Ch 13 – Microbiology – Flashcards

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virus characteristics
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-small infectious agents
-can infect most living things
-bacteriophages attack bacteria
-reproduce at high rate (require host)
-can mutate
-acellular (no cytoplasm or organelles)
-no metabolism of their own
-replicate using hosts machinery
-possess DNA or RNA never both
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Ivanowski
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-in 1892 shows that the tobacco mosaic disease is caused by an agent
that passes through a porcelain filter
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viral genome
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-Single or segmented, circular or linear molecule of nucleic acid functioning as
the genetic material of the virus
-Can be single-stranded or double-stranded DNA or RNA (but never both)
-Codes for the synthesis of viral components and viral enzymes for replication
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capsid
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-Protein shell surrounding the genome
-Usually composed of protein subunits called capsomeres
-Protect and introduce the genome into host cells.
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viral envelope
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-Composed of phospholipids and glycoprotein
-Derived from host cell membranes by a process called budding
-Depending on the virus, envelopes may be covered by spikes made of
carbohydrates-protein complexes that helps the virus to attach to the
host cell
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enveloped viruses
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-Nucleic acid surrounded by either a
helical or polyhedral core and covered by an envelope (herpes)
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binal (complex) virus
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Pleomorphic (irregular shape), or
have complex structures
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virus size range
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5-300nm
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helical viruses
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nucleic acid surrounded by a hollow
protein cylinder or capsid and possessing a helical
structure (tobacco mosaic)
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Polyhedral viruses
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nucleic acid surrounded by a
polyhedral (many-sided) shell or capsid, usually in the
form of an icosahedron (Mastadenovirus)
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classification of viruses
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-type of nucleic acid
-shape of capsid
-enveloped or naked
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viruses with ds DNA(+/-)
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-the (-) DNA is directly transcribed into viral mRNA
-bacteriophages, papovaviruses, adenoviruses, herpesviruses
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viruses with (+) DNA or (-) DNA
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-once inside the host, it is converted into ds DNA and the (-) strand is transcribed into viral mRNA
-Phage M13, Parvoviruses
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viruses with (+) RNA
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-a (+) RNA is copied into (-) RNA that is transcribed into viral mRNA
-Picorna viruses, Togaviruses, Corona viruses
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viruses with (-) RNA
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-the (-) RNA is copied into (+) RNA which functions as viral mRNA
-Orthomysoviruses, Paramysoviruses, Rhabdoviruses
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viruses with ds RNA (+/-)
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-the (+) RNA functions as viral mRNA
-Reoviruses
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viruses with (+) RNA
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-the (+) RNA is reverse transcribed into (-)DNA that makes a complementary copy to become (+/-) DNA
-the DNA is transcribed to make viral mRNA
-Retroviruses
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viral replication of bacteriophages
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-lysogenic and lytic cycle
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steps of lytic cycle
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-attachment
-penetration
-biosynthesis
-maturation
-release
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attachment (lytic cycle)
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-by chance, no energy required
-involves attachment site on virus and receptor site on bacteria
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penetration (lytic cycle)
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-phage lysozyme is released and breaks down a portion of the cell wall
-phage injects DNA
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biosynthesis (lytic cycle)
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-synthesis of viral nucleic acids and proteins in cytoplasm
-host DNA is degraded
-viral proteins interfere with transcription and it ceases
-translation is repressed
-early phase-many copies of the phage DNA are synthesized using the host's nucleotides and enzymes
-late phase-host's ribosomes, enzymes, and amino acids are used for translation of viral proteins
-during this eclipse period, the virus is not infectious
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maturation (lytic cycle)
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-assembly of capsid around genome
-complete virions are produced
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release (lytic cycle)
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-plasma membrane lyses to to action of phage lysozyme
-virions released to infect other bacteria
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lysogenic cycle
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-does not necessarily end with host cell death
-these phages are able to incorporate their DNA into the host cell DNA
-virus remains latent(inactive)
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lysogeny leads to...(3)
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-lysogenic cells are immune to re-infection of the same phage
-phage conversion (cell exhibits new properties)
-specialized transduction
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example of phage conversion
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-Corynebacterium diphteriae
-diphteriae caused by toxin
-gene encoding toxin is carried by a phage
-so it only produces toxin when it carries the lysogenic phage
-similar with Clostridrium botulinum
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Animal virus infection steps (6)
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-attachment
-penetration
-uncoating
-biosynthesis
-maturation
-release and reinfection
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attachment (animal virus)
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-binding of attachment sites on viral surface with receptor sites on host cell membrane
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penetration (animal virus)
