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Virology Study Guide Midterm 2

by: Madeline Abuelafiya

Virology Study Guide Midterm 2 BIOL 5325

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Madeline Abuelafiya

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In class Notes for Virology whole section for test 2
Dr. Harrod
Study Guide
Virology, Harrod
50 ?




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This 17 page Study Guide was uploaded by Madeline Abuelafiya on Tuesday March 29, 2016. The Study Guide belongs to BIOL 5325 at Southern Methodist University taught by Dr. Harrod in Winter 2016. Since its upload, it has received 14 views. For similar materials see Virology in Biology at Southern Methodist University.


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Date Created: 03/29/16
February 16, 2016 Chapter 7 Important questions in the chapter Adaptive immune response: adaptive, sterilizing, highly specific from memory Antibodies produced by B PLASMA CELLS Memory immune response- will never get that infection again Triad model of disease ** Changes in the host: if immune system is under developed/more susceptible than others Genetic background could effect susceptibility to infection- if there is no cofactors (?)- people that cant get hiv Host Changes: Age, nutrition, fever response, genetic factors, dual infections, and species resistance Shingles: chicken pox virus (a herpes virus) – can never clear the virus- latent and can become reactivated  trace peripheral nerve endings with immune suppressed individuals (old people) Fever Response: Don’t pay too much attention to diagram, Macrophages take in a pathogen Release inflammatory cytokines (not prostaglandin) Induce hypothalymus to produce prostaglandins then elevate body temperature ** Fever response: first line of response to any infection This is to try to denature bacterial proteins- stopping bacterial replication Non specific Immunity: innate immune response: reacts against any pathogen- no associated memory. This limits spread of infection Dendritic cells- motile can go to site of infection : degrade virus into small peptides Antigen presenting cells present MHC Class 2** present onto immune system stimulated adaptive immune response 3 types of antigen presenting cells: dendridic cells, macrophages, Memory B cells ** MHC Class 2 – antigen presenting MHC1- on every cells Immunological synapse: between MAC CLASS 2 and Antigen presenting cell stimulated immune response by helper T cells (??) Every cell has MHC class 1- self from not self Pore forming granuals kill cells Mechanical immunity and Phagocytosis Body defense cells contain pattern- recognition receptors (PRRs) that recognize pathogen associtated molecular patterns (PAMPS) PKR- stimulates inferon response (PAMPS) – markers of a viral infection Ds RNA- unique to a viral infection Kinase in the cell called PKR binds to ds RNA and activated 3 major classes of molecules that shuts off cellular translation and kills the cell Phagocytosis: macrophages, neutrophils, blood monocytes Dendritic cells derived from monocytes- motile and go to cyte of infection to internalize pathogen and process it into peptides and then go to lymph notes to present antigen to helper t cells. NK (Natural Killer) cells: Innate immunity : recognize cells that don’t have MHC1 on their surface Or that have tumor antigens (tumor infiltrating lymohocytes) Supposed to kill cell before it releases particles and spreads infection Perforins, granzyes, chemokines- put holes in the cell Interferons are cytokines Cytokines: intercellular communication dsRNA activated PRK cell tells itself it is infected by a virus phosphorlylates/inactivates translation in the cell stopping viral protein making RNAse L degrades RNA in the cell and kills the cell Prevents spread of viral infection Inferferons were immediately put into clinical trial: effective against cancers and viral and bacterial infections Apoptois: programmed cell death Cytopathic viruses (high kinetics) can induce apoptosis Incephalitus: inflammation of the brain and nervous tissue: apoposis in brain and nervous tissue Compemet cascade: when you activate complementary protetiens formation of MAC Hypocomplementemia: cannot activate system and has weakened immune response Antibodies bind to viral comotents to neutralize the infection Cell