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RUTGERS / OTHER / OTH 132 / section 7 mutations study guide a

section 7 mutations study guide a

section 7 mutations study guide a

Description

School: Rutgers University
Department: OTHER
Course: Microbiology for the Health Sciences
Professor: Skelly
Term: Spring 2017
Tags: Bacteria, bacteriophage, Viruses, Transformation, transduction, replication, transcription, mutagens, and mutations
Cost: 50
Name: Microbiology for the Health Sciences Study Guide
Description: These notes cover the processes of transcription, replication, and translation. They also talk about transduction, transformation, and specialized transduction. Various types of viruses will also be discussed. Mutations and the different types of mutations that have varying impacts on an organism.
Uploaded: 03/02/2017
55 Pages 256 Views 0 Unlocks
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What happens when we want ot make a copy of RNA?




What does the DNA double helix look like?




-what do we have in our mouth?



February 13, 2017 Chapter 7: Genetics Definition of a Gene -the basic unit of heredity; a linear sequence of nucleotides of DNA that form a  functional unit of a chromosome or a plasmid -Genes with different information at the  -can be a structural RNA, so not all genes are coding for a particular protein, a lot of  times they code for structWe also discuss several other topics like How many skeletal muscles do we have?
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ural components -usually we’re talking about a diploid eukaryotic organism -and along the chromosome there are areas for different genes -genes can have alleles, two alleles, one is coming from each parent -the location can be referred to as loci or location -because prokaryotes only have single copy of a chromosome, they generally have  only one version or allele of each gene -sometimes they have 2 copies of a particular gene, but bacteria don’t have 2  copies of an allele of a gene -diploid for just those two genes -it’s essential that that copy gets passed down to the progeny Fig 7-2a Bacterial DNA is referred to as chromosomes -very often the chromosome of bacterial cells are circular but can be linear -can be two copies of a circular genome and on one circle there is certain genetic  info, genetic info is split between the two chromosomes, some organisms have a  circular chromosome and have a linear chromosome (depends on organism) -rembember you only see one copy of each gene -looks like a clock going from 0 min to 180 min -if you have econjugation pilus it would take a full 100 min for DNA to transfer to other organism -after 20 min, it would take certain amount of DNA to go through -out in the envt, environmental motions pull them apart, never really have  100 mins to make the entire transfer of DNA -for a lot of the bacterial organisms, scientists have isolated the  chromosomes of organisms, and have sequenced all the genome (know every base,  can make predictions as to what the genetic info is)-what do we have in our mouth? Sometimes scientists can’t grow up the  culture. They have to isolate the DNA from tract or mouth and sequence the DNA  and put it through algorithms and sort of place them in a family -this is supercoiled in the bacterial cell and a lot of times it’s so densely  packed= nucleoid -if you were to spread out the DNA, the DNA takes up a lot more room than  one cell -has to be tightly wound -when you have to DNA replication, enzymes help unwinds and replicate the  DNA What does the DNA double helix look like? Fig. 7-1 -ribose sugar – 5 carbons -has a phosphate hanging off -other end ahs a nucleotide base (A, C, T, or G) -this double helix has a base pairing with the other strand  -G-C (3 h bonds) -T-A (2 h bonds) -hydrogen bonds hold bases together  -the two strasnd are bought together as nucleotide bases = Watson and crick  -to get double helix, they realized that the strands go into two different directions  (antiparallel) -the 5th prime refers to the 5th carbon in this ribose group that holds the phosphate -the 3 prime carbon holds the hydroxyl group -so when dna polymerase adds nucleotides = add going into 5 to 3 prime direction -the 5th carbon phosphate is always being add to the 3rd carbon hydroxyl group -the carbon 2 is missing a hydroxyl group -in RNA it has it -DNA polymersase will add the 5th carbon phosphate group to the 3 carbon hydroxyl  group -needs to work in that direction when it copies either strand -the strands are referred to as antiparallel-allows DNA to be formed -the colors are trying to help figure how dna polymerase works -this double helix isn’t strung out in cytoplasm, it’s supercoiled and bound to itself -when I want to copy this DNA, I will always do it in a semiconservative way -going to open up this double helix, enzyme called helicase that breaks bonds between the bases and allows RNA or DNA polymerase to break through the  nucleotide sequence -whetehr I’m going to cpy the DNA or open the DNA to make RNA I know I have to  unwind and break these basese and have either DNA polymerase or RNA  polymerase to copy these strands Fig. 7-3 -can use dna as a template to make RNA = transcription -once I have copies of RNA = mRNA uses ribosomes to make protein = translation There are some viruses that have RNA as their genetic information, not all viruses  have DNA as their genetic info -RNA => DNA (reverse transcriptase) -HIV (rna virus when it enters body, converted to DNA, gets integrated into  chromosomes = impossible to be cured) Fig. 7-4b -scientists learn a lot using bacteria, because they defined the enzymes and how  DNA replicates DNA Replication -2 strands broken and unwind, helicase opens up double strand, immediately a copy is made from each strand = end up with two copies of DNA (there is an original  strand and copied strand= semiconservative) -always one strand from the original and one copy  Fig. 7-4a When dna gets copied, there is a particular sequence that allows DNA polymerase  to recognize start of replication -both strands need to be replicated simultaneously because as soon as you copy  there is another enzyme making that supercoiled links wind up the DNA again -as fast you open DNa there is a DNA that winds it up again -the polymerase can only add the 5th carbon phosphate to the 3 carbon hydroxyl =  works in 5 to 3 direction-adding the 5th carbon phosphate group to the 3 carbon hydroxyl -when I want to copy my 3 prime I can start copying immediately -yelolow is moving from 5 to 3 direciton = leading strand -it will maintain antiparallel nature and make a copy of semiconservative strand -DNA polymerase only added in the 5 to 3 direction How do you copy the purple strand -have to open DNA enough and read backwards -lagging strand, waiting for replication fork to open up Okazaki put dna in a test tube -showed that DNA could be replicated, when he analyzed the products, saw a  long strand being copied and little fragments being made = as replication fork is  opening, thi strand going into 5 to 3 direction is being copied in the 5 to 3 direction,  little sections of dna are being copied and eventually a ligase goes in and copies so  that you have one long strand -lagging strand = have to open up the DNA helix to let the DNA polymerase  to make copies What happens when we want ot make a copy of RNA? Fig. 7-5 Just like with DNA, you have to open up the double helix =opening either one of those strands -as you open up the strand, you have RNA polymerase that recognizes a specific  sequence and recognize that that is the start of the transcript -it starts copying one of the stradns in the double helix Couple differences between rna and dnd -sugar is different (one is deoxyribose and the other is ribose) -there is a nucleotide base change -we don’t have a parigin iwht T, we have A pairing with U- -the RNA polymerase adds in a 5 to 3 direction too, expending a lot of ATP to  make these covalent bonds and eventually get a new strand of RNA = going to be  used for different purposes -some is structural, some carry mRNA to make protein -cells expend a lot of energy in making DNA, make proteins and transcripts when  they need toWhen talking about bacteria, dna replication and transcription happen in cytoplasm -in euk, where is DNA replication and transcription occurring?  -in the nucleus -all of your transcription for euk cell takes place in nucleus -dNA polymerase and RNA polymerase work silmiar whetehr it is euk and prok -but different when taking antibiotics that are inhibitors of replication of  bacteria, in RNA replication so that we don’t inhibit our own DNA or RNA synthesis -antibiotics are grouped according to what they are in a bacterial cell -don’t bother our cells because our DNA is different than a bacterial cell Fig. 7-6 Eukaryotic cells have a unique feature that bacteria don’t -transctip is created as coding regions as an exon -then the exon a lot of times is broken up by an intron -have another exon that makes up the mRNA -in eukaryotic cells, have mRNA that is the exon that codes for the aprticular  protein sequence -introns get spliced out (in nucleus) -ultimately cell decides what particular exons gets put together = become  mature RNA that get secreted into the cytoplasm from nucleus -why are there intervening sequences? Not coding for proteins, they are regulatory  sequences -why they want to replicate in this way, can mix and match exons from differenet  transcripts = create a diversity of mRNA = create of diversity of protein in a euk cell with a minimum amount of DNA -there wouldn’t be enough room to hold DNA = mix and match exons from  different DNAs to create diversity with minimal amount of DNA = UNIQUE TO  EUKARYOTES -critical that we can splice together exons from RNA to make proteins Fig. 7-10 We ultimately wind up with 3 important types of RNA -wind up with mRNA = it’s holding the message that ultimately that gets  translated into proteins -holding code that will establish what amino acid gets placed on the  mRNA to make that protein-rRNA= structural RNAs, ribosomes are sites whre protein synthesis takes  place, ribosome comes together to make that 70s ribosome and is where protein  synthesis takes place, and ribosomes move along and that code is read to mke that  protein (not translated into protein ) -structural RNA not a message = transfer RNA = it’s transferring something  to the ribosome , transferring the amino acids that the mRNA is asking for at that  particular position -at transcription, we have tRNA and rRNA, and many different kinds of mRNA  -when mRNA is being copied off of DNA, since this is taking place in cytoplasm,  ribosomes can jump onto the mRNA before the mRNA is being finished and copied Fig. 7-11 -looks like strings hanging off, strings of mRNA -before mRNA is completely made, ribosome jumps on  -unique to bacteria becaue it is still inside the nucleus = polyribosomes that  jump onto mRNA = string of pearls and know direction of mRNA because  polyribosome get longer and longer and falls off DNA -RNA hasn’t ended and ribosomes jump on to start translation -because euk it happens in cytoplasm Fig. 7-7 -recognizes start of mRNa because there is a unique sequence where