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-fusion with the host membrane
-endocytosis
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uncoating (animal virus)
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-capsid is digested
-release of viral genome
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biosynthesis (animal virus)
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-viral genome directs the host cell's metabolic to synthesize viral enzymes and viral parts
-early phage- viral genome replicates thousands of times
-late phase-viral structural proteins and enzymes involved in maturation are produced
-during uncoating and replication, virus is not infectious
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viral structure proteins
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-capsid and matrix proteins
-envelope glycoproteins
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maturation (animal phase)
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assembly of capsid around genome
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release and reinfection (animal virus)
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-virus obtains envelope by budding
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number of viruses that can be made from one host cell
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10k to 50k
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viral latency
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-some ds DNA viruses like herpes virus and retrovirus are able to remain latent for long periods of time without replicating or causing harm
-some remain latent in cytoplasm
-others are able to integrate their DNA into host cell chromosomes(provirus)
-results from the lack of production of specific host cell proteins that are required for activation of viral genes
-activation of host cellls DNA in response to extracellular stimuli can lead to synthesis of specific host cell proteins required by virus
-these proteins now activate viral genes leading to burst of replication via the productive life cycle
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examples of latent viruses
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-herpes simplex virus (HSV) (oral, genital)
-Epstein-Barr virus (EBV)-replicate in epithelial cells, latent in B lymphocytes, mononucleosis
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persistent (chronic) viral infections
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-occur gradually over a long period rather than appearing suddenly
-cervial cancer (HPV), AIDS-HIV-1, liver cancer HBV
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Herpesviruses
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-large genome 120kb, linear, ds
-among most widespread of all infections
-can establish latent infections which can reactivate years later producing acute infections
-100 herpesviruses identified from oysters to humans
-8 infect humans
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more on herpes
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-disease is initiated by direct contact (oral genital brain)
-cause cytopathologic effects (degenerative changes in cells)
-avoids antibodes by cell to cell spread
-establishes latency in neurons (hides from immune system)
-activated from latency by heat, cold, UV, stress, or immune suppression
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Herpes Simplex Virus (HSV)
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-common human pathogen
-cause painful by benign lesions and recurrent disease
-both type 1 and type 2 cause cause significant mortality when infecting eye or brain, in immunosupressed person, or newborn
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Varicella Zoster virus (VZV)
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-causes chicken pox (varicella)
-when reactivated causes herpes zoster or shingles (rash along entire skin)
-establish latent infections of neurons
-characteristic blister-like lesions
-spread predominantly by respiratory route
-smallest genome of herpesvirus
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Hepatitis A virus (Acute Viral Hepatitis A)
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-common in US
-30% of population show evidence of past infection due to anti-HAV antibodies
-most infections are asympotomatic-confers lifelong immunity
-long incubation period (15-50 days) before symptoms
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more on HAV
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-during incubation period, virus replicates in intestinal cells and shed in high concentrations in stools
-transmitted via fecal-oral route (water, food, dirty hands)
-outbreaks usually originate from common source (water supplies, restaurant, daycare)
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Hepatitis B Virus (HBV)
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-one of the most frequently reported vaccine preventable diseases in US
-HBV causes acute and chronic hepatitis
-spread though sexual contact, blood transfusion, exposure to blood via open cuts, opens spores, needle/razor sharing, ear piercing
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more on HBV
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-can be spread from mother to child from birth
-incubation period 4-25 weeks
-90% are considered acute
-10% chronic may progress to cirrhosis, liver failure or liver cancer
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HIV/AIDS
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-33 people worldwide living with HIV/AIDS
-14 million AIDS deaths since beginning of epidemic
-close to 1 million US AIDS cases
-caused by HIV-1 or HIV-2
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HIV structure
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-enveloped RNA
-2 copies of (+) RNA genome
-9 viral genes
-encodes viral proteins (gp41, gp120)
that mediate infection of target cells
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human cells possessing CD4
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-T4 helper lymphocytes
-monocytes
-macrophages
-dendritic cells
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HIV disease mechanism
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-results in progressive immune deterioration due to decreased number and function of CD4+ T lymphocytes (helper T-cells)
-initial infection of dendritic cells or other macrophages in epithelium
-moves to lymphoid regions where replication reaches critical levels
-macrophages are persistently infected creating a major reservoir and means of distribution
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more on HIV disease mechanism
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-CD8 T cells can kill infected cells but CD8 T cells require activation of CD4 T cells
-as CD4 decreases, CD8 decreases
-reduction of CD8 correlates to disease progression to AIDS
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Human papillomavirus
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-very common infection
-20 million people infected
-at least 50% of sexually active people acquire genital HPV at some pt in their lives
-by age 50, 80% of women will have acquired genital HPV infection
-6.2 million get a new genital HPV each year
