forms spherule/sporangia filled with endospores. SW US, Mexico |
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Paracoccidioides brasiliensis
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PRIMARY systemic fungal infxn: (DIMORPHIC)
"Captain's wheel" morphology on stain Ulcerative lesions (face, GI mucosa) |
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What are the 3 impt HIV enzymes?
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RT
Protease (modify transcribed proteins to become fully fxnal) Integrase (integrate viral provirus into host genome) |
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What 2 major human cells does HIV infect and what do they have in common?
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CD4+ T cells
Macrophages They both have CD4 |
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Explain HIV entry into host cells.
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gp120 binds CD4 → virion conf change → expose gp120 → bind chemokine receptor → allows gp41 to penetrate membrane and lead to fusion
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Name the impt host chemokine receptors for HIV entry into cells.
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CCR5 - used to ID/infect macs
CXCR4 - used to ID/infect CD4+ T cells CCR5 mutations = resist HIV infxn! |
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Why are concomitant infxns with HIV so bad?
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HIV LTRs (on both ends of HIV genome) have NK-kB binding sites.
Any activation of immune system (bact, viral, vaccine) can stim T-cells → ↑NK-kB (TF) → stim replication/pathogenicity of HIV genome |
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What are the EARLY HIV genes? (regulatory)
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tat - trxn of other genes
rev - exports immature RNAs (Rev Responsive Elements) out of nucleus, req'd for late genes nef - activates T-cells, downregulates CD4, MHCI |
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What are the LATE HIV genes? (structural)
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gag - internal capsid
pol - 3 impt enzymes: RT, protease, integrase gag/pol - due to ribosomal fram-shift env - envelope (gp120/gp41) |
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What is APOBEC3G?
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Host antiviral protein; induces mutation in viral DNA (C→U) so that the virus can't replicate
Only works in Vif(-) HIV. HIV that are Vif(+) degrade APOBEC3G. |
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What are the important helper T cell cytokines in normal viral infxns and what happens in HIV?
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Th1 - produce IL-2, IFN-γ → help CTLs (CD8+) to kill infected cells
Th2 – produce IL-4 → help B-cell produce neutralizing Abs HIV kills these helper T cells |
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What is the timecourse of HIV-1 infxn?
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-2-6 wks: Flu-like Sx
-~10yrs: aSx phase (depletion of CD4 -T cells) -Symptomatic phase -AIDS: CD4<200 (opportunistic infxns) |
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What is the origin of HIV-1?
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Cross-species transmission of Simian Immunodeficiency Virus
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2 impt viral wapons for HIV:
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Integrase: can establish latent infxns
RT: error-prone enzyme (muts) |
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Name a complication/syndrome of HAART.
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Immune reconstitution inflammatory syndromes - reestablishing your immune system causes you to detect/attack latent infxns
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Orthomyxoviruses: Genome, Transmission, Clinical.
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(-)ssRNA
Transmxn:resp secretions Clinical: first URT then LRT; high fever, tiredness, m ache, HA |
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What are the 3 types of Influenza virus?
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Type A: Ag shift/drift
Type B: Ag drift only Type C: Ag drift only |
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Structure of influenza virus
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Spikes:
HA (80%) - binds SA, endocytosis NA (20%) - cleaves SA M1 - packaging of RNA, budding M2 - ion ch involved in penetration |
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What are influenza virus' pathogenic talents?
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Cap stealing - viral endonuclease steals host cap and transfers it to viral mRNA
High mutatation/recombo rate of ssRNA Molecular evolution due to selective pressures |
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What is Antigenic Drift? (influenza)
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Minor changes → seasonal epidemics
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What are the important helper T cell cytokines in normal viral infxns and what happens in HIV?
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Th1 - produce IL-2, IFN-γ → help CTLs (CD8+) to kill infected cells
Th2 – produce IL-4 → help B-cell produce neutralizing Abs HI kills these helper T cells |
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What is the timecourse of HIV-1 infxn?
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-2-6 wks: Flu-like Sx
-~10yrs: aSx phase (depletion of CD4 -T cells) -Symptomatic phase -AIDS: CD4<200 (opportunistic infxns) |
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What is the origin of HIV-1?
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Cross-species transmission of Simian Immunodeficiency Virus
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2 impt viral wapons for HIV:
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Integrase: can establish latent infxns
RT: error-prone enzyme (muts) |
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Name a complication/syndrome of HAART.
