theme 1: virus and prion

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what is a virus
a simple micro-organism
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are viruses capable of independent existence? if not, what do they need to survive?
not capable of independent existence. need host cell to replicate-> steal energy, metabolic intermediates and enzymes
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whats the structure of a virus
genome, capsid, envelope lipid bilayer, poss own enzymes too
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what type of human viruses exist?
dna and rna viruses
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what are the stages of virus life cycle?
1)adsorption (interacts with host cell receptors), 2) penetration (via endocytosis/membrane fusion), 3) uncoating (unsheath the nucleic acid), 4) synthesis (make that fatty nucleic acid/proteins), 5) assembly (put the virus together), 6) release(bud)
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what is virus classification based off?
structural differences
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what are the 2 ways of virus classification?
1)genetic material (dna v rna, ds v **, + v -) and 2) envelope?
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how is hep b/herpes ;) similar to parvovirus?
both DNA viruses
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how is hep b/herpes different to parvovirus
hep b/herpes is DS and enveloped (guarded and sm more) and parvovirus is the opposite (**,unenveloped)
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what does ENRHH stand for?
enterovirus, norovirus, rhinovirus, hep A, hep E (every n really hates ham)
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why are enterovirus, norovirus, rhinovirus, hep A, hep E (ENRHH) similar to hep C, rubella
all + rna viruses
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how is ENRHH different to hep C and rubella?
enterovirus, norovirus, rhinovirus, hep A, hep C= unenveloped (more of them, they trying to compensate), hep c/rubella=enveloped
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what does IMMRSV stand for?
influenza, mumps, measles, resp syncytial virus (I must move: rapid, speed, velocity)
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what are IMMRSV classed as?
- RNA, enveloped (-ve so need the guard)
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why does rotavirus seem to be on a rota?
as is both + and - gASP
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whats the only retrovirus we need to know? and its class
HIV- + RNA via DNA, enveloped
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main characteristic of herpes
ability to establish latency (there but no symptoms) and reactivate (cause symptoms again)
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how many types of herpes can infect humans?but how many do we need to know?
9 (extras are 6A,6B,7,8) and only learn 5
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what is herpes simplex virus 1 known as?
HSV-1 - cold sores
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what is a cold sore?
fluid filled vesicle probs on mouth
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how are HSV1 and HSV2 epidemiology similar?
both exist worldwide and humans are only known reservoir
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how are HSV1 and HSV2 different in epidemiology?
HSV1- 80% of UK have had/have it but only 10-20% got HSV2
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What is herpes simplex 2 known as?
HSV-2, genital herpes
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how are both HSV1 and HSV2 transmitted?
direct contact with vesicle fluid from lesions, latent in sensory nerve ganglia (HSV1-trigeminal, HSV2-sacral ganglia) with periodic reactivations
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what clinical syndrome is for HSV1 only?
encephalitis=brain inflammation - can be severe/fatal
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what clinical syndrome is for HSV2 only?
1)meningitis=can follow an outbreak of genital lesions, 2) neonatal herpes= vertical transmission from genital tract to baby, can spread through babys body (severe disseminated viraemia)-life threatening
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what clinical syndromes are for HSV1 and HSV2?
Vesicles/ulcers to skin/mucous membrane (HSV1=mouth)(HSV2=genitals/buttocks)
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why are chicken pox and shingles/herpes zoster both names for varicella zoster virus
primary (first) infection=chicken pox, but reactivation=herpes zoster/shingles
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how different is prevalence in UK to tropics for chicken pox?
in uk by 20 95% of people have had it, but in tropics it decreases to 50%
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how is the mode of transmission for chicken pox and shingles different/similar
-just chicken pox transmitted by resp droplets from infected person, -both transmitted by direct contact of vesicle fluid
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how is latency established for varicella zoster virus?
in dorsal root ganglion of whole CNS
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how many ways does varicella zoster virus present as a clinical syndrome?
2