mediated response: cytotocic T lymphocytes activated by __ go kills the cells (target cell killing) Adampted immune response remains a week after infection Requires memory response B and T cell Lymph fluid: interstitial fluids cleaning B lymphocytes- White blood cells diffrintialte in the lymph notes to B blasma cell Humoral Response IGA- mucosal immunity B cells activated by helper t lymphocytes in the lymph nodes Antigen: anything that can stimulate an immune response Feb. 23 Humoral B cell immunity B cells create neutralizing antibody: 2 binding sites that can recognize an antigen Antibodies coat the virus and neutralize the infection by binding to the virus preventing It from binding to cell receptor preventing infection Antigen presenting cells presents antigen to helper T cells Antigen presenting cells process cellular antigens*** have the ability to process antigens by phagocytosis present on MHC Class 2: by internalizing the pathogen, chewing it up, and presenting it on MHC Class 2 Helper cells are CD4+ lymphocytes T-cells can undergo DNA rearrangement Cytokines: soluable growth factors B cells differentiate in lymh nodes** T cells mature in the thymus *** B Plasma cells secrete antibodies to neutralize the viral infection Variable region: DNA level exchange in the B cells- chances Constant region: binds to cell surface 2 binding receptor sites on each antibody IgM antibody: major neutifulizing antibodies that increase first during infection: linked my J chain- junction region. Found in spleen and immune organs. First produced in response to infection. Multiple binding sites. (pentamer) First neutralizing antibody IgG: response to vaccine and major neutralizing antibody (does not have a junction)- 1 and 2 present in the blood. Can cross placenta and help fetus with viral infection. Allows mother to protect fetus from viral infection (monomer) 23 day half life – high level of total serum immunoglobulin. If already exposed to pathogen. IgG will occur earlier and a very high titer. Adaptive immunity. IgA: secretory antibody: junction region involved in secretion (dimer) Viral Neutralizing Antibidies Want to identify the particle virus that are most immunogenic An effective vaccine will generate highest neutralizing response This is measured by taking blood plasma and reacting it against the viral particles and seeing whether or not it would cause infection HIV envelope contains hypervariable regions allowing them to accumulate mutations of the glycoproteins and escape the immune system Neutralizing antibodies are highly speicifc to the antigen ____antibodies_____?Rapid, sterilizing, and dependent on cell memory. AIDS patients have a lot if CD8+ t cells but do not work without helper T cells so because they are being destroyed and targeted, therefore CD8+ cannot function Cytotoxic T cells induce targeted cell killing. Bc ells recognize whole viruses and whole protein antigen T cells recognize short viral peptides MHC Class2 process antigen internally but external antigens are phagocytosed MHC Class1  recognize intracellular antigens: internal antigens on the cell surface prosseced by proteasome. Virus already in the cell CTL: cytotoxic T lymohocytes Dendritic cells, macrophages are important for antigen presenting All cells have MHC class 1 Helper t cells become active  make cytokines (specific for B or T cells response: th1 and Th2) Cytotoxic t cells are immature cD8+ cells and mature into cytotoxic t cells Then they travel to the site of infection Cytotoxic t cell binds to peptide in MHC class 1 molecule Helper t cells recognize MHC class 2 Makes perforins and granzymes and cytokines to kill the cell thorugh lysis/death and apoptosis before it can release more infection This causes inflammation and can end up being dangerous: inflammation in gut or liver In brain: leads to encephalitis Inflammatory cytokines: dangerous Cytotoxic t cell response in certain organs can cause dangerous inflammation Vulnerable population: young , old nK cells: non specific cell killing (t cells) activate complement cascade : aggragate proteins that induce pores in infected cells resulting in cytolysis. Macrophages and monocytes: peroxynitrite non specific cell killing (kill infected cells and surrounding cell) IFN: cell stops making proteins and degrades made proteins  induces cell death Dentritic cells (APC) serves as