Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
24 Cards in this Set
- Front
- Back
|
Innate response to viral infection
|
infected cells produce IFN a/B, IL-6, 12, chemokines (RANTES) to attract NKs and DCs
complement-mediated lysis of virions opsonization and phagocytosis of virions |
|
|
role of IFN-a in viral infections
|
rel by infected cells as part of innate immune response
acts on uninfected cells to induce anti-viral state if these host cells become infected, they are armed with PKR(~DAI)that is is activated by dbl-stranded RNA and inhibit protein syn; also have RNAse1 to degrade viral RNA (also preventing protein syn) LIMITS VIRAL SPREAD |
|
|
Cell Mediated Adaptive response to viral infection
|
TH1 and CD8 control intracelllular infection; lyse infected cells-->resolution
APC phagocytose free virion NK and APC rel early cytokines APC present to TH0: upreg CD80/86, MHC on APC TH0-->TH1, TH2; upreg MPh, PMN CTL activated B cells activated |
|
|
humoral response to viral infections
|
Prevent spread by blocking extracellular virions
Ig neutralize, opsonize virus; removed via ADCC, NK (with Ig providing specificity |
|
|
primary adaptive response to viral infection
|
IFN-g
MPh and DC as APCs virus specific CD4 and B cells proliferate B cells prod IgM, IgG, IgA virus specific CD8 proliferate |
|
|
secondary response to viral infection (memory)
|
Ig circulating (M, G, A)
virus specific memory B, T cells secretory IgA prevents re-infection via mucosa |
|
|
role of IFN-g in viral infection
|
enhances MHC expression by host cells-->enhances killing of infected cells; allows differentiation of CD8s
activates NKs for enhanced killing of infected cells |
|
|
viral evasion of host immune response
|
antigenic variation-results in many serotypes that are less efficient
downreg MHC1- prevent recog of infected cells downreg accessory mol for immune recognition (communication/activation) infect immunoprivileged sites-difficult for immune cells to enter infect cells of immune system |
|
|
HPV: general charac
|
ds, circular DNA
naked nuclear replication |
|
|
HPV: epidemiology
|
transmitted via direct or indirect inoculation of skin, mucosa
STD prevention: education, vaccine |
|
|
HPV: clinical disease
|
cutaneous or mucosal warts
carcinoma of cervix, anus, rectum diagnostic: inclusion bodies in vacuoles of epidermal cells |
|
|
HPV: pathogenic mxn
|
stimulates cell growth
viral proteins bind/inactivate p53, pRb (p105Rb)-->promotes cell growth infected cells are active, replicating basal cells of epidermis virus replicates as cell replicates as cell layer moves apical and differentiates, virus makes new capsid, proteins when host cell is dead, sloughed-off keratinocyte, virions are rel |
|
|
HPV: prevention, resolution
|
innate- IFN, NKs
complement opsonization adaptive- prevents infection with blocking Ig resolution of infection via opsonizing Ig; CTLs |
|
|
Influenza Virus: gen charac
|
ss, -sense RNA
enveloped (from PM) segmented genome can be cleared peplomers: hemagglutinin (H) for attachment and entry (endocytosis); neuraminidase (N) for release (removes sialic acid residues) |
|
|
Influenza: immune evasion
|
antigenic drift:
aa mutaions-->slow change, epidemic strains (new mutants ea yr with slight variation) antigenic shift: reassortants-->sudden, extreme change prod virions with entirely new peplomers-->pandemic strains |
|
|
Influenza: epidemiology
|
spread person to person
resp droplet reservoirs: human, bird, pig (pig for both avian and human flu; would allow reassortment) |
|
|
influenza: clinical disease
|
FEVER
chill, headache, myalgia, cough sequelae (pathological cond resulting from disease) serious in elderly Guillan-Barre (influ A,B): autoimmune attack on peripheral nn. Reyes (influ B): children taking aspirin for flu-like sx. |
|
|
influenza: prevention and resolution
|
innate-
IFN, NK Complement with MAC lysis adaptive- blocking Ig Resolution adaptive- CTLs, opsonizing Ig |
|
|
Herpes Simplex Virus: gen charac
|
ds, linear DNA
enveloped |
|
|
HSV: epidemiology
|
reservoir: man
transmission: direct, indirect contact with skin, mucosa STD, transplacental |
|
|
HSV: mxn
|
productive in epithelial cells; infects neurons and becomes latent until stressed or immune repression; activated production of virions that infect more epithelial cells;
symptomatic or asymptomatic but with shedding |
|
|
HSV: cytopathologic effects
|
latent in neurons
HSV I: trigeminal root ganglion (oral) HSVII: sacral n. ganglia (genital) form intranuclear inclusion bodies |
|
|
HSV: clinical disease
|
cold sores
genital herpes fever, malaise followed by vesicular lesions no cure |
|
|
HSV: prevention and resolution
|
innate-
IFN, NK complement opsonization in extracellular phase adaptive- resolution: opsonizing Ig, CTLs |