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what are the two clinical syndromes varicella zoster virus present as?
1) chicken pox: febrile illness with widespread vesicular rash, 2) shingles/herpes zoster= reactivation causes unilateral vesicles in a dermatomal distribution
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what disease is epstein barr virus known to cause
glandular fever/infectious mononucleosis
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why is EBV the dodgy virus? ie: how is it transmitted
saliva/genital secretions-kissing disease
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what herpes virus infects 90-95% of the UK by 25, and 50% of infected before 5 years?
epstein barr virus
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what clinical syndrome for primary infection is shared by epstein barr virus and cytomegalovirus? what % is caused by EBV
infectious mononucleosis, 80-90% by EBV
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how does infectious mononucleosis present? part of this includes the reason why it is called 'mononucleosis'
-tonsilitis, fever, lymphadenopathy (affects lymph nodes), hepatosplenomegaly.-get atypical lymphocytes on the blood film that looks like monocytes
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how does the latency for epstein barr virus to cytomegalovirus
ebv= in b cells, cytomegalovirus=in myeloid progenitors/monocytes/dendritic cells
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when can EBV be reactivated and what is it associated with?
when unwell/immunosuppressed, associated with malignant b cell lymphoproliferative disorder
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whats wild about the prevalence of CMV?
% prevalence= ~ age
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what two ways can CMV be transmitted?
-saliva/genital secretions, - donated blood, stem cells, solid organs
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apart from infectious mononucleosis how else does CMV present as a syndrome?
congenital CMV infection (when mum is infected in preg and passes it to infant)
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how do the symptoms for congenital CMV infection of the neonate differ to the symptoms of reactivation of latent cmv in immunosuppressed patients?
congenital- retinitis, deafness, microcephaly, hepatosplenomegaly. -reactivation= retinitis, colitis, pneumonitis
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who can get rhinovirus?
anyone worldwide, epidemics in autumn,winter,spring
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how is rhinovirus, influenza, respiratory syncytial virus transmitted?
aerosolisation of respiratory secretions (rhino-also droplets from eyes/nose)
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how does rhinovirus present as a clinical syndrome?
common cold- sneezing, coughing, sore throat, headache, fever, nasal obstruction & discharge
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which respiratory virus can spread between species-animals and humans? and when does it peak?
influenza with peak in winter annually
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how many types of influenza exist and which one mutates regularly leading to yearly variation in strains?
A,B,C- A mutates regularly
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how are the influenza viruses named?
according to the variant of the surface proteins: H and N, e.g. H1N1-swine, H3N2-seasonal
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how does primary influenza illness differ to post-influenza?
primary= initially fever & myalgia (muscle aches) THEN headache, cough, sore throat, nasal discharge, post= secondary bacterial lung infection (common in elderly)- by s.pneumoniae, H.influenzae, s. aureus
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even though respiratory syncytial virus is distributed worldwide, what group of people does it affect the most?
young children
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how does RSV present as a clinical syndrome?
bronchiolitis= inflammation of the smallest airways (bronchioles) leads to cough, wheeze, hypoxia and apnoea, affects under 2 year olds
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where are 70% of the 36.9 million people living globally with HIV found?
sub-saharan africa
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what 3 ways can HIV be transmitted and how?
-vertically via breast milk, needlestick via blood, sexually via genital secretions
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what part of the immune system does HIV affect?
cd4 cells (helper t lymphocytes)-part of cell-mediated immune system
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what/when does the initial stage of HIV infection look like?
2-6 weeks after transmission can get acute seroconversion illness (when start making antibodies)- flu like symptoms
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how is the chronic infection stage different to the AIDS infection stage of HIV?
chronic= asymptomatic, steady state between virus and immune system (cd4 cells regenerate as hiv destroys them) last 5-15 years, AIDS= rise in viral load and fall in cd4 count
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how does AIDS kill a patient?