translation  should start -small and large subunit -has to start transaltion at start of protein -30s and 50s come togheter to make 70s and goes onto mRNA -ultimately, the ribosome moves along mRNA every 3 nucleotides, those 3  nucleotides are called a codon and those 3 nucleotides are asking for a specific  amino acid a tRNA is dropping off an amino acid -the growoing polypeptide chain grows through a large tunnel in the subunit -gets to stop codons because they don’t ask for any amino acid, ribosome  know that that’s the end of translation, ribosome can then start translation for  another RNA Fig. 7-8 -3 nucleotides represent an amino acid -universal table because euk and prok use the SAME LANGUAGE whether you are a  bacterial or eukaryotic cell-that universality is why we can express human genes in bacteria (HGH, or insulin)  can recognize the codons in those genes and express them -AUG codes for Methionine = has 1 codon -start codon for EVERY PROTEIN -the ribosome not only sees the sequence they also see the AUG -three stop codons: UAA, UAG, UGA, ribosome stops translation and peptide falls  away from ribosome How does the amino acid get involved when codon is in mRNA/ -the codon is recognized by an anticodon (3 nucleotide sequence) that is in  the transfer RNA Fig. 7-9a Structural tRNA -it’s delivering the particular amino acid that is being asked for because the  anticodon is base pairing with the codon in the mRNA -for every codon there is a tRNA that can bring in that particular amino acid Fig. 7-9b what a tRNA looks like Table 7-1 Properties of the different kinds of RNA Transfer RNA has to drop the amino acids to the ribosome Fig. 7-12 part 1 -recognize 5 prime end of RNA -ribosome is made up of RNA dn ribosomal proteins -the ribosme attaches at start -have AUG codon = start codon -p site = first nucleotide that will come in A site= second amino acid will come in here -ribosome is reading every 3 nucleotides i Fig. 7-12 part 2 -tRNA comes in and methionine is ready to maek first peptide bond with next amino  acid dictated by certain codon Fig. 7-12 part 3 -base pairing, making peptide bond between methionine and aspartic acid -there are enzymes part of ribosomes allowing pepted bond to be formed Fig. 7-12 part 4Fig. 7-12 part 5 -growing polypeptide chain moved = new amino acid asking for isoleucine -this proceeds until finally you get to the mRNA Fig. 7-12 part 6 -this is all translation Translation in our body works in similar way, Many antibiotics we use actually inhibit translation -streptomyocin causes a lot of error -dna polymerase and rna polymerase have high fidelity, when make error,  they stop and correct it, these enzymes don’t want to make errors, can cause  mutations in DNA = cancer, the dna and rna polymerase try to correct and will stop  replication -same thing with translation: high fidelity, the correct amino acid is put in the right  place -anitibotic interferes with this (streptomyosin) -inhibit peptide bond formation -some inhibit progression of ribosome -when you look at targets of antibioics = protein synthesis -our system is different enough (ribosomes 80s), when taking antibiotics, don’t  inhibit protein synthesis in our cells Ending with protein synthesisFebruary 15, 2017  2nd Half of Chapter 7 Last Monday, DNA replication, transcription and translation An organisms spends a lot of their ATP to transcribe their mRNA  -organisms do not like to waste energy making things that they don’t need to make -they have regulatory mechanisms when they need to make a particular protein,  don’t waste energy And so orggniaims have ways of sensing what they need and regulating so that they don’t waste valuable ATP Fig. 7-13 FEEDBACK INHIBITION -end product of a pathway is coming back to inhibit the first step in a pathway -in this case, a 5 step pathway to make an amino acid threonine -has an enzyme at each one of these steps -when there are loads of threonine there’s no point in making anymore, the amino  acid can come back and bind at the allosteric site -when threonine is at a low level, the amino acid can’t bind to enzyme 1 anymore -good way to preserve wasting a lot of energy in the enzymtic pathways -reversible, when threonine falls off, can go through pathway again -one aspec of regulating what’s needed -the threonine is regulating the enzyme 1 and the pathway -makes sense that enzyme 1 should be sotpped, right at the beginning, very  reversible allosteric inhibitor -one mechanisms organisms have -another mechanisms in enzyme Induction (catabolic reactions) -the susbrstae is available, you wil turn on the genetic info the enzymes need to break down a particular substrate -organisms in a cell usually cluster their genes that work in a particular  pathway -so that you can control the genetic info = operon -the bacterial cells will cluste those genes, controlled upstream, since all of  these genes work together in this operon  Ex: the lactose operon, is the operon that makes the beta galactocitase,  makes a permease that helps bring lactose into a cell -there’s another gene that helps break down the lactose-the genes are grouped together in an operon, region of DNA called the  promoter, the promoter (particular sequence that allows RNA polymerase to bind to  promoter site to start transcription) -we also see a region called the operator, another ac=rea that regulates this  operon, if it’s bound by a repressor protein, the promoter cannot read through and  make the transcripts for these three genes, so when you have repressor protein  bound to operator = turned off operon -why waste time and energy to make proteins to make lactose when sugar  isn’t available through the cells?  -the repressor protein is expressed usually on another part of the DNA doesn’  thave to sit enxt to operon, expressed on another part of DNA of organis -always there in the cell, when ean enzyme is always present  (constiative enzyme, always present, always made, always expressed) -better have enough repressor to make sure operon stays off  -an organism given a choice of a particular carbohydrate = glucose is  preferred ATP provider, organisms are already three, the enzymes are constitatively  expressed ot break down glucose What happens when we use up glucose? Will then express proteins made  from the transcript -when lactose is present, the sugar physically sits on the repressor,  repressor can no longer bind to the operator -good way to run on this promoter by having lactose present -I don’t want the operator not bound when lactose isn’t present, a godo way to sequester it is let lactose bind to it so that repressor can’t sit down -example of ENZYME INDUCITON -getting operon to turn on when lactose  -usually pathways involving catabolic reactions -usually the operator is regulated through an induction, through  presence of lactose for operator to be induced and turned on Enzyme repression: look at lactose, see how a repressor protein can work to Ex: of tryptophan synthesis -an organism that can make amino acid has an operon and number of genes  that are supporting genes in pathway -work similar to opern -RNA promoter upstream, an operator (sequence that can be bound by a  repressor protein)-anabolic pathway -number of enzymes will reduce tryptophan -too much tryptophan, no point in orgnaims making anymore, tryptophan will  bind to the repressorfor the tryp operon, when it’s boudn to repressor, repressor can now bind to the operator -a lot fo tryptophan, want the operator to be attached and shut off all of the  genes down stream -start urnnign of tryptophan, not enough of it to bind to repressor, can’t bind  to operator, now RNA polymerase sit on promoter and read through enzyems  eneded for production of trpyophan -the product rpohtn is needed ot activte the repressor protein when it is in  short supply, operator falls off -example whre tryphoha is repressing, and lactose is inducing -looking at anabolic reacitons where you have to make something -end product goes back and turns off repressor -all of these pathways are going on, not doing just one or the other -minimizing breaking down ATP -looking at the lac operon, glucose is the consitiave enzyme, glucose will always be  used up first, then lactose Fig. 7-15 There’s a lag = glucose is used up but you don’t immediately continue growin -plateau= is caused by needing time to get mrNa translated to make  eznymes availbael to break down lactose = catabolite repression  =when a cell has a choice of the 2 sugrars = even though lactose is present,  operon won’t be turned on until all of glucose is used up, then the operator can be  turned on -lactose will sequester that repressor -lactose has to be used up complertely and then you make the enzymes  using the lactose -catablite repression (won’t turn on that lac operon) Talked how mRNa can make protein Now start talking about how we can understand pathway by making mutations of  these steps along the way = how you can start defining pathways When talking about DNA-as being a genotype j-the genotype is basically the DNA the info to make those proteins -the DNA ultimately gets translated into a phenotype (characterisics) What are the characteristics you are expressing of the cell? -by changing the DNa, making a mutation, that’ shwere you see the change and  seed if that change leads to a change in the phenotype To undrstnad any amino acid pathway, people study mutations in the pathway to  discover what enzymes are needed? Do you think a change in the genotype will always cause a change in the  phenotype? No -not all mutations lead to a phenotype change What could happen to cause changes in the phenotype? What are the enzymes replicating DNA need to be doing? When an enzyme copes DNA what does the enzyme need to be doing to present  this form happening -has to have a very high fidelity -DNA polymerase has to recognize error and stop and correct it -there are always errors, even with the hgihes fidelity = spontaneous  mutations -some genes are more prone to mutations -another gene might require 6 million divisions befreo you find a mutation -can study mutations by looking at sponsaous mutations = slow procedure  What can we do to induce mutations? Especially if the target is the DNA? -UV light, give them chemicals and ingesting chemicals like carcinogens to  induce mutations especially if they want to study a particular protein to be aberrant Fig. 7-16 can have point mutations -just one nucleotide, error in DNA, spontatnoeu mutation, when this is  transcribed get UUA, get a new amino acid, from phenylalanine to Leucine -deping on where the substitution is, may inactivate the protein, the  substituation wasn’t at the active site of the enzme -what is a critical enzyme? What is at the active site? -even though you change genotype, may not see phenotypec) have a G and mRNA as UUC, there’s more than one codon for a particular maino  acid -this is relally a silent mutation, new base but it deosnt matter stiil going to  insert phenylalanine at that postion Then we have other mutations that are much more severe Fig. 7-17 -either inserting a base or taking away a base (frame shift mutatioins) -a base pair is either inserted or deleted = reading frame is completely off  kiltered -if G leaves, I have a