bridge to stimulating the second line of defense: antigens and cytotoxic c cells, b cell differentiation 7.5 Cytokines target B cells (IL 4,6,8,12)  b plasma cell T cell cytotoxic t cell Some of these will be long lived: memory Stimulated through initial infection and vaccine Viruses escape immune system They can down regulate MHC Class 1 Can escape neutralizing antibodies though hyper variable regions: immune escape variance Immune response is a selective pressure Cancer Causing Viruses: Viral latency: down reg MHC class . (ie. EBV- infects B cells) Molecular mimicry: look like cellular proteins and not recognized Can make decoy molecules to inactivate neutraphols. Decoy antigens to distract immune response (ebola virus) Inhibit apoptosis – cancer virus- macrophages and monocytes can be infected without killing the cell itself INF: PKR inactivates to block interferon signaling Passive antibody therapy Convalescent serum : blood/serum neutralizing antibodies from surivors to help infected patients. Very useful for viruses we don’t have a vaccine against. Must be a blood type match. Treatment against Hep A and ebola virus Complications: serum sickness: develop immune response against antibodies present Skin lesions, redness/itching, fever, swollen lymph, flushing: reacting against serum Vaccination: best way Hard for HIV b/c of hypervariable region or ebola Traditional vaccine killed or inactivated vaccines or live attenuated viruses History of smallpox vaccine One of the first vaccines produced was the Rabies Vaccine: 97% mortality rate before vaccine Generate an attenuated virus: take a cytopathic virus of one species and inject it into a different species that does not support the virus. The virus will adapt to effect that host. Then when taken out- it is attenuated and can no longer cause infection in original target Heat (denature proteins) or chemical inactivation of viruses (look like normal) Problems with inactivating virus: the chemical may not completely inactivate all viruses. Any life virus particles may cause disease. Attenuated virus much safer but can still revert back to wild type virus Production of attenuated viral vaccine Low yield of vaccine strains and have low shelf life Recombinant DNA methods: very safe Subunit vaccine: subunits of protein coat of virus, individual glycoprotein or capsid/coat protein/ immunogenic parts (peptides) No danger in inverting back and causing disease Can induce an allergic response Live vector: safe vector that will contain the specific glycoprotein Recombinant HBV vaccine introduced into yeast vextor transdorm cells_ break open yeast cells Yeast: eukaryotic cells!! Coat proteins are glycosylated!! So they can be recognizing. This IS NOT IN BACTERIA ** Vaccina- can vaccinate wild life Reassortant virus vaccines . Different genomes from different viruses. Seasonal types of flu. Hybrid viruses that express proteins of multiple types of strain. DNA vaccines: not every effective – difficult to get it into the nucleus and the plasmids will be degraded. Edible plants-profalactic: effective, cheap, and good for developing countries Plant cells infected with bacteria that has the infectious gene. 7.8- Do not vaccinate immunosuppressed host Even if its an attenuated virus- can cause infection in an immunosuppressed host/person So how do you protect an immunosuppressed host as those with : cancer, transplant patients, HIV infected individuals Never use live vaccine or attenuated vaccine Vaccine side effects Allergies Preservititve/ additives can cause allergies and immune response Vaccinosis Ways which the vaccine is delivered Experimental vaccines often fast tracked Preclinical- stage 1 – animal studies CIinical- Phase 120-80: healthy indivisuals, is there adverse response Pase 2 – 100-200: does immune response happen. Increase neutralizing agents placebo included Phase 3- full scale, vulnerable population, 100-1000- placebo included Phase 4: Available to public but monitored for safely / side effects 2-10 years for full process many companies work on influenze, childhood vaccines- large market 7-1 Ebola virus highly viremic but absense of phagocytes to fight infection and NO antibody response, inhibits interferon respons Two forms of Ebola GP- Hard to generate vaccine when there is no antibody response. Feb 25, 2016 Chapter 8 What is epidemiology: studies causation