vulnerable to opportunistic infections (AIDS defining illnesses)= pneumocystis pneumonia, cryptococcal meningitis, Kaposi's sarcoma
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5 viruses are hepatotropic and can induce hepatitis. what do these terms mean?
hepatotropic= has an effect on the liver. hepatitis= liver inflammation
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how are hep A and E similar in terms of transmission?
-both faeco-oral spread as virus is shed into faeces
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how do both hep A and E present as a clinical syndrome?
-both present with: nausea, myalgia, fevers, jaundice (as bilirubin isnt being excreted by damaged liver), right upper quadrant pain (both self limiting-resolve without treatment)
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where is hep A and E endemic and why?
in developing world as associated with contaminated water
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in europe what % of adults have the antibody for hep A and what does this show?
10-50%, shows previous exposure (A for antibody, hep A)
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in west europe/north america what animal are cases of hep E associated with?
pig/undercooked pork (pigE)
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how do the symptomatic populations for hep A and E differ?
hep A= kids- asymptomatic, adults-50% asymptomatic, hep E= 95% asymptomatic
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what groups is hep A associated with?
lower socio-economic groups, returning tourists, MSM
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why is hep E in pregnant women big yikes?
25% get fulminant hepatitis (liver failure) with high mortality
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are more people infected chronically by hep b than infected by hep c?
yes, 248 million worldwide chronically infected by hep b (people DIE), 170 million infected worldwide by hep c
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is vertical and sexual transmission more common in hep b than hep c, and what other ways can they both be transmitted?
blood borne viruses-yes (hep b+ parenteral (not via digestive tract)), (hep c+major=sharing needles, needlestick injuries, transfusion of contaminated products)- C for Sharp
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what can happen first after transmission of both hep b and c? and is this symptomatic?
acute clinical hepatitis - (25% of hep c) (hep b=90% kids, 50% adults= asymptomatic)
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after acute clinical hepatitis, what two things could either happen in both hep b and c?
clears (15% for hep c) OR becomes chronic (hep b=risk of this is inversely proportional to age, perinatal more likely to become chronic than adult)(hep c=85%)
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how does chronic hep b and c progress?
cirrhosis--> hepatocellular carcinoma (HCC)
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Though prevalence of hep c is low in developed countries (0.5-2%) what group is 50% prevalent with hep c
people who inject drugs (PWID)
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why is norovirus and rotavirus named as they are?
noro-from norwalk (first outbreak), rota- looks like a wheel
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is norovirus common and if you have it are you safe from getting it again? where is it most common to get it?
90% of adults have had it but immunity is short lived, point source outbreaks- confined areas and a single person has it- speedy spread
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what group is rotavirus most common in and when? why is it so scary for developing countries?
80-100% of it affects kids (1-3 years) especially in winter, big cause of infant mortality in developing countries
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how are both norovirus and rotavirus transmitted and what extra way is rotavirus transmitted
ingest/inhale aerolisation of vomit particles, rota= also faeco-oral route so contaminated h2o/fud/ aerolised poop too
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major syndrome of norovirus
vomiting
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major syndrome of rotavirus
fever, vomiting, watery diarrhoea
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what is polio, echoviruses, coxsachie A and B all apart of?
enteroviruses group
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when and who does enteroviruses mainly affect? and is it asymptomatic?
peaks in summer/autumn in UK tho worldwide distribution, 75% cases are under 15 yr, 90% asymptomatic or have mild febrile illness
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how do enteroviruses enter the body and where do they spread?
enteric route (faeco-oral/contaminated fud/h2o) and go from gut to lymph nodes to blood
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where does enteroviruses replicate but not cause symptoms/
the GI
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what three ways can enterovirus present as clinical syndromes?
1) fever-rash syndrome in kids (hand/feet/mouth), 2) meningitis (most of viral meningitis cases are coz of enterovirus), 3)severe disseminated disease in neonates
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how is mumps, measles, rubella and parvovirus spread?