whole new reading frame, by chance an AAA codes for  phenylalanine, going to be detrimental -if you insert a base, a C, reading as phenylalanine -these frame shift mutations are rather serious unless it happened it at the  very end of the transcript -when you have a point mutation, what kind of a point mutationt or nucleotide could be inserted that would cause a protein to be truncated so that you’d never make  the full length protein if this nucleotide was inserted = stop codon -would be observed would cause protein to be truncated sooner than it  should have been = change the characterisitcc of the protein Table 7-3 types of mutations and their effects on Organisms -Table 7-4 sometiems add chemicals to induce organisms -can incorporate base analogs -that base is altered but can get incorporated into DNA -whent aht alterd base Is replicated, the wrong partnered is added to that  copied strand -can do things directly to the bases like an amine group -can add methyl groups to the base -all these alterations of bases lead to incorrect pairing -all of these are inducing point mutations, used for their scientific work -acridine orange that intercalates into double strand, DNA polymerase is  either adding a base pair or changing a base pair Ex: of base analog is 5-Bromouracil Fig. 7-18 -fi this gets into DNA, will not base pair properly -having this ability to do amage, potetnital drugs used in cancer  therapy, cells that are growing at a rapid rate will incorporate the Fig. 7-19Feb 22, 2017 Transformation: when an organism can take up naked DNA Transduction: the bacteriophage (specific for each general of bacteira) infects the  bacterial cell and brings chromosomal dna from the previous host Conjugation: cell to cell contact, dna is passed from one cell to the next -must involve a conjugation pilus Fig. 8-6 Lederberg’s experiment: discovery of Conjugation -worked with two different bacterial strains -there were individual strains, each one were auxotrophic for a particular  gene -a,b,c,d,e, represent genetic info (positive means wild type) -this strain can make d,e,f for wild but was deficiecnte in a,b, and c -but in other strain, d,e,f couldn’t make the whild type but a,b,c, couldn’t -mixed the strains, and plate them onto growth medium that did not supply  a,b,c,d,e,or f -as expected when trying to plate cells from other tube, was missing the  three factors -when mixed the two cells together, when plated out, there were colonies  there,  -only way it occurred was cells were able to make all 6 factors -dna went form one cell to the other -the cell produced could now express all 6 nutrients Conjugation -two living cells have to be brought together -differs between 2 mechanisms 1. have to have a cell that will be donor and recipient cell that is receiving the genetic info =always have a donor and reciepient cell 2. can transfer much larger quantities of DNA than through transformation or  transduction -as long as they are together through the conj bridge, may be able to  transfer an entire chromosomeEx: would take 100 min to allow chromosome to leave the atone cell  cell and enter the other cell Fig. 8-7 -that donor cell is actually the cell that makes the conjugation pilus -the F stands for fertility, the cell that makes that pilus can recognize a cell,  something on the cell, an outside receptor and knows it can mate with that  particular cell -the receptor is the one that can accept the dna -th pilus recognized something no the outside of that cell being able to mate  with that cell Fig. 8-11b -pasmid: extracellular piece of dna, usually transferred with the chromosomal dna during binrary fission -replicated just like any other piece of DNA -can be lost -gives extra pieces of info to a cell, they are non essential genes -the plasmid DNA can add useful genes to a cell -usually a cell that has this has a selective advantage that it can have  another property -the genetic info to allow this to occur is coming rom a plasmid (f  plasmid for a feritiliy= info for making conj birdgge and making the transfer that the donor cell has) The Transfer fo F plasmids -they are ircular, double-stranded, can be different sizes -always refer to the F positive cell as making the conj. Pilus -the F- does not have the fertility plasmid -this F pilus: creating that bridge to allow for the transfer to go from the F+ to the F- =an F- to an F- nothing would happen - An F+ to an F+ would not happen, no reason to be mating - Always have that F+ supplying the conj pilus and always looking for the F pilus Fig. 8-8 -Follow the colors when looking through the chapter-the f plasmid contains the info to make the pilus and all the necessary protines to  allow for transfer to recipient -starts initiating at an intitiatino sequence into the recipient -not known whether the dna travels down the bridge or the conj. Pilus pull the pilus  together -conj. Bridge is allowing for that DNA transfer -at inititiation seuqnce, first part of DNa goes in -only single strand of plasmid enters reciepient Why couldn’the whole plasmid transferred over to the recipient cell? -have to have a single strand, automatically starts getting copid -the F+ then would be F- -you convert your F- cells to F+ -the original F+ copies its single stranded plasmid -end up having both cells that are F+ -only the single stranded plasmid enters host because you don’t want to lose  the plasmid = lose ability to conjugate -realized that conj, bacterial cells sometimes had a very high freq, of  recombination -when they had the f plasmid in their cell, it seemed like the dna on the chromosome fereq recominbe with the recipient (HFr cell) HFr-cell: had the F plasmid inside the host chromosome, these cell had  a high freq ofrecombination with the recipient dNA Realized that the f plasmid incorporate insete into the cell chromosome Hfr -the f plasmid can now integrate into the host chromosome -the Hfr strain would look for the f- cell and the Hfr strain can make the conjugation  pilus and can start transferring material into F- cell and the intiiateing segment,  except this tiem, when the f plasmid starts entering the recipeitn cell, it’s dragegin  begind it chromosomal dna -the plasmid is starting to transfer and is taking some chromosomsal dna  from the Hfr strain and that’s what’s entering into the new recipient cell -difference, plasmid is inside host chormosme, this time it’s pulling some of  the chromosomal dna from the Hfr strain Fig. 8-9 High frequency reocombinations-once integrate into host chromosome = hfr strain making conj pilu and  looking for f minus cell -plasmed starts entering recipient, first part is initiating sequence and pick up red plasmid dna, start pulling the purple dna into the f- cell -the plasmid is pulling in some of the Hfr’s dna and as the purple dna enters  there is a recombination event = F- strain ahs purple a and b, and c,d,e, and g are  all green -only a small portion of pplasmid came in (would have to sit for 100 min to  bring in the whole plasmid, chances of it happening are small) -in this case, mating only went for about 20 minutes -if I did bring in the whole plasmid would become hfr strain, small chance of  happening -recombinant is because genetic info of a and b now entered this reciepinet = recombinant -recombined with green a and b and became purple a and b -the F- did get new genetic info, jus tnot converted to an Hfr-strain because I  didn’t pull in the complete plasmid -another form of a conjugation event, that allows recipient cell to pick up new information  There wwas aanother novel conjugation event, when this plasmid popped out of the strain and accidnetlay when it popped out, when plasmid pops out, sometimes it  pulls some adjacent dna with -random evet, sometimes makes mistake and grabs a little bit of the Dna that was adjacent to it -refers to as an F’ plasmid -the fertility plasmid, but it also contains some host chromosome -can bring in genetic info besides jus thte info to bring in the f plasmid -we have an F’ cell mating with the F The transfer of F’ Plasmids -F’ plasmid has more info than just to transfer itself, has chromosomal DNA from the host that it’s sitting in -looking for F- cell, making conjugation bridge, and transfer DNA Fig. 8-10 The formation and transfer of F’ plasmids -f’ cell is perfectly happy as long as that plasmid stays in the cell (has  essential genes on it)-enters F- as a single strand -recipient cell has a plasmid, it’s more or less an F’ cell except I have 2  copies of A and B -this is the one exmaples, where you might have a cell with 2 coopies  of a particular gene (it’s not a whole chromosome0 -if this green chromosome had A and B that were mutant, the a and b  could compensate for the mutation -how they can aquire new characterisitcs -bacterial cell that are in close genera can conjugate Plasmids -we really just talk about the F plasmids -the fertility plasmids have a lot more info they contain = give the organisms  advanatgage -the plasmids are always selected for Ex: dividing during binary fission may hold onto the plasmid for  selective advantages -can be refereed to resistane plasmids: for resistance to antibiotics -can be resistant to penicillin Ex: super bugs, organisms resistant to all the antibiotics in a clinical  setting -have these plasmid that have all the gentic info for a bunch of  antibiotics -other plasmids have bacteriocidal proteins called bacterioicins -antimicrobrial, want to secrete these proteins out in the envt. so that it kills their close relatives so that they can dominant the space -these break down in the body too fast 4. virulence plasmids: carry traits that cause disease In ch. 19-24 (has the toxin information in their genes making them  virulent is found in a plasmid) -these plasmids contain info that make them have a selective  advantage spreading via conjugation = why organisms evolve so fast -why a doctor is reporting a new case resistant, matter of weeks and  other doctors will be reporting this plasmid in other organisms because of the  spread through conjugation5. tumor-inducing plasmids cause tumor formation in plants -support bacterial growth 6. plasmids that contain info for catabolic enzymes -break down chemicals (mercury, tolulene) =to clean up soil Fig. 8-11c a typical resistance plasmid can carry genes for resistacne to various  antibiotics and to inorganic toxic substances =plasmids can hold a lot of genetic info -the antibiotic resistance plasmaids can be accidently transferred  thorugh a bacteriophage -plasmids could contain so much genetic info to so many antibiotics -don’t want these plasmids entering our normal flora organisms =  infected with pathogen, normal flora could echange plasmid with pathogen = real  problems -do a lot fo explaining as why drug resistance is so fast Trasnposon -genetic sequence contain info to let that piece of dna to move form one prositon in  chromosome to antoher -transporalbe element inserts itself into a particular sequence and can mov to  another area on a chromsomes -has athe dna to make that the eznyem to allow for it to repliecate and move to  another area on a chromosome -very often a plasmid may have a transposon:  -if plasmid comes into cell, may bring in transposable element can  