of disease, risk factors, transmissibility, what populations are infected, symptoms caused Triad model of disease: host, pathogen environment SARS: example of a pandemic: spread across geographical boundries: associated with travel Epidemic: local outbreak ie. Influenza Endemic: persists at a steady state in certain geographical areas. Zika- south America Sporadic: no associated pattern Morbidity: ability to cause disease Mortality: ability to cause death Incidence: number of new cases: a measure or morbidity. Prevalence: Number of cases in an exhibit population at a specified time. Total cases Carrier: asymptomatic individuals that can transmit the disease to susceptible individuals Incubation time: time between infection of a virus and onset of symptoms. (flu: 1-3 days) dependent on the threshold of infection: the titer of the virus you were infected with Fever, chills everything looks like the flu early on Prodromal period: earliest, non specific signs of symptoms of an illness: fever, chills Convalescence: recovery period: cold, flu short. Ebola: long, more tissue damage Mode of transmission- how an infectious disease is spread or passed on Etiological: causative Etiological agent/ pathogen- disease causing agent Reservoir: the host, what carries the disease. What etiological agent lives, grows, and multiplies (mosquitos) Case definition: a standard set of criteria that is used to identify who has the disease being studied Communicable Period: period of transmission Convalescence: recovery period Zoonosis: any infectious disease transmissible from animal to humans- including vector borne diseases 8.2: history of epidemiology Edward Jenner: observed milkmaids were not badly scarred and disfigured from small pox: they appeared to be immune. Protected due to cross immunity: protection from one virus conferred protection from another virus. He made the first vaccine from lesions on milkmaids. John Snow: Cholera outbreak in London. Three major suppliers of water. 2 of which associated with sewage outlets that would drain into water supply. Less cholera if upstream or away from one water pump. Sewage contamination drains cholera into water supply. Mapped the sick people and water supply. Identified source of contamination. Tracked the source of infection. Florence Nightingale: modernized nursing practices. Mapped mortality rates of British Soldiers during Crimean War. Soldiers were dying from infections instead of wounds. Made a wedge diagram of cause of death. Identified lack of sanitation and hygiene in the hospital caused most deaths. 8.3 Complexities of Disease Transmission Factors associated with increased risk of disease: age(old/young) , sex (HTLV effects women) , race, immune, nutrition, behavior Pathogens: stability in the environment (hanta virus), virulence factors, immune evasion, drug resistance , enhanced mode of transmission Environment: how many susceptible hosts, population density, sanitary conditions, climate change, environmental changes(esp. vector borne) , blood products (HIV blood supply), geographical locations, zoonotic infections Modes of transmission: airborne, direct contact, fecal oral, mosquito vectors, Chain of Infection: How to break the chain: starilization of fomites, rapid identification, sanitation, barrier techniques, hand washing, waste, aseptic techniques, identify high risk individuals. Concept of Herd Immunity: Reduce number of risked people. Vaccinated people. If people avoid being vaccinated: more susceptible individuals 8.4 Epidemiology today: What epidemiologists wants to know: Case definition, Person, place, time, risk factors Descriptive studies are observational Restrospective: past Cross sectional/prevalence: present Logitudinal/prospective: future Football game spread of disease: Norwalk virus Quarantine: isolation of individuals War and Religion impact of viruses Sitenal chicken surveillance program March 1, 2016 Baby fae did not have tissue rejection Sushruta- rhinoplasty Hippocrates- recorded symptoms of disease Galen: a heart can beat outside the body Da vinvi: anatomical drawings. Improved by Vesalius who dissected human cadavers Vasalius: The father of modern anatomy Edward jenner: vaccine small pox Louis Pasteur: first attenuated vaccine Robert Koch: developed stiteria for classifying infectious agent Elizabeth Black well: 1 woman to go to American