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Virology test 1 lecture 8

front 1 Pathogenesis of viral disease	back 1 no data
front 2 sites of virus entry in a human	back 2 eyes mouth nose scratch/injury needle stick resp track urogenital tract anus
front 3 transmission of communicable disease	back 3 direct horizontal contact - kissing/sex airborne droplets vertical contact (mother -> baby) vector indirect (vehicles) touching objects/surface (contact) - fomites food, water, biological products airborne droplet nuclei aerosols
front 4 human to human	back 4 blood transfusion/injection respiratory saliva fecal-oral venereal

front 5 zoonoses	back 5 infection acquired from animals biting arthropod vector vertebrate reservoir vertebrate reservoir/arthropod vector
front 6 body defenses	back 6 eyes tears lysozyme resp. tract mucus ciliated epithelium aveolar macrophages genitourinary tract washing of urine acidity of urine vaginal lactic acid lysozyme skin anatomic barrier antimicrobial secretions digestive tract stomach acidity normal flora
front 7 reaction of host cell to viral infection	back 7 most viruses -> host cell death poxvirus, polyomavirus, papillomavirus -> proliferation of host cells RSV, measles, sendai, herpes -> fusion of membrane of adjacent cells to form multinucleate hybrid cells polyomaviruses, herpes, adeno, RNA oncogenic virus -> transformation of normal cells into malignant cancer cells rubella, some adenoviruses -> no histologic change in host cell appearance for several weeks
front 8 viral inclusion bodies in some human diseases	back 8 herpes nucleus cytomegalovirus nucleus rabies cytoplasm adenovirus nucleus measles nucleus vaccina cytoplasm

front 9 determinants of viral disease	back 9 nature of disease target tissue portal entry of virus access of virus to target tissue tissue tropism of virus (viral attachment protein) permissiveness of cells for virus replication viral pathogen (strain) immune status competence of the immune system prior immunity to the virus severity of disease cytopathic ability of virus immunopathology virus inoculum size length of time before resolution of infection general health of the individual genetic makeup of individual age
front 10 types of infection	back 10 inapparent infections virus infect but doesnt cause anything (dont know ur infected) acute infections see things that happen to infection localized stay same place virus go into person + replicate localized + localized spread -> disease + shedding of virus generalized travel through bloodstream virus -> entry -> blood/lymph so travel? cause disease at target organs shed no significant effect on other organs can spread thru nerves (ex: rabies) Port of entry, implant, locally spread -> peripheral nerves instead of blood -> spread to target organ (central nervous system) -> can cause the disease and/or shed to go into the environment to spread congenital persistent infections usually dont cause disease. Sometimes blow up transformation
front 11 Pathogenesis of congenital viral infection	back 11 Can be congenital transmitted Mother w/ fetus gets infected, then go to blood stream -> placental invasion -> fetus infected - then baby may die in uterus, or recovers - in some cases, baby born w/ disease -> can lead to clinical infection which can lead to persistant infection, recover, or gets killed -> can also lead to development of defects/abnormalities
front 12 Slow Infectious Diseases	back 12 bc of prions How theyre diff from viruses - viruses are filterable, so are prions - ONLY have protein - no morphology - none of this kills prions - not affected by proteases, heat, etc. Immune system important against viruses Prions have LONG incubation period – don’t know you have it for months/years Prions are transmissible spongiform encephaloptathies Deposits of extracellular proteins form plaques transmittable no signs of inflammation transmission of disease to experimental animal by intracranial injection of a homogenate of diseased tissue and subsequent serial passage to further animals

front 13 scrapie - infectious disease of sheep known since early 1700s	back 13 2-3 year incubation period cause irritability, itchiness and lack of coordination - fatal transmitted to goats in 1957 and mice in 1961 for animal experimental studies
front 14 kuru: fore tribe of papua-new guinea	back 14 "laughing death" restricted to that area loss of coordination (ataxia), partial paralysis, death devastated tribes for decades high familial prevalence in closely intermarried community affected children and women most Ppl. In tribe being infected + dying for years - usually women/children died - what happened: scientist in autralia working for NIH - he stopped in papua new guinea, heard abt this, became interested and started studying it - the ppl who were infected suffered loss of coordination, partial paralysis, and death
front 15 "infectious" nature of kuru: TSE that resembles others	back 15 noted it was similar to CJD, though diff parts of the brain noted it was similar to scrapie in sheep
front 16 CJD	back 16 rare neurogenerative disease "spongiform encephlopathy" worldwide occurrence 10-15% inheritied (familial (f)CJD) shown to be infectious also procedures: corneal transplant, intracerebral electrodes, injection of human growth hormone, or gonadotropin, tissue implants in brain

front 17 prion protein	back 17 Usually harmless and most ppl have the normal protein that can transform into the disease one (on top) Becomes all twisted and becomes like bottom one (becomes infectious)
front 18 how this occurs	back 18 Normal one = PrPsc (protein of scrapie, normal) PrPc – cellular form If one of them changes, then cascade of proteins contacting each other and transforming them -> hypothesize that it interacts and changes the protein - so its not created, but modifies existing proteins
front 19 PrPC	back 19 form polymers as PrPC is converted Aggregate – they form polymer -> causes disease
front 20 Progression of transmissible Creutzfeldt-Jakob disease	back 20 Progression of disease is slow - infection occurs, and incubation can be 1-30 years 3-5 months before disease, see progrone - get like dementia stage – see fibers are in brain -> leads to death

front 21 prion transmission	back 21 How spread - some species transmission maybe be possible (scrapie from sheep, caused mad cow disease) btw species - but no proof of showing can go to humans Can amplify and cause more disease in a species
front 22 brain areas affected	back 22 cerebral cortex CJD eats holes in brain -> lead to dementia + death cerebellum kuru + gerstman disease -> dementia thalamus fatal familial insomnia brain stem bovine spongiforn encephalopathy (mad cow disease) -> has infected thousands of cows
front 23 protein concentration in human vs animal brain	back 23 Study of brain extracts showed that there are 3 types of CJD where more concentrated protein in middle (humans) But in animal, the top part is more concentrated But type 4 in human is like the animal one Pattern of prion masses: Know diff types of infections (latent, acute, etc.)