transpose itself from plasmid to chromsoomes, problem if enters into host  chromosome on essential gene could cause a mutation -tranpsoable elemtn also carry other genes, those other genes are information to  make the cell resistatnct ot a particular antibiotic Fig. 8-12 -the transponson do have other genes as part of their body and so when I move out  of this plasmid and I enter a host I can now transpose this sequence and make this  host have a gene for antimicrobial resistance -in this case a penicillin derivative -transposons have ability to bringing in genetic info and potential to bring in genes  into copy of host chromosome-these are mechanisms where we can define why antimicrobrial resistance was  occurring  -plasmids can really express any gene, why don’t we let microorganisms work for us and express genes that we would like expressed? -make E. coli do work for us? -put genes into plasmids, blood clotting factors, growth horomone -you could phhyically put any gene into a plasmid, there were  restrictive enzymes and bacteria make them, could take them in a test tube, and  insert genes of interest that we want to express -this was the start of recombinant DNA technology -can genetically modify bacteria to make human proteins for us -we’re using things in the clinic, purify insulin from bacteria Recombinatnt DNA techonolgoy 1. manipulation of DNA in vitro 2. recombination of another orgnaims’s DNA with bacterial DNA in a phage or a  plasmid 3. The cloning, or production of many genetically identical progeny, of phages or  plasmids that carry foreign DNA -the start of DNA technology was an exploitation of what bacteria have been doing  for thousands of years -could force e. coli to express human proteins Fig. 8-15 Producing Recombinant DNA -using endonucleases that cut inside DNA -the restriction endonucleases cut specific sequences -cut up human DNA, ex, insulin gene, so that I’m cutting out a specific sequence,  when cutting an inverted repeat sequence, when the enzymes cut they leave these  little overhangs called sticky ends -when the dna is cutting by restriction enzyme, here is our human insulin gene -have sticky ends, can then go into plasmid that I cut using the same restrictive  enzyme and this plasmid opens up and I have a sticky end on each cut of the  plasmid -the sticky ends base pair and ultimately get sealed up =now have plasmid with insulin gene, can get into recipient cell a number of ways -like a modified transformation-can now select for the cell that took up the plasmid -grow the cells with the plasmids in gigantic vats -after a certain amount of time, they’re making insulin, keep it inside  them, in the end you physically grab all the cells, lyse them, chemists downstream  purify the insulin out of the cells, the human insulin protein is isolated and  ultimately cleaned up = injection to somebodyFebruary 20, 2016 / Lecture 9 Fig. 7-24 -the antibiotic wasn’t induced by the antibiotic, the mutations are happening at a  random spontaneous event by exposing them to media that have antibiotics in  them =antibiotic resistance (mutation is being caused by antibiotic) -you want to know why that microorganism is resistant to that particular  antibiotic -does the ribosome change so now the streptomycin can’t change -but it’s a tedious job to find these mutations, so when you have a culture  where colonies are equal distances from each other -so if I wanted to place each of these colonies in the agar, it would be very  tedious to pick up each colony -looking at antibiotic resistance -do a procedure called Replica plating (sterile velveteen-covered block) -stab the velvet cloth onto the plate, the velvet cloth or filter paper will pick  up cells from each of these colonies, and they’ll be on the plate = can stab any type of growth media -in this case, these colonies in red are growing, can find them on the master  plate  -it’s replica plating, because this stab can go onto many different plates -the cloth is like an inoculating needle -ex: scientist named Dr. Ames -realized that you could study potential carcinogens by using bacteira -can see if you can take a bacterial mutant, a cell that could not make  a particular amino acid for itself -so normally if we look for mutations, we are looking for a wild type  (induce it using UV, chemical) => want auxotrophic mutant (a nutritionally deficient mutant, can’t process a sugar or amino acid0 -scientists have a wild type cell, no mutation in the protein, and are  looking at the mutant -he could really use an auxotrophic mutant => exposed to UV and get  it back to the wild type -in an industry when using a chemical, have to verify it if it’s a  mutagen -he realized intead of using animals, why not do it in bacteria -came up with the Ames test Fig 7-25b -could not grow without histidine in medium -he saturated that filter paper in the chemical, then he spread out the  auxotrophic mutant -after an incubation, he looked to see if he could find any colonies around the  disc -what he wanted to see if there were colonies on the plate -wanted to see if chemical grew  -the colonies reverted back to the wild type -taking a mutant and see if he could recover the wild type -on the filter paper, it didn’t induce a mutation Fig. 7-25a -only 3 of them have a disc on it -what about the control that has no disc? -not exposing it to carcinogen -spontaneous mutations -the one which has a lot of colonies seems to be a stronger mutagen  -the Ames test (good indication as to whether the chemical is a carcinogen) In A, can grow without the chemical, didn’t have to induce it = spontaneous  generations Whenever you have a mutant, best way to define a mutation, pick up colony off  plate, and sequence the DNA = PCR (polymerase chain reaction) -dealing with an enzyme, a way of amplifying DNA  -can amplify so that you can study the DNA Pg. 197 -if we wanted to amplify that DNA to confirm by sequencing -do the PCR -first step: separate DNA strands -done in a test tube, supplying the reagents -take histidine gene that we thought reverted back to the wild type -we know the gene sequence -we went from the auxotroph to the prototroph -works at very high temp (DNA strands melt) -h bonds come apart, melting double helix -we make a primer, a little sequence of nucleotides that sit at each end, once the  primers sit down at each pair, you have DNA polymerase that can work at a high  temp -use the extremophiles, hot springs, realized the enzyme from those  organisms could be useful, invented in PCR -once you add DNA polymerase, you can extend and amplify to two  semiconservative strands, then you go and you repeat it, then melt these two  helices and then add primer, then you have 4 then 16  -finally you get enough of your DNA and do all sorts of things with it -is this the histidine gene? Did the chemical correct the base for that? -if I have specific primers, people identify microorganisms by putting them in  different types of media -people will try to use specific primers that will only amplify specific organisms -this test can be done VERY FAST, all you need are very specific primers in a  particular organism Ex: primer in e. coli, or mycobacteria tuberculosis -they don’t have unique primers that are specific to unique organisms -in the future, that’s what people are looking to do -people amplify it all the time, need enough to sequence it Done with chapter 7  Chapter 8 -when talking about mutations, a mutation changes a characteristic in a cell -we know a mistake can be made during DNA replication -chemicals and UV damage can result in a mutation -those are way we can generate diversity in organism -not all genotypes result in a phenotype -in Ch. 8, is how DNA can go from one cell to another cell in that time period-actually looking at the exchange of DNA among bacteria -this exchange of info is a tremendous way of picking up diversity -organisms are so promiscuous  -2 mechanisms (transformation and transduction) wed will be  conjugation -this is how organisms start picking up new traits Ex: if you see it in e. coli, can see it in salmonella, etc. Ex: that’s why antibiotic resistance is such a problem -no one ever predicted the resistance that we see, because of sharing info Gene Transfer -you are moving info from DNA organisms -Recombination, once genetic inof goes into one cell, it has to be incorporated into  the recipient cell -you don’t just take a chunk of DNA, and it just sits there, has to get  incorporated into the recipient’s chromosomes -vertical gene transfer: when genes pass from parents to offspring -horizontal lateral gene transfer: passing genes that are living next door to each  other in the same time frame -happens by 3 different way (transformation, transduction, conjugation) -all going on in nature Transformmation: naked DNA, it died, and now it’s out in the growth media, not in  the cell anymore, spewed out of dead cell Transduction: involves a bacteriorphage, a virus of bacteria, bacteria has to deal  with viral infections too Conjugation: when two cells come together, one makes the conjugation pilus, and  the DNA goes through the bridge So transformation -you’re altering the characterisitcis of an organism because you transferring genetic info -talking about naked DNA, it gets spewed out of a dead cell, has to be taken up  pretty fast into a live cell becaue DNA out in the envt. gets chewed up by nucleases -the recipient cell actually makes a protein factor called a competence factor and is  released into the growth medium and facilitates the entry of DNA into cell-there’s a number of enzymes involved in actually bringing DNA from the  outside -we have DNA transport proteins -can help bring DNA across membrane -and have exonuclease that cuts up DNA is also needed (can only bring small  fragments) -loads of enzymes involved in transporting DNA across membrane and  peptidoglycan layer -DNA has an overall negative charge, asking a negative molecutle going across a  negative membrane, because why is something negative going to go across  something negative? Fig. 8-1 -defines transformation -before scientists knew that DNA carried the genetic info -thought it was the protein that carried genetic info -done at Rockefeller university -studying streptococcus pneumonia -the cells they are quite lethal to mice (injecting the wild type will kill the  mice) -the wild type has a smooth capsule and inhibit the mouse -also work with mutant strain, it wasn’t virulent, no capsule, live = colony  looked rough because there was no capsule = referred to as the rough strain the  non-capsulated strain, the mouse survived -took wild type capsulated cell, heat killed it, mouse lives -the only strain that killed mouse was the live capsule -they took a living avirulent rough strain and heat killed capsule, mouse dies,  there were capsulated virulent strain present = where did this capsule come from -coined the term transformation -his heat killed strain transformed the rough strain into the virulent  capsulated form -confirmed that it was the DNA that was heat killed that transformed  the strain Fig. 8-2 The Mechanism of Bacterial Transformation -the red DNA is from the heat killed smooth strain-you can’t put a whole chromosome across -there are nucleases