college of medicine Emily Jennings Stowe: first female physician in Canada to attend medical school Retrovirus: can only infect dividing cell: HIV, HTLV- virus also infects dividing cell- nuclear envelop dissolves to transport the particles into the nucleus of the host cell. They integrate randomly and can lead to tumors and cancers. Can also lead to silencing of gene expression Adenovirus: dividing an nondividing cells. Stimulates cells to divide. Do not integrate in genome in the host. Maintain in episomes in the host. Therefore, the cells will discard the genetic material. Also can cause an immune response. Common for generating vaccines- then can look at the immune response Adeno-associated virus: satellite virus dependent of adenovirus (helper virus). Had targeted integration into genome of the host Herpes simplex virus: large genome, can infect cells of the nervous system. Causes immune response Vaccinia or MVA pox virus: replicate in cytoplasm- amount an immune response- good for vaccine. Limited repeat treatment REPLICATION DEFECTIVE PARTICLES** Virusees are engineered so that they cannot replicate and destroy or harm cells of the patient. One round of infection.  March 3, 2016 Porcine can shed infectious viruses Rabies: zooinotic infection from transplants Rabies can persist at the site of the bit and in the nervous system for years No treatment for clinical rabies History of Cancer Viruses and Tumors: It is not the goal of the virsus to transform the cell Cancer causing viruses induce cell proliferation: proviral replication Virus introduces cell proliferation to replicate their genome without expressing many viral proteins which allows it to hide from the immune system Chimney Sweep scrotal cancer carcinogens can cause cancer Viruses cause cancer: Retrovirus: Rous Sarcoma Virus Sarc is a tyrosine kinase in growth factor receptor signaling Oncogene= positively deregulates cell growth and proliferation: have the ability to drive cell division 10.2- Major Viruses that cause cancer in humans Hepititus B/C virus, HPV- cervical Cancer EBV- infectious mononucleosis and lymphomas Kaposi Human T-lymphotropic virus type 1 Cancer Bio Terms: Oncogene=a gene that has the potential to convert to a normal cell to a cancerous or transformed cell c-onc= cellular oncogene v-onc= viral oncogene- a viral gene responsible for the oncogenicity of the virus proto-oncogenes- cellular genes that promote cell growth and proliferation viruses can induce genomic instability cancer- malignant phenotype- invasive- and can spread to secondary sites telomeres are repetitive sequences that cap the chromosomes and stabilize the genome lose cap fusion Changed in metabolism- rapid growth Telomere cap becomes stable, don’t lose telomere ends- immortalization Cancer not recognized in the immune system because derived from self tissues Human tumor cells into nude mice because they don’t have a thymus- no immune response 10.3 How do viruses cause cancer-moleular m In addition to genes involved in replication – SRC causes transformation ALV picked up SRC RSV 2 major mechanisms for viruses to cause cancer 1) Insertional mutagenesis: insertional activation of a cellular proto- oncogene – promotor protein protooncogene instead of viral genes 2) Integration of DNA that contains a viral oncogene (RSV): integration of proviral DNA containing a v-onc 3) PDGF receptor- ability of cells to recruit a blood supply Oncogenes of viruses- transcription factors Not homologs of cellular genes EBV- induces cell proliferation- destabilized genome- maintaine episome copies in the genome EBV- infectious mononucleosis- the kissing disease. Lytic vs latent form of disease ELEVATED COUNT OF B CELLS – WBC coult- shedding virus Who gets Burkitt lymphoma- associated with molar tooth development and pathogens Latent infections Chromosomal 8- c-myc gene mutation  drives proliferation of these cells KSHV causes rare skin cancer- also causes B cell lymphoma Hepatitus B Virus (HBV) Hepatocarcinoa Hepititus due to the immune response *HBYOne of the first vaccines to prevent cancer caused by virus HPV Hpv- more than 100 kinds- mainly cause benign infections and tumors called papillomas High risk hpv- genital warts- spread certain types of High risk- cause cancer- cervical, vulva, vagina, anus and penis cancer types 16/18 Low risk0 warts papilloma Memebers of the