respiratory droplets
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what group is mumps an endemic in worldwide?
children
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what two childhood diseases (occur in adults too tho) are highly infectious
mumps and measles (after 2 hours-environment is still infectious)
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how does mumps present?
POM: -acute parotitis (parotid gland inflammation uni/bilateral), -orchitis (testicular inflammation, 4-5 days after parotitis), -meningitis (in 15% of mump cases, before mmr was bigger cause)
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what can meningitis caused by mumps lead to?
meningoencephalitis and sensorineural deafness
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how does the prevalence of measles and rubella in UK differ?
used to be common with 2-3 yearly epidemics for measles and 6-8 yearly epidemics for rubella, now occurs in clusters of unvaccinated but rare (rare for both)
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what are the symptoms (3 c's) of primary measles and what follows?
fever, coryza (stuffy nose), cough, conjucitivitis, Kopliks spots on inside of cheek, then maculopapular rash (flat red area with raised bumps)
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what can happen 7-10 days after acute measles infection?
acute post infectious measles encephalitis: immune mediated, high mortality rate, more common in under 1's (1:1000)
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what can happen 7-10 years after measles infection?
subacute sclerosing pan-encephalitis SSPE: progressive, degenerative and fatal disease of the CNS (1:1000000)
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what two ways does rubella present as clinical syndromes?
1) primary rubella, 2) congenital rubella
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how does primary rubella present? what two symptoms occur in 30% of adults?
-mild illness, fever and maculopapular rash -arthalgia/arthritis
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what is the triad of congenital rubella?
-bilateral cataracts (lens clouding), sensorineural deafness (lesion near auditory nerve/inner ear), microcephaly, risk of it is highest in first 12 weeks of pregnancy
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what is parvovirus b19 known as?
slapped cheek syndrome, fifth disease
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when does parvovirus peak and what % of 15/90 year olds have it?
spring, 50% of 15 year olds, 90% of 90 year olds
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what is the characteristic clinical syndrome of parvovirus b19 (where its other name comes from)?
erythema infectiosum= fiery red rash to cheeks, lacy body rash, fever, coryza
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parvovirus can also cause transient aplastic crisis. why?
parvo kills erythrocyte progenitor cells-> transient anaemia leads to crisis as not enough Hb, affects those with high erythrocyte turnover e.g. sickle cell
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what effect is infection of parvovirus in pregnancy especially in first 20 weeks going to have?
7-10% foetal loss, 2-3% of foetuses develop hydrops fetalis as severe fatal anaemia-> heart failure--> oedma, ascites (abdo fluid swelling)
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what is a prion, does it have protein, does it have nucleic acid?
small infectious particle contains protein but no nucleic acid
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how can prion proteins become abnormal? 4 steps
1)gene mutation causes changes in protein folding pattern, 2) becomes resistant to protease enzyme, 3) they accumulate abnormally in cell, 4) promotes other proteins to abnormally fold
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how can you get abnormal prions? 2 ways
1)inherited (gen defects) 2) transmitted to you via consumption/direct exposure
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what 4 properties do human prion diseases share?
1) manifest in the CNS, 2) make spongiform changes in brain tissue, 3) have long incubation times, 4) progressive and fatal
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what is the older form and newer form of creutzfeld-jakob disease (CJD)?
old-sporadic (gene mutation, very rare), newer=new variant CJD
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what did sporadic CJD lead to?
progressive ataxia (lose control of body movements), depression, dementia then death
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why is nvCJD linked to BSE (bovine spongiform encephalopathy)?
-same structure prion therefore associated with eating infected beef
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Card 2

Front

are viruses capable of independent existence? if not, what do they need to survive?

Back

not capable of independent existence. need host cell to replicate-> steal energy, metabolic intermediates and enzymes

Card 3

Front

whats the structure of a virus

Back

Preview of the front of card 3

Card 4

Front

what type of human viruses exist?

Back

Preview of the front of card 4

Card 5

Front

what are the stages of virus life cycle?

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Preview of the front of card 5
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