there to break up the whole chromosome -making a competence factor -the fragments that come over are no more than 7-10 thousand nucleotides f-the rough strain made competence factor and you brought in fragments (had to be about 5-10 thousand nucleotides) -come in as a single stranded molecule -once inside these fragments can’t sit around in cytoplasm -to get expressed they have to recombine -the single stranded molecule comes in and lines up because of homology  with the recipient DNA, line up with purple A and B, do an equal exchange =  incorporate the small a and b into the chromosome -the a and b is the corrected copy to make the capsule, when the rough strain picked up the small a and b it can now be converted to the wild type -the single strand displaces the original host strand, and then the progeny all  have the red a and b -involves naked DNA, competence factor, and other enzymes, come in as  single strand, have to have a recombination event where they line up with  homologous genes -so an organism can be transformed to pick up a new trait (like antibiotic  resistance) -generating diversity -any transformation would be one that gives a selective advantage to survive  and replicate Transduction -the DNA is moved from one cell to another because of a virus -called bacteriophage (a virus that can infect bacteria) -phages: composed of a small amount of nucleic acid called the core that is  covered by protein coat -because the virus is so simple, don’t have to a lot of genetic info, have to  hijack a host cell, don’t have the info to make a ribosome or ATP, rely on host cell -phage is capable of infecting a bacterium attaches to a receptor site on the  cell wall -can be flagella on the fimbriae-the phage is very specific as to what kind of bacteria it will infect (e.  coli)  -need to see that particular receptor on that cell = high degree of  specificity -can be used to kill bacteria -virulent phage: capable of causing infection and the destruction and death of a bacterial cell -detriemtnal, destroys host cell, left with dead bacterial cell, all the  phage lyses out of the bacteria, will go on to infect another host cell -temperate phage: does not cause a disruptive infection -goes into host cell, incorporates into host chromosome and stays  there because it’s under suppression, there’s a protein keeping it there, at various  teims I can induce to be a virulent phage for a new cycle  -prophage -carry genetic info that maeks the bacteria pathogenic -the organism that causes Diphtheria, has a prophage in DNA, that  prophage codes for toxin that makes diphtheria the disease that it is  -the bacteriophage often contains info that makes the bacteira pathogenic -lysogeny:  -lysogenic strain -as long as prophage is not induced, the strain of bacteria that harbors  a prophage is lysogenic, (e. coli contains a prophage, a bacteriophage that can  infect e. coli) Fig. 8-3 Bacteriophage Life Cycles -usually have a complex structure -head surrounds their DNA -have fiber or tails that help them recognize the cell they can infect -leave all their body parts outside of the cell, leave their tail and head out of  head -just inject DNA into host cell, have lysozymes that break down peptidoglycan layer to do this -the nucleotides are used to make new viral DNA, the DNA is transcribed and  translated using enzymes from bacteria -ultimately the bacteriophage puts itself together, makes sure it’s assembled  before it leaves, releases a lysozyme that breaks out of the peptidoglycan layer-THIS IS A virulent phage -temperate phage: undergoes lysogenic cycle -inject DNA into host cell, put red pice of DNA into host chromosome, can go  on for many division, there’s a repressor protein that keesp the DNA in the host  chromosome -very often the dna from the phage may contain virulent genes, giving ability  to make a toxin for the cell -if I induce this red DNa to pop out, go through a lytic cycle, when I go back  into a new host go thorugh the lysogenic cycle -if they pop out can go through lytic cyle 1 round -the virulent phage only goes through lytic cycle How do they carry info to the host cell Fig. 8-4 -when it’s induced to pop out of chromosome, can take a little bit of the red DNA  with it = specialized transduction because the DNA it can take out is just the  adjacent DNA -Transduction: -specialized: due to the temperate phage -and so sometimes you can induce the black phage to come out, sometimes  it may pull out the red adjacent dna with it and the bacteriophage goes on to have a lytic cell -and when this DNA which has a little bit of red goes into new host, it  integrates, you see a little bit of red dna from first host cell in the chromosome of  another infected host cell -this new host has picked up a trait from the previous host -when the prophage enters the host, enters at a unique site, when it takes  DNA, it’s very specific DNA that was adjacent ot wherever the prophage inserted  itself -the opposite of specialized: generalized transduction -generalized is caused by your virulent phage -so those phages that go through the lytic cycle  Fig. 8-5 Generalized Transduction -you assemble yourself-sometimes by accident, instead of taking blue phage DNA you accidentally  pick up red chromosomal dna into the head, and they assemble and lyse  themselves out of host -and now when phage infects Bacteria, a little of the DNA from first host can  get incorporated into the new host cell -generalized because it’s random, I can take any particular portion of this  chromosome and by accident incorporate = random -specialized transduction, can only take the ADJACENT DNA from where the  prophage was inserted -in generalized, it could be any chromosome by accident -virulent infections, in real life bring in new info -transduction plays a role in antibiotic resistanceFebruary 27, 2017 Micro Lecture 11 Tomorrow Viruses go up on website (Ch. 19-24) -bring notes with you on Wednesday Pop Quiz -briefly explain what causes spontaneous mutations (1.5) -random, occur spontaneously due to any DNA replication errors due to base  pairing -exposed to chemical or UV = inducing mutations What is a nonsense codon? -doesn’t code for specific amino acids, refer to three stop codons One performs PCR to do this -amplify DNA Write the full name of the RNA that contains the anticodon -tRNA Memorize all the viruses, and understand all the genetic transfer mechanisms -Introns don’t code for protein, play a role in specific messages getting expressed Prokaryotes generally don’t have mRNA that need to be spliced (Eukaryotes do) Viruses Fig. 10-1 -very small, nanometer range = electron microscope to look at them -exception to rules = extreme environments = large seen in microscope = rare -are there living? Cannot replicate without a host to support their replication -because they’re really simple, don’t have a lot of genetic info -minimal amount of genetic info -either come as an RNA or DNA -the nucleic acid sometimes is segmented (influenza virus I 8 pieces each  containing different info) -can have single stranded DNA or RNA as part of genetic info -DNA expresses protein like the capsid that covers up the nucleic acid-this capsid takes on unique characteristics = how virus is describes based on how the capsomeres form around the nucleic acid -it’s basically nucleic acid covered by capsid -a lot of times it has an outer membrane -pinching off from host cell = enveloped virus = if virus surrounded by  membrane -when buds off from host cell form this envelope -proteins project out of membrane = spikes == carbs and proteins  (recognize specific things on host cell) -human viruses not only recognize we’re a human, like to go to  particular tissue (skin, intestine) -spikes are what contains a particular feature to recognize something  on our cells (lock and key fit = successful replication) -spikes sometimes embedded in nuclear capsid = depends on virus  what it’ll look like -doesn’t rely on host for translation, can’t make ribosomes, uses host  cell’s ribosomes and ATP and enzymes and structures = come with ability to  replicate DNA with enzymes Fig. 10-2 Sizes of viruses Picornavirus: small as ribosome in a eukaryotic cell -all sorts of shapes -spikes in adenovirus -helical virus tobacco mosaic virus -bacteriophage – capsid and tail fibers -has a fiber to allow DNA to get released into the head and be injected  through outer membrane and peptidoglycan into cytoplasm of the host -E. coli sitting within a liver cell Viruses get their name from what they look like -corona virus unnumbered p 278 -assigns a description based on what it looks like Fig. 10-3c bullet shaped -causes rabies virus-unique looking viruses -what a virus looks like depends on genetic info telling it how to look -it’s not an easy thing to name a virus -had to come up with a convention for naming viruses -ICTV: came up with a universal way to name viruses -try to group viruses on biochemical and molecular characteristics -unusual protein that this virus has (ex: reverse transcriptase in  retroviruses) -type and structure of nucleic acids (segment, single strand, double strand) -method of replication (cytoplasm? Nucleus of host?) -host range (does the virus infect many different mammals? Or is it very  narrow -if virus infects human does it go after specific cell type or lung or can it infect many different types of tissue) -host range and specificity is dependent on recognition of host cell  -other physical and chemical traits -because we can sequence DNA from viruses = helps classify viruses  There is a convention: virus names put into families, genus, and species -we have a family: genus: species Ex of a virus: retrovidiae: family -families that can go from RNA strand back to a DNA strand -genus: Lentivirus -species: HIV (human immunodeficiency virus) = type 1, 2 based on  strains Now one interesting characteristic of a family of virus are the herpes viruses: table  10-3 -common trait: latency (potential to reside in your body in a latent form) -it always seems to part of your cells in a stable non-replicating form and at  certain times it might start reestablishing an actual infection in your body Simplex virus: herpes simplex type 1,  -skin problem, but goes to neural tissue-it seems to hang out in neuronal tissue (like a provirus) not replicating  but always there -virus never gets completely cleared from body  -varicellovirus: chicken pox -once a person recovers from chicken pox, will stay indefinitely =  shingles, virus is replicating in neuron tissue down leg and back (nerve problem) -cytomegalovirus: usually not a problem for healthy people -those who are immune compromised: can cause severe infections -biggest problems = teratogen = any agent that can cross into  placenta causing birth defects in developing fetus -can cause severe problems for the baby -epstein-barr virus: infectious mononucleosis -shown to be associated with cancer, goes into b cells and b cells make your antibodies = b cell lymphomas -human herpesvirus 8 = cancer linked to AIDS, causes overgrowth in blood  vessels, cancer of the blood vessel lining -in group because they share one common feature: once infected, they don’t seem  to go away, always have possibility to infect, coming out of dormancy