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Immune reconstitution inflammatory syndromes - reestablishing your immune system causes you to detect/attack latent infxns
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Orthomyxoviruses: Genome, Transmission, Clinical.
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Genome:(-)ssRNA
Transmxn:resp secretions Clinical:first URT then LRT; high fever, tiredness, m ache, HA |
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What are the 3 types of Influenza virus?
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Type A: Ag shift/drift
Type B: Ag drift only Type C: Ag drift only |
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Structure of influenza virus
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Spikes:
HA (80%) - binds SA, endocytosis NA (20%) - cleaves SA M1 - packaging of RNA, budding M2 - ion ch involved in penetration |
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What are influenza virus' pathogenic talents?
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Cap stealing - viral endonuclease steals host cap and transfers it to viral mRNA
High mutatation/recombo rate of ssRNA Molecular evolution due to selective pressures |
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What is Antigenic Drift? (influenza)
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Minor changes → seasonal epidemics.
eg. errors in RNA replication |
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What is Antigenic Shift? (influenza)
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Major changes → pandemics
eg. recombination with other strains |
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What is the H & A variant of Avian Flu?
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H5N1, very high mortality rate, strong environmental survival
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What is the flu vaccine production timeline?
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Jan-May: Virus selection and production
Summer: FDA approval and packaging Fall: Vaccination Vaccines are usu an inactivated vaccine |
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Paramyxoviridae: Genome, Major genera, Unique features
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(-)RNA
Morbillivirus (measles) Paramyxovirus (parainfluenza) Rubulavirus (mumps) Pneumovirus (RSV) Henipaviruses (Nipah and Hendra virus) Abs are not effective bc can spread directly from cell-to-cell via host cell fusions (cell-mediate immunity is critical!!) |
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Paramyxoviridae: Morbillivirus (measles): Genome, Hallmarks, Complications
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(-)RNA
Koplik spots (white spots on buccal mucosa) maculopapular rash that starts on head and spreads Live attenuated vaccine is good Complications: Subacute sclerosing panencephalitis (Δmental, spasticity, blindness) |
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Rubulavirus (mumps): Genome, Hallmarks
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(-)RNA
Parotitis (salivary glands), orchitis, meningoencephalitis MMR vaccine: 95% lifelong imm |
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Pneumovirus (RSV): Hallmarks
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Rales (auscultation), CXR hyperexpansion, patchy infiltrates;
NO viremia/systemic spread; syncytia formation (multinucleated "giant cell"), immunity doesn't protect against reinfxn Infants: Pneumonia/bronchiolitis Adults: URT Infxn |
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Paramyxoviridae: Paramyxovirus (parainfluenza): Genome, Hallmarks
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(-)RNA
Limited to resp tract (URT), NO viremia/systemic spread |
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Henipaviruses (Nipah and Hendra virus): Genome, Hallmarks
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(-)RNA
Hendra/Nipah more closely related to eachother (70-80%) than other paramyxo's (50%) Extended Zoonotic virus: Hendra - bats, horses Nipha - bats, pigs |
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Rhabdovirus: Lyssavirus (rabies): Genome, Hallmarks, Tx
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(-)ssRNA
Hydrophobia, anxiety, cardiac arrest, Negri inclusion bodies in brain, long incubation phase bc virus takes longer to replicate in muscle Tx:pre/post-exposure before Sx (if symptomatic, only supportive care) |
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Togavirus, Flavivirus: ArBoviruses: Genome, Hallmarks
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(+)ssRNA = "capped" mRNA
Togavirus - Equine Encephalitis Flavivirus - Dengue & Yellow Fever, West Nile Cytolytic, arthropod-borne, systemic/viremia, can induce host IFN Some vaccines, otherwise supportive care |
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Togavirus: Rubella virus: Genome, Hallmarks
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(+)ssRNA = "capped" mRNA
Resp virus that ONLY infects humans Fetus: severe congenital defects Children: rash, lymphadenopathy Adults: bone/joint pain, thrombocytopenia, encephalitis |
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HBV: Genome, Hallmarks, Complications, Vaccine, Tx