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more on HPV
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-more than 100 different types
-some cause benign skin warts or papillomas
-common warts are spread environmentally or skin to skin contact
-seperate group of 30 HPVs are through sexual contact
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High Risk HPVs
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-about a dozen can cause cancers (most mostly cervical cancer)
-HPV induced cancers often have viral sequences integrated into the cellular DNA
-some of the HPV "early" genes (E6 and E7) are known to act as oncogenes that tumor growth and malignant transformation
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oncogene
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-modified gene or set of nucleotides that code for a protein that increases the malignancy of a tumor cell
-some usually involved in early stages of cancer increase chance that a normal cell develops into a tumor cell possibly resulting in cancer
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growing viruses (4)
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-growing virus in living animals
-growing virus in embryonic egg
-growing virus in cell culture
-growing bacteriophages
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growing viruses in living animals
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-used to be the only way
-not extensively used anymore except for growth of viruses that develop in an animal
-ex. Coxsackievirus A-painful blisters in mouth, thoat, hands, feet, conjunctivitis (eyelid swelling)
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growing virus in embryonic egg
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-viral growth is indicated by damage/death of embryo or lesions on egg membrane
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growing virus in cell culture
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-a tissue is treated with enzymes to separate the cells
-cells are suspended in culture medium
-normal cells or primary cells grow in a monolayer across glass or plastic container. Transformed or continuous cells do not grow in the monoculture
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growing bacteriophages (plaque method)
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-a sample of bacteriophage is mixed with host bacteria and melted agar
-mixture is poured into a petri plate containing a layer of agar growth medium
-each virus infects a bacterium, multiply, and release hundreds of new viruses that will infect other bacteria
-destruction of bacteria produces a clearing or a plaqueviro
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viroids
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-small circular single stranded molecules of infectious RNA lacking a protein coat
-cause of few plant diseases
-viroid RNA does not code for any protein
-usually transmitted by seed or pollen
-infected plants can show distorted growth
-ex. Potato spindle tuber disease-all tomatoes and potatoes are susceptible and there is no natural resistance
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Hepatitis D
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-only known disease to be caused by viroid
-delta agent is a viroid enclosed in a Hep B virus capsid
-there is extensive sequence complementarity between Hep D viroid RNA and human liver cell 7S RNA, a small cytoplasmic RNA
-causes liver death by sequestering 7S RNA of cleaving it
-can only enter human cell if enclosed in a capsid that contains a binding protein (it obtains this from Hep B virus)
-the delta agent that enters blood can be transmitted via blood or serum transfusions
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prions
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-small proteinaceous particles
-controversy if it contains nucelic acid (if so, it has very little, not enough to code for protein)
-infect and propagate by refolding into a structure which is able to convert normal protein into abnormally structured protein
-cause neurodegenerative disease by aggregating in CNS to form plaques called amyloids which disrupt normal tissue structure
-this disruption is characterized by holes with spongy architecture due to loss of neurons
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isoforms
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-the proteins that prions are made of
-found throughout body
-prion protein found in infectious material has a different structure and is resistant to proteases
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PrP^c
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-normal protein found on membrane of cells
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Prp^Sc
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-infectious isoform of Prp^c
-able to catalyze formation of other normal proteins into infectious ones by changing conformation
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Prp^Sc mechanism of infection
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-prp is produced by cells
-prpSc acquired or produced by altered gene
-prpSc reacts with prp on cell surface and converts it to prpSc
-new prpSc converts more prp
-prpSc is takin in cell by endocytosis
-prpSc accululates in endosomes
-prpSc continues to accumulate as it is transfered to lysozomes
-results in cell death
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Bovine spongiform encephalopathy (mad cow disease)
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-fatal neurodegenerative disease
-transmissions occurs when healthy animals come in contact with infected tissues
-was widespread in Europe in 1987 due to meat and bone meal and animal cadavers used as cattle feed
-can be transferred to human beings who eat or inhale material from infected carcasses (Creutzfeldt-Jakob
disease)(nvCJD or vCJD)
-first symptoms of CJD is rapidly progressive dementia, memory loss, personality changes, hallucinations,
speech impairment, jerky movements, balance and coordination dysfunction (ataxia), rigid posture, seizures
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Kuru
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-laughing sickness
-first noted in New Guinea in 1900s
-by 1950s anthropologists reported that kuru (trembling with fear) was rampant throughout South Fore
-due to ritual acts of mortuary cannibalism
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symptoms of kuru first stage
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-ambulant stage-unsteadiness of stance, voice, hands, eyes, deterioration of speech, tremor, shivering, loss of coordination in lower extremities that moves slightly upwards, slurring speech
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symptoms of kuru second stage
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-sedentary stage
-no longer walk without support, more severe tremors and ataxia, shock-like muscle jerks, outbursts of laughter, depression, mental slowing
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kuru symptoms 3rd stage
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-terminal stage
-inability too sit up without support, severe ataxia, tremor and slurring of speech, urinary and fecal incontinence, difficulty swallowing, deep ulcerations
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