like a repeat  of a cold sore = latent -in ch. 10, look at viruses as being the teratogens causing birth defects and cancer -read up on emerging viruses -Ebola has been around for a long time, pockets in Africa = spread to big  cities, large populations potentially exposed -must be in some animal but no one knows where it is -this past summer = zika virus  Problem of viruses: -from a vector like a mosquito or some other vector -because we have travel, you really have people mixing easily potentially  spreading -because viruses can grow fast, can mutate fast  -don’t have a good arsenal of antiviral compounds = rely on a host, not a lot  of targets = how are we going to get something specific to kill them and not our  cells -can target reverse transcriptase in HIV-specific proteins unique to the virus = useful for HIV -for hepatitis: treating symptoms hoping immune system kicks in  -Zika virus: crossing placenta causing deformities -read chapter on emerging viruses -these viruses are more easily spread because mosquitoes are increasing =  going into colder climates that are now warming up Fig. 10-8 bacterial cell attached to complex viruses -virus recognizes bacteria Fig. 10-10a  -head, unique shape based on capsomeres -tail fibers will recognize something on the host cell -DNA comes down the tube and be injected into bacterial cell -all these parts of virus stay outside of bacteria (only DNA or RNA goes in) Fig. 10-11 Cycle of Bacteriophage -think of lytic virus, not a virus into host chromosome -tail fibers recognize something outside of cell (outer membrane protein, pilus,  flagella) -adsorption -once virus sits down = penetration -injects DNA and lysozyme to break peptidoglycan layer -once DNA is inside = will start breaking up chromosomal DNA, the nucleic acids can be used to make new copies of the virus DNA = biosynthesis -making all the new DNA molecules -transcribing mRNA and translating that to make viral proteins -see parts coming together -going into maturation step -bring all parts together -head has just enough room for head of DNA, package a whole head of DNA  don’t want to be shy of any genetic info I need before leaving -release enzyme called lysozyme opening peptidoglycan = released from cell-leave just like how I entered -one bacteriophage might cause a release of 200 phage particles = don’t just make  one phage = usually hundreds made -they go on to infect 200 bacterial cells -since the phage lyses the host cell -look at lytic phages as being antibacterial agents = phage therapy -a person cannot recover form an infection with antibiotics = chronic problem -they find out what the particular bacterial infection (salmonella, clostridia),  try to find a bacteriophage specific to that bacteria, give an injection of the virus -the specificity of the phage will only attack that pathogen and leave the flora alone -for the antibiotic resistant strains, this is what is going to be the ultimate  cure of that infection  -only works for lytic phages  -you need to have the phage be willing to infect cells and lyse out of them -used for problems where they are highly resistant to antibiotics -you have the specificity, the chances of the pathogen becoming resistant to  virus is not great because the viruses grow exponentially = this growth of virus  takes care of those pathogens quickly = pathogen gets outnumbered by phage  particles Fig. 10-12  Growth Curve: y-axis: after 20 minutes: from absorption, biosynthesis and maturation= released  200 phage particles -eclipse period: wouldn’t find any phage particles -slowly overtime would start seeing phage particles -depending on phage = can be 20 minutes to 2 hours depending on virus getting  through all stages Fig. 10-13 phage experiment -host and virus that attacks E. coli -mix in a test tube the virus and E. coli -spill that out into an agar plate -since you have E. coli, E. coli will start growing on plate, but embedded within the  lawn will be these little clear areas = plaques= the plaques just like colonies and count them = plaque comes from one virus that entered one bacterial cell released  viral particles and attached to other bacteria in the neighborhood = counting  plaques = cloudy is E. coli = each plaque represents one infectious viral particle  that infected one bacterial cell -can figure out how many viral particles you had in original infectious test tube  =plaque forming units Fig. 10-16 human virus has same steps but there are differences -have to have an adsorption step -virus happens to have a membrane can actually fuse with host cell -difference is WHOLE VIRUS COMES IN = NOT JUST THE DNA -penetration step -just have capsid once inside, then strips capsid, DNA virus goes into nuclear  membrane -have an uncoating step -will do replication, and make mRNA and translation in cytoplasm -depending on virus, assemble in nucleus or in cytoplasm = ultimately in this case  need to get not only capsid need to get that membrane again = budding off from  host cell picking up membrane from host and viral proteins -came out the same way I came in -depending on virus, can come in through fusion OR endocytosis -sometimes some viruses burst, they release themselves by lysing the host cells -especially if you don’t need the membrane from the host Fig. 10-17a RNA Viruses -this one is coming in and doesn’t have a membrane = don’t see fusion of  membrane -many RNA viruses that have membrane -coming in through endocytosis = penetration -when you have RNA, single stranded molecule = described as having a plus  sense RNA or a minus sense RNA -either a positive sense or a minus sense that you come in as - a positive sense RNA is a virus that can be translated immediately, so if  you’re a single strand and plus sense, this plus sense is mRNA = can be translated-ribosomes attach = making viral proteins = an RNA polymerase a  transcriptase that will copy your plus sense and when you make a copy of your plus  sense it makes a copy of a minus sense =the minus sense has to get copied into the plus sense that will get  copied  -problem comes in when you are minus sense: when you come into the cell, it is not mRNA have to be transcribed or copied to the plus sense so I can make  protein and be translated, ultimately makes protein and then the plus sense that  was made from transcription will have to be copied to make minus sense  -they bring in transcriptase = copy the minus sense to the positive  sense Another RNA virus concerned about = HIV It’s a positive single stranded RNA -when it comes into host cell, brings in reverse transcriptase, bringing in a  copy of DNA, ultimately that single strand DNA is copied into double strand = will  integrate into our host chromosome =once integrated can stay there indefinitely =  DNA can start being replicated into viral RNA = start translation of viral proteins =  HIV buds out of host cell -once infected with HIV = you have the virus for the rest of your life because  there’s no way to get rid of integrated DNA from infected cells -all the antiviral compounds keep the concentration at a low level -problem is this DNA is always present in cells = need to figure out how to get rid of copy in host chromosome = this is a plus sense RNA which is in the family of  retrovidiae that makes rna to dna Fig. 10-17b Budding  -eventually kills host cell Fig. 10-18a and b HIV recognizes 2 specific proteins on our cells  Fig. 10-19 -endocytosis depends on virus Table 10-6**** COMPARE BACTERIOPHAGES IN THE ANIMAL VIRUSES -subtle differences  Fig. 10-21 what do we use to study human viruses? -this is chicken eggs used to study influenza virus -replicates in embryonated chicken virus-injects virus into eggs, embryo supplies tissue to allow viral growth –  pharmaceutical industry purify the virus from the eggs Fig. 10-22a -nice healthy looking cells -if you put a virus in there = Fig. 10-22b virus inside causes swellingFeb. 27th Lecture Points 1.The basic components of a virus are a nucleic acid (DNA or RNA), capsid ,  envelope and possibly spikes projecting from the virion particle. 2. A virus is classified into a Family, Genus and Species. The ICTV requires  the common English name be used to designate a viral species. 3. Know the 5 steps of viral replication for both animal viruses and  bacteriophages. 4. What would a growth curve for a bacteriophage look like? 5. What are the two ways a enveloped virus can enter a human host cell? 6. How does replication of a DNA virus differ from a RNA virus? 7. Why does a (-) sense RNA virus need to bring a transcriptase into a host  cell but the (+) RNA virus does not need to? 8. Define Viral Latency. 9. Viruses can be cultured in animals, embryonated eggs (Influenza Virus  propagated this way), and Tissue Culture. The damage caused to tissue  culture cells by the virus is called the cytopathic effect (CPE). 10. Define Teratogenesis. What viruses are know to cross the placenta? 11. Prions (PrP) are small proteinaceous infectious particles. There is a  normal form of this protein in human cells (especially brain) and if it comes in contact with the misfolded prion protein (PrP), it is thought that the wild type  protein is converted to the misfolded form. The misfolded proteins start to  stick together in fibrils. Ultimately this leads to brain cell death and to the  diseases collectively referred to as transmissible spongiform  encephalopathies. These diseases are fatal and on autopsy, one can see  holes in the brain tissue. Kuru, CJD, new-variant CJD, Scrapie and Elk Wasting  Disease are some of the diseases caused by prions. Refer to pages 789 -  792 for more information on these diseases. 12. Many viruses are associated with human cancers. Integration of viral  DNA into host DNA can cause expression of viral proteins which may result in unregulated growth of the host cells. Viral DNA may also integrate into host  growth suppressing genes thereby inactivating them. RNA viruses may even carry genetic information from a host cell that it previously infected and  these genes are referred to as proto-oncogenes. If they become expressed inthe new host cell this may lead to uncontrolled growth. Know which viruses  are associated with cancer such as Papillomavirus. March 1st Lecture Points Study These Viruses in Chapter 18-24 Chapter 18: HIV (AIDS) (pages 563 - 571) Chapter 19: Rubella, Measles, Chickenpox, Smallpox, Human Papillomas Chapter 20: Herpes, Cytomegalovirus Chapter 21: Rhinovirus, Parainfluenza, Influenza, RSV, SARS, Hantavirus Chapter 22: Mumps, Rotavirus, Hepatitis Viruses Chapter 23: EBV Chapter 24: Prion Disease, Rabies, West Nile Fever, Equine Encephalitis, Polio 1. HIV: 2 important strains HIV1 and HIV2. The virus targets cells of the  immune system such as macrophages and T cells which not only makes a  person immunocompromised but helps spread the infection to other organs.  