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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)
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
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
nuclear replication
HPV: epidemiology
transmitted via direct or indirect inoculation of skin, mucosa
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
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
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
Complement with MAC lysis
blocking Ig

adaptive- CTLs, opsonizing Ig
Herpes Simplex Virus: gen charac
ds, linear DNA
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
complement opsonization in extracellular phase
resolution: opsonizing Ig, CTLs