papova virus family Non enveloped Icosahedral DNA CIRCULAR DNA GENOME Early, immediate early, late Late gene: structural genes Early: regulatory: transcriptiom How does HPV cause tumors HPV lies dormant in the dermal cells even if you get it frozen off, it can come back Keratin- connective protein associated with differentiation Skin cells are dead cells without intact nucleuses Warts: highly infectious because they shed virus particeles. Differentiated cells spreads virus particel Undiffentiated cells hold the virus but do not spread until they have been differentiated Cervical cancers/head and neck cancers Benign cancers become a transformed HPV destabilized the genome- inactivate P53 and Rb HPV allows cells to proliferate in the presence of carcinogens. Esophogyl cancers have a very high morality rate because generally far along when discovered Tree man Generalized verrucisis- repeated surgeries to remove outgrowths Low risk papillon virus in an immune suppressed patients can Produced keratinized epithelium and systemic tumors all over the outside of the body 10.6 March 15, 2016 Not enveloped DNA virus SV40 – circular ds DNA virus Early proteins: transcription factors and replication factors large T and small T antigens Late proteins: VP proteins that form the capsid – VP1,2,3 Small t: lytic effect Large T: oncogenic transformation and cell proliferation SV40- nonhuman 1 Oncolytic viruses and viral therapies will not be tested on Only transforming viruses March 17, 2016 Chapter 11 POLIO Test will cover CH 7- CH 12 Fecal contamination – more polio virus infection Nigeria, Pakistan, afganistan  no vaccine Or vaccine associated polio from attenuated vaccines Oral route or oral fecal contamination and in saliva 95% of all polio virus infection are asymptomatic but are still shelding virus stiff neck, back and legs in mild form less than 1%, major form of disease (in high populations, this is still a lot) motor neurons destruction , flaccid paralysis- systemic weekness recovery can take up to two years and still be incomplete Three Forms of Major Illness 1) Spinal paralysis: more common: asymmetric paralysis- occurs on one side 2) Bulbar Paralysis: ipper spinal chord- more serius because effects breathing, swallowing, many patients but on iron lung or respirator 3) Bulbospinal- combination of spinal and bulbar paralysis PPS- disease return Atrophy of muscle tissue and deterioration of the muscle Muscle fibers affected from the primary disease  nerve endings also begin to die  permanent weakness Treatment: pain management, inflammation repression, anti nerve gas New nerve endings recovery  regenerated muscle function  muscle degeneration  new nerve degeneration Classification and structure of poliovirus 4 major coat proteins, icosahedral self assem non enveloped, no glycoproteins or lipid bilayer highly resistant to stomach acid- acid stable extrememly difficult to denature a virus particles chlorine can denature these types of particles +ssRNA genome same orientation of mRNA therefore *genome is infectious highly stable, very difficult to denature resistant to many proteases, detergents (bc no lipid bilayer), alcohol, pH, either, chloroform, disinfectants, etc. can persist for a long time outside of body 10.5 most common method: isolate cirus from stool sample pathogenic in any human or monkey kidney cell lines cytopathic affects (lysis of the cell zones of killing causing plaque formation) antibodies can be used to identify specific subtypes- no cross reactivity genomic sequencing can also be used 11.6 Cellular Pathogenesis humans and nonhuman primates are the only known natural hosts of polio viruses they do not infect other experimental animals because they don’t have the poliovirus receptor Once polio is in the body, it will replicate into Peyer’s patches- immune of the gut  primary viremia and tonsils and route to lymph to the blood stream infects secondary organs (muscle and motor neurons)  secondary viremia of the CNS associated meningitis and encephalitis Inflammation attacking the motor neurons. Immune system will recognize the infected neurons and attack them March 22 Polio- non enveloped, no glycoproteins- major capsid proteins- VP1,2,3,4 VP4 taken in via receptor mediated endocytosis Replicated in cytoplasm of the cell Encodes an rna dependent rna polymerasw VPg viral protein associated with