The virus is a retrovirus and integrates into the host cell's DNA. The reverse  transcriptase makes a lot of errors when copying the RNA into DNA so the  proteins on the virus surface can change frequently and causing it to become resistant to antiviral compounds fast. That is why a cocktail of antiviral  drugs is used to treat the infection. HIV infected people often develop the  malignancy called Kaposi's sarcoma which is caused by the Human  herpesvirus 8. The transmission of the virus is by sexual contact, blood, dirty needles and mother to child. Why is it so hard to make a vaccine to it? The  follwing link is an animation of HIV infecting a host cell. http://www.sumanasinc.com/webcontent/animations/content/lifecyclehiv2.html 2. Rubella (also called German mesles): This is a virus that can cross the  placenta and causes Congenital Rubella Syndrome. The virus is a  component of the MMR vaccine. 3. Measles (also called called Rubeola): Koplik's spots on the lips and cheek  appear before other symptoms occur . Complications caused by this virus are measles encephalitis and subacute schlerosing panencephalitis. This virus is  included in the MMR vaccine.4. Varicella-Zoster: This Herpesvirus causes chickenpox and can cause  complications such as damage to blood vessels. Since it resides in ganglia of  the head and neck in its latent form, it can be activated and cause Shingles.  There is an attenuated virus vaccine that is available to protect against  chickenpox and it is still not know whether this vaccine will completely  protect against Shingles. 5. Smallpox: The one success story of ridding the human population of a  dreaded virus. A successful vaccination program across the planet was  required for this to happen. 6. Papillomavirus: There are many strains of this virus and most cause warts  but two strains numbered 16 and 18 are know to be involved with cervical  cancer. A recent vaccine from Merck called Gardasil is available to prevent  infection with those strains as well as a couple of other strains but the  vaccine appears to do nothing to an already established infection in a  person. Genital warts are referred to as condylomas. 7. Herpes Simplex Virus (HSV): HSV1 is predominately found in cold sores  and HSV2 (sometimes called herpes hominis virus) predominately found in  genital herpes. This is a latent virus that resides in ganglia and it can lead to more serious complications such as encephalitis, lung, liver, and spleen  infections. Another complication from an active infection is Neonatal Herpes. 8. Cytomegalovirus (CMV): Approximately 80% are carriers of this human  herpes virus-5. This virus can cross the placenta and cause severe damage  to the fetus. It is also a problem in patients receiving a transplant since they  need to take drugs to suppress their immune system and can't fight off this  virus as easily as a healthy person. 9. Rhinovirus: Most common cause of a cold (coryza). So many different  strains make it impossible to produce an effective vaccine. 10. Parainfluenza: It is localized mostly to the mucous membrane of the nose and throat. Croup, which is an obstruction of the larynx, causes a "barking"  cough and is a hallmark of the disease. 11. Influenza: Is composed of 8 fragments of RNA which codes for the viral  proteins. Hemagglutinin and Neuraminidase are required for the virus to be  infectious. Changes in the genes coding for these proteins results in the  different viral strains. These changes are referred to as antigenic drift and is  the reason why every year there are different viruses that make up the  vaccine. Since the viral RNA is in different fragments, it is know that if 2  different viruses infect a host cell simultaneously, there is a chance for gene  reassortment of these different RNA fragments. This is called antigenic shift and is why the "Bird Flu" is a concern to us since it is know that in cases where people become infected with the Bird Flu there is a high mortality rate with it. Imagine what would happen if the genes causing this high mortality  rate were transferred (by gene reassortment) to the influenza strains that  infect humans! The vaccine is produced every year with a few different  strains that are most predominant that year. The virus is made in  embryonated chicken eggs but this is very inefficient which is why there  have been vaccine shortages. Currently a tissue culture system has just  been developed to grow the virus in which can be used in future vaccines. 12. Severe Acute Respiratory Syndrome (SARS): It caused by a coronavirus  and has a high mortality rate associated with it. It is know that it resides in  civet cats in China as well as domestic cats. The virus is contracted by close  contact with infected people and it is monitored by the World Health  Organization (WHO) as an emerging virus. 13. Respiratory Syncytial Virus (RSV): This is the most common lower  respiratory infection in children under 1 year old. Hospital workers need to  be careful not to spread this virus in the nursery wards. 14. Hanta Pulmonary Syndrome: This is an emerging virus that showed up in  this country during the last 15 years. The source of the virus seems to be  only in rodents so far. It has a very high mortality rate and is an infection of  the lungs. This virus has been seen in other countries for over 50 years but  it is different since it causes hemorrhagic and renal symptoms without lung  involvement in those countries. 15. Mumps: Humans are the only host of the virus. It is a part of the MMR  vaccine. There are complications caused by this disease such as male  sterility if an adult is infected with the virus. Also it can cause  meningoencephalitis. 16.Rotavirus: Causes viral enteritis among infants and young children. Hospital workers have to be careful not to spread the virus in the children's  ward. There is a vaccine for it. In developing countries, there is a high  mortality rate associated with this virus since children do not receive fluids  lost from diarrhea. 17. Hepatitis A,B,C: Hepatitis B is caused by a DNA virus and the other two  are RNA viruses. Hepatitis A is transmitted by the fecal - oral route. There is a vaccine to it. Hepatitis B is transmitted by blood and blood products. It can  also cross the placenta. A person can carry this virus in their body for many  years after recovery. There is a vaccine to this virus which is part of the  recommended immunization schedule for children and all health care  workers. This virus is implicated in some cases of liver cancer. Hepatitis C is  transmitted from blood products. It can become a chronic infection in some  people and has been implicated in some cases of liver cancer.18. Epstein-Barr Virus (EBV): This herpesvirus causes infectious  mononucleosis and targets the B cells of the immune system. It also remains latent in the B-cell after recovery from the initial infection. This virus can  lead to complications in immunocompromised people and it can cause the  tumor Burkitt's Lymphoma as well as nasopharyngeal carcinoma. 19. Polio: There are two forms of the vaccine (Salk and Sabin) and since  everyone in this country is vaccinated we would most likely only see cases of it in someone not vaccinated coming from another country. The complication caused by this virus is complete or partial paralysis. The WHO has  attempted to get all countries to participate in a vaccination campaign to  eliminate the virus from the planet but so far it has not met with the same  success that smallpox vaccination has. 20. West Nile Virus: Is transmitted by a mosquito and has spread across the  country in the short time since it was introduced in this country. It can be  thought of as an emerging disease and will be hard to control since birds are  a reservoir for the virus. 21. Rabies Virus: This virus is found in many mammals and it is critical that  dogs and cats continue to be vaccinated. Some cases of rabies that show up today are not only from rabid animal bites but cuts exposed to viruses. For  example, infectious material from a rabid animal can gain entry into the  human body through broken skin. 22. Encephalitis: There are 4 different viruses causing inflammation of the  brain (Eastern Equine, Western Equine, Venezuelan Equine and St. Louis  Encephalitis Viruses). These viruses can be thought of as emerging viruses  and the virus seems to need to pass through birds before the mosquito can  pass it on to humans and/or horses. There are tables in the book that break up the different fungal viruses,  condensed version of bacteria in each chapter -know common names for viruses, are there vaccines, associated with  cancer, is it a teratogen, did the viruses have any unique characteristic  complication -make sure you start committing to memory now March 1, 2017 Ch. 10: prions: infectious proteins, why is it in the chapter on viruses?-the slow viruses, Jakob was a disease caused by a slow virus -Transmissible Spongiform Encephalopathies  =prions -first infection to be described as this result of an infection in the  brain resulting from these wholes = resulting from a slow virus -sheep get the same thing, all the prions head toward the  neuronal tissue and lymph tissue -damage usually neurological -if they are in your body long enough will die Prion is misfolded, we have a normal type in our brain, and we  come in contact with abnormally folded protein, can travel to neuronal tissue -wild type is present in brain, when the misfolded protein starts  converting the wild type correctly folded to the aberrant folded protein=  accumulating brain = tangles cause cell death = start seeing the tissue  becoming necrotic causing holes in the brain tissue -scrapie’s is similar to crightsfold yakob -all considered transmissible spongiform encephalopathies -can get them from contaminated food -variant = called mad cow disease = developing the  transmissible spongiform encephalopathies = once it starts can’t stop it =  keep contaminated food out of our meals and animals -scrapie’s = from sheep, can cross hosts -prions seems to cross different hosts  What is really happening? Still seems unbelievable that is associated with  protein, some believe there has to be some other factor to start these  tangles -if exposed to acids = destroy the infectivity -exposed to UV damaging agent, this still is infectious -it is an infectious protein, seems unbelievable -ensuring animals ARE NOT infected, don’t harbor prions -that’s why it is in chapter on viruses Chapter 18= HIV-t cells help b cells which make antibodies -HIV and HIV-2 are two different strains -1. Targets cell of immune system: T cell, macrophages which can spread  virus to other organs. Opportunistic Infections When t cells fall below critical level = opportunistic infections -these organisms will take advantage and infect people -normal organisms that we would come in contact with, people who are immunocompromised can’t fight those opportunistic infections -people with HIV infection if not given therapy and T cells fall below  certain level, die from infection that can’t be treated Fig. 26.36 HIV biology -could spread infection, but never seemed to get very sick -majority of people with HIV cause them to be immunocompromised, in the beginning there were no antiviral agents = aids -scientists wanted to know why a group isn’t getting sick, maybe  they’re making an antiviral compound, not really -HIV virus not only recognize receptors on t cells and macrophages,  CD4 lock and key, not just looking at one receptor, recognizes 2 receptors on host cell -co-receptors (CCRS) -people that never progressed to AIDs had a mutant form