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Circular, partially dsDNA, enveloped
Jaundice Outcome based on age of infxn Birth: aSx, chornic, no anti-HBs Adult: Sx, not chronic, anti-HBs (resolution) Complications: cirrhosis, hepatocellular carcinoma (5yr survival 3%) Vaccine: 3 shots, long-lasting Tx: (NOT curative, but helps liver regen) - IFN, nucleoside analogues |
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HDV: Genome, Hallmarks
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Circular ssDNA, enveloped
Obligatory coinfxn with HBV, "superinfxn" when HDV happens on top of a CHRONIC HBV infxn Again anti-HBs is the key to resolution in acute coinfxn |
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Adenovirus: Genome, Hallmarks, Impt genes
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linear dsDNA, non-enveloped = lytic
Disease (serotype): Resp (4/7), conjunctivitis (8), gastroenteritis (11), cystitis (40/41) Can persist and reactivate E1A – inhibits host pRB (TSG) E1B – inhibits host p53 (TSG) E2 – pol/replication E3 – immune evasion L1-L5 – Late proteins (structural) |
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Parvovirus: Erythrovirus B19: Genome, Hallmarks, Complications
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(+)DNA and (-)DNA
Child: Erythema infectiosum - "Fifth / Slapped Cheek Disease" Adult: arthritis Infects nasopharynx, URT, BM (RBC precursors, anemia) Complications: Aplastic anemia in sickle cell pts Chronic anemia in immunocompr Hydrops fetalis in pregnancy |
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Papovovirus: Papillomavirus: Genome, Hallmarks, Impt genes, Vaccine
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Circular dsDNA
Tropism to stratified squamous epith HPV16, 18, 31 → cervical cancer E6/E7 inhibits p53/pRB (TSGs) Gardasil against HPV6/11/16/18 |
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Papovovirus: Human Polyomavirus: 2 types
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JC - Progressive Multifocal Leukoencephalopathy (PML) in HIV
BK - hemorrhagic cystitis in BM transplant, ureter stenosis in renal transplant |
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Picornaviruses: Genome, Impt ones
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(+)ssRNA = "capped mRNA," non-enveloped = lytic
Enterovirus (Poliovirus) - bind CD55 Rhinovirus - bind ICAM-1 |
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Picornavirus: Poliovirus: Genome, Hallmarks, Vaccine
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(+)ssRNA
Fecal-oral transmxn, lots of serotypes, Sx depend on secondary target tissue 90% aSx > resp/gut > meningitis > poliomyelitis > paralytic disease UMN: Bulbar poliomyelitis LMN infx: Paralytic poliomyelitis mm deterioation: Postpolio syndrome Polio enterovirus vaccine (no non-polio enterovirus vaccines): Salk - inactivated, 4xIV Sabin - attenuated, oral=easy |
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Picornavirus: Rhinovirus: Genome, Hallmarks, Tx
(Respiratory viruses) |
(+)ssRNA
Lots of serotypes!, mcc common cold, limited to resp tract due to acid sensitivity (inactivated pH<6) and grows better in colder temp in lung (33°C) vs. GI; I-CAM-binding receptor is hidden in groove, not recog'd by Abs Tx: cough suppressant, decongestant, fluid/rest (No Abx or antihistamines) |
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Coronavirus (SARS): Genome, Hallmarks
(Respiratory viruses) |
(+)RNA, largest RNA virus, has 5'cap/polyA tail, synthesizes nested set of subgenomic RNAs, enveloped, glycoprotein "corona" is protective in intestine
Coronaviruses (a/w enteric infxn) are URTI (2nd mcc common cold after Rhinovirus), but SARS can also cause serious LRTI SARS begins with ssytemic Sx (high fever >38°C!!), followed by resp Sx (infiltrates) Supportive care |
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Reovirus: Rotavirus: Genome, Hallmarks
(Respiratory viruses) |
Segmented dsRNA, non-enveloped, two-layer capsid
Single most important cause of severe diarrheal illness in young (lots of virus in stool) R(resp), E(nteric), O(rphan) virus Two-layer capsid (non-infxs), cleaved in GI and can infect enterocytes Vaccine, Supportive care |
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Flavivirus: HCV: Genome, Hallmarks, Tx
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(+)RNA, enveloped, quasispecies (Abs don't protect against recurrent)
Acute: 70% aSx > jaundice, LFT Dx: Bx (gold std) Global challenge: No preventative vaccine, Tx ineffective, leads to CHRONIC infxn → hepatitis, steatosis, insulin-resistance, cirrhosis Transmxn (blood): IV drug use > sex Tx: Genotype 1a/1b don't respond to IFN Genotype 2/3 respond to IFN Genotype 3a → steatosis Transplant |
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Picornavirus: HAV: Genome, Hallmarks, Vaccine
|
(+)ssRNA, non-enveloped, 1 serotype
mcc acute viral hepatitis > HBV > HCV; replicates slowly without direct CPE Fecal-oral, jaundice more severe >14yo; no chronic sequelae (only acute) Acute/current infxn: anti-HAV-IgM Past infxn: anti-HAV-IgG Pre-exposure: Vaccine, Ig (travelers) Post-exposure: Ig |
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What are the 8 HHV?