of a  particular receptor, virus needs to see both receptors -virus could enter host cell, but was impeded because it wasn’t real  receptor that attached to this virus -attempt to create a vaccine -why is it hard to create a vaccine It is an RNA virus, comes in as a single stranded RNA 2. error prone reverse transcriptase causes changes in viral proteins so  antibodies can’t recognize protein -reverse transcriptase makes a lot of mistakes, always changing HIV The antibody has to work outside host cell and be there before it enters host  cell, once it enters host cell, T cells recognize the viral cells, a vaccine would have to kill a virus mounting your antibody response and T cell response =  difficult to do without using an attenuated strain (a virus or bacteria,  are live organisms but it’s crippled so that it can’t cause an  infection but it does give you an immune respone that portesct you  against the wild type) -would have to use an attenuated strain of HIV -problem with that is that you now are giving somebody a live  attenuated strain, can mutate back to wild type, we know it’s a  retrovirus, so once you make a copy of RNA to DNA, integrates into  a host chromosome = nothing preventing strain from doing that too Difficult problem to make a vaccine because of the life cycle of the virus -virus keeps changing = antibody doesn’t work -attenuated vaccine = can complicate other cells of body 3. HIGHLY active antiretroviral therapy -best thing to do -a cocktail of different antiviral compounds -virus has a lot of unique proteins -been able to come up with enough antiviral compounds so that a  person can live a healthy life due to very unique proteins that are targeted to HIV -since virus mutates so readily, it can become resistant to one antiviral  compound very fast, that’s why it’s a cocktail amount P. 281 -body does fight during first stages of HIV -the very cells the virus goes into are needed to kill the viral cells -after a while, the immune system can’t keep up anymore -start getting sick with things that are not typical -may get herpes infections, not a good enough immune system -may get anemia HIV-related symptoms if not treated develop -cancers -a wasting disease, metabolism thrown off, emaciated -ultimately go onto stage of AIDS It is the last stage -dies of opportunistic infection -Metabolism is off -don’t necessarily die of HIV virus This table was made before the antiviral retroviral therapy was made -no one really knows, because the drugs haven’t been given that long before  they every progress to AIDS -even if you’re on antiviral therapy you’re still infectious, but we try to keep t  cells high enough so they don’t progress to AIDS 4. Transmission:  -sexual contact, blood contact, dirty needles, mother to child -in utero, mother can pass virus on but nowadays the mother being  treated, the transmission rate isn’t that great anymore 5. vaccine -once you have virus, it never goes away, because you have that DNA copy  in your chromosomes Chapter 19: skin involvement Rubella: lead to congenital rubella syndrome, if pregnant virus can cross  placenta especially during first trimester can cause severe problems -can be referred to as a teratogen 2. vaccine (MMR) made up of measles, mumps, rubella -attenuated viruses in this vaccine -virus that has been crippled so that it cannot cause an infection as if  you saw wild type virus -the rubella rash isn’t life threatening but CAN CROSS PLACENTA -can be called German measles Measles: nasty virus, get a rash or fever 1. Keulik’s spots (blue lesion in mouth) (immunosuppression) 2. Measles encephalitis -can get into brain tissue causing encephalitis3. subacute sclerosingpancencephalitis -can have it as a kid can come back -= high mortality rate -can happen in kids who get infected at young age  4. (MMMR) vaccine -a lot of people who have measles, still are immunocompromised a few years later = interfere with normal immune system = more vulnerable to  other infections Varicella-zoster virus: Herpesvirus -stays in neuronal tissue -dormant but can be triggered -complications: blood vessel damage -fever, rash, chicken pox, can become infected -can get scar tissue -sometimes it’s not just skin but blood vessels -shingles: activation of viruses, that reside in ganglia of head and spine -vaccine: attenuated virus but is there a problem with latency -is it going to be a problem since it is not going to go away, there is  also a vaccine given to adults to prevent shingles, immune system given a  boost, hopefully keep varicella zoster to grow -nowadays most people are getting vaccinated, interesting to see if  numbers of people who get shingles increases or decreases -once you get chicken pox, you’re protected for life but can get  shingles Small pox: eradicated by vaccination -Jenner used cow pox virus to protect against small pox Papilloma virus: virus that causes warts, physical lesions -but it was realized that is associated with cervical cancer -good group of strains “16” and “18” that caused  -warts are caused by papilloma virus -those associated with cervical cancer don’t show visible lesion-by being able to take cervical tissue that was cancerous = had viral  DNA -vaccine to protect against cervical cancer: men can spread virus but  there is penile cancer Gardasil by merck -need to be vaccinated before acquiring virus -genital warts: condylomas Chapter 20: sexually transmitted  HSV 1: cold sore HSV 2: genital herpes. Virus shedding without visible signs of open  wound in skin, no symptoms of lesion -latency: reside in ganglia -a lot of pain with these lesions because of neural tissues -complications: can spread to any organ in body more a result of  someone who is immunocompromised -encephalitis, lung, liver, spleen infections -neonatal herpes- usually during delivery is infected or  somehow contact with mother that is shedding virus -basically, don’t have active immune system yet =  death = not many antiviral compounds -she doesn’t have to have active lesions Cytomegalovirus: CM HHV-5 -techniques to detect it -most people infected with it, not a virus that causes a lot of symptoms - 80% a lot of people can be adult carrier -doctors should be describing this to pregnant women because it can  cross the placenta = damaging fetal tissue -want until they could start screening for the virus through PCR to look  for viral DNA in baby - immunosuppressed patients (people with HIV, or transplant patients  are being affected by this virus) -people should be talking about CMV -if a child is born with problems, exposed to infection in utero -it’s in the sexually transmitted chapter because of placental  transmission Chapter 21 – upper respiratory tract Rhinovirus: most common cause of colds -no vaccine to treat all common colds -very hardy, can stay out in environment unlike bacteria that can’t survive  outside moist area = phomite (inadamant object) that can harbor things like  viruses possibly bacteria = important to keep clean Corona viruses are another common cause of colds  -sore throat Parainfluenza: infects nose, throat, mucous membranes of nose, throat,  -croup – obstruction of larynx may cause “barking” cough  -respiration-strider -no vaccine for it lower respiratory tract -Influenza:  -always new strains being developed -segmented virus, 8 RNA STRANDS -spikes are hemagglutinin -H1N1: allows virus to attach to the host cell -N protein: helps virus can get through mucus that may be on lung  tissue and nasal passages, and helps release virus from host cell -every year there seems to be dominant strains in the virus so they  always know what  =always mutates: antigenic drift, as RNA replicated = mistakes made  = differences in H and N proteins = these proteins are critical for virus to be  infectious = why they always need to give a new cocktail -antigen: ability to create an immune response -changing the protein on outside of virus due to antigenic drift -antigenic shift: another reason virus changes from year to year-can have one host cell getting infected with 2 viruses at the  same time, might not be 2 human virus, may have human and pig influenza  virus in same cell that both have 8 segments of RNA -1 host cell could have 8 fragments then of pig and 8 fragments of the  human -can exchange fragments of the RNA = antigenic shift = shift  before switch = wind up with virus that now has copies of info from both the  pig and the human -that pig info could give a new characteristic for influenza to  more easily attach to our host cell -if human is infected with bird flu = high mortality rate -if bird RNA mixes with human influenza even more virulent -that’s why the protein H and N because of antigenic drift and shift can  cause the change -once you’re sick and damage is done with lung tissue, vulnerable to  bacterial infections -can cause pneumonia, because lung tissue is damaged if came  in contact with another bacterium, gives opportunity for infection -RNA fragments, also gene reassortment (antigenic shift) -antigenic drift- mutation in RNA Bird flu Vaccine: embryonated chicken egg SARS: severe acute respiratory syndrome -it’s a coronavirus (SARS-CoV) -high mortality rate especially in markets selling food products -cats seemed to harbor virus  -spread very fast to many other countries -luckily because of quarantine, it didn’t get established -like an emerging infection, has caused diseases in past, seemed like  they could contain it, but because of travel, viruses could move fast -middles eastern respiratory syndrome = high mortality rateRespiratory syncytial virus: most common infections agent in children under  1 yr of age -kids in nursery unit, person will have to be very careful not to spread it -not a lot of antiviral compounds, just treating the symptoms -hanta virus Pulmonary syndrome: in rodents, mice, shed virus, high  fatality -breathing it in causes severe respiratory problems Chapter 22: Gastrointestinal Disease Mumps: human, only host -MMR vaccines Complications: sterility, meningoencephalitis Rotavirus: infection of intestinal tract, viral enteritis among infants and  young children. Hospital acquired -vaccine become available in last 10 years = protects Hepatitis: A B C B: DNA virus A and C are RNA viruses A: often gotten from contaminated food Fecal = oral B: vaccine, can get it rhoguth blood, body fluids, liver cancer -carrier state -having a chronic infection can lead to liver cancer -people that are carrier that are healthy but are still shedding virus is a  problem C: get it rhough blood products -if you get it, not only does it lead to horrible infection -people can become carriers -it is involved in liver cancer Chapter 23Epstein-Barr virus: infectious mononucleosis -herpesviral  -inflamed lymp tissue: b cell attached originally and virus remains latent in B  cell -barkitt’s lympohone, masopharyngeal carcinoma -immunocompromised Chatper 24 Polio: salk and Sabin vaccine -vaccinated -close to eradicating West nile virus: mosquito infected -immunocompromised can cause encephalitis Rabies: many mammal’s hosts -protected, immunized -out in wild -once you show symptoms of rabies it’s over -equine encephalitis: mosquito transmitted: bind: attacks horse or human

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