|
HSV1
HSV2 VZV CMV HHV6 HHV7 EBV Kaposi's Sarcoma assoc HV (HHV8) |
|
What are the differences between the 3 groups of HHV?
|
α – short replication cycle
β – long replication cycle γ – generally infects immune cells (eg. B cells) |
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HHV: HSV1/2: Genome, Hallmarks, Impt genes, Complications, Tx
|
dsDNA, α (short replication cycle)
Prevalence: HSV1 > HSV2 HSV1 - oral/eye HSV2 - genital Lytic and Latent cycles Acute/lytic: VP16 gene - master ctrl gene that turns on gene expression Latent: viral DNA remains as episome in ganglionic cells (antiviral drugs ineffective here) Immunocompr - disseminated infxn, CNS, HSV can enhance HIV acquisition Tx: acyclovir - targets HSV-1 thymidine kinase to stop DNA elgonation |
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HHV: VZV: Genome, Hallmarks, Tx
|
dsDNA, α (short replication cycle)
Primary: Varicella - mostly children, rash Reactivation of latent from DRG: Zoster - pain along affected nerves Tx: acyclovir |
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HHV: EBV: Genome, Leads to 4 diseases, Hallmarks, Tx
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dsDNA, γ (infects immune cells)
Acute: in epith cells Latent: in B-lymphocytes (can cause immortalization here → malignancy) Leads to: 1. Infectious mononucleosis (Heterophile Abs; Triad: lymphadenopahty, splenomegaly, pharyngitis) 2. Burkitt's Lymphoma (t(14;18), c-myc) 3. Nasopharyngeal Carcinoma 4. Hair oral leukoplakia in AIDS Supportive care (no Abx/vaccine), life-long immunity |
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HHV: HHV8/Kaposi's Sarcome-associated HV: Genome, Hallmarks
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dsDNA, γ (infects immune cells)
Found in AIDS-related B-cell lymphomas |
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HHV: CMV: Genome, Hallmarks, Tx
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dsDNA, β (long replication cycle)
OI, latency in leukocytes, 80% of all adults have CMV Abs, Owl eye inclusions 1. Cytomegalic inclusion disease - mc viral cause of congenital defects 2. CMV mononucleosis 3. CMV retinitis, pneumonia (immunocompr) Tx: Gancyclovir and Foscarnet – inhibit CMV DNA pol |
|
Name a strategy of immune evasion (1)
|
Ag variation
S. pneumonia: lots of subtypes that differ in capsular polysaccs Influenza virus: Ag drift - mutations in H epitopes → seasonal Ag shift - reassortment b/w strains → pandemics |
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Name a strategy of immune evasion (2)
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Latency - for escaping eradication and for reactivation
HSV: hides in sensory neurons (also VZV, EBV) M. tuberculosis - hides in macs |
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Name a strategy of immune evasion (3)
|
Manipulation of immune system - resistance to immunity
M. tuberculosis: prevents phagosome-lysosome fusion (hids in macs) |
|
How does HIV avoid immune response?
|
Avoid Abs;
1. HIV envelope is heavily glycosylated 2. gp41 is masked until CD4 is engaged by gp120 3. high mutation rates (RT) Avoid CTLs 1. Downregulate MHCI 2. Tat/Rev system turbocharges HIV gene expression 3. Virions can be released b4 immune recog Chen's research: Mutation in CTL epitope of AIDS helps it escape MHCII |
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Filovirus: Genome, Genera, Hallmarks
|
Linear (-)ssRNA
Marbug virus Ebola virus Leads to: severe hemorrhagic fever Host fruit bats don't die bc they carry PKR (dsRNA-dep protein kinase R) |
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Poxvirus (Smallpox): Genome, Hallmarks
|
dsDNA, replicates in cytoplasm
Guarnieri inclusion bodies Smallpox (vs. Chicken Pox): 1. Rash on lower extrem (face/trunk) 2. Vesicles appear all at same time (diff stages) |
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Bunyavirus: Genome, Hallmarks
|
(-)ssRNA
Transmission via Aedes mosquito in California encephalitis Hanta virus (no insect vector, a/w rodent feces) |
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Areavirus: Genome, Hallmarks, Tx
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(-)ssRNA, ambisense RNA that fxn as both (+) and (-)
Rodent feces/urine Infects Macs → activate T cells → tissue damage due to T-cell-mediated inflamm Non-fatal: Lymphocytic choriomeningitis Fatal: Lassa fever, Machupo, Junia Tx – Ribovirin |
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- What is a key charac of picornaviruses that contrib. to ability to be transmitted effic via oral fecal rotue?
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o Nonenveloped viruses with relatively stable capsid
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- When delivered to cyto of a permissive host cell, the genome of picornaviruses:
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o These are positive strand so….. serve as template for host ribosomes to translate the viral proteins
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- Enteroviruses are one of several groups of viruses which gain access to human body thru GI. However, rarely cause GI disease and in fact cause wide range of diff clinical manifestations. Why do these viruses cause a wide variety of disease syndromes?
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o The secondary target tissues to which specific enteroviruses spread and replicate are different.
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- Frustrated teacher comes in with 3rd rhinovirus infxn of year. Why does she keep getting it?
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o Reinfxn is common cuz there are >100 serotypes.
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- Which of the following viruses is hep A most closely related to?
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o Poliovirus (picornavirus)
HAV is a Picornavirus |
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- 14 yo with acute illness with jaundice, fatigue, nausea and tests indic elev ALT. what form of viral hepatitis do you suspect he has contracted?
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o Hep A: distinguishing feature is acute
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- Of the following chronically infected Hep C pts, which statistically has highest probability of achieving SVR (sustained viral response) in response to combo therapy with IFN and ribavarin?
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o 30yo Caucasian female infected with genotype 2a
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- HBsAg negative person comes into clinical complaining that she has chronically felt tired with ab discomfort, loss of appetite and digestive disturbances for years and now appears jaundice. Blood transfusion in 1991. What hep virus?
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o Hep C
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- To avoid flu virus spread the use of a regular face mask ...
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o May offer reasonable protection
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- 3 mo infant presents with 3 day Hx of fever, cough and poor feeding. On exam, baby appears ill and temp of 102 and RR 32. CXR shows bilateral patchy infiltrates in lungs. Which is most likely etiologic agent?
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o Respiratory syncytial virus (infants under 1yo RSV is most common cause of pneumonia like symptoms)
(Corona and Rhinoviruses stay in upper resp tract so not that) |
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- 1yo had common cold but now has voice that is hoarse and cough= that sounds harsh and brassy and worse at night. On exam, child has trouble drawing air into lungs btwn coughs and trouble drawing air into lungs. Visible stridor on inhalation. Most likely to be...
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o Parainfluenza
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- Which of the following disease can be prevented by vaccine except:
Dengue, Measles, Polio, Rubella, Flu |
o Dengue fever
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- Vaccination strategy for child born to chronic carrier mother (Hep B)
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o 3 Hep B vaccine (0, 1, 3 mo) + HB Ig
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- What determines if a newborn will become a chronic carrier or not
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o Viral load of mother
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- Antiviral Tx for Hep B:
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o IFN
o Nucleoside analogs: target reverse transcriptase |
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- Who gets hep D infxn?
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o Those with hep B
o Coinfected: worse than Hep B alone. o Superinfected: get worse and stay worse |
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- Chronic HBV criteria:
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o longer than 6 mo with HBsAg circulating
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- Why does geographic distrib of hep B matter?
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o People are travelling to those areas.
o Carriers. |
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- Chronic Hep B rates going down because:
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o vaccines.
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- How do you get hep B?
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o Bloooooooooooooooooooooooood
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- What are the important reqts for HIV-1 entry into target cells?
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o Receptor is CD4rec
o CCR5,CCL4 are coreceptors |
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- What is the consequence of HIV 1 infxn?
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o Cd4 drops cuz this is the target.
o Also macrophages are infected but for some reason the functional aspect is not as striking as CD4 T cell. |
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- Why does T cell activation lead to inc in HIV replic—molecular mech?
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o Infection causes T cell activation and this is what HIV targets CD4 T cells so it increases.
o 2 binding sites for NF-kB |
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- How does HIV establish latency?
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o Integrate its DNA into host.
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- What is the possible mech whereby swine flu virus H1N1 evolves?
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o Antigenic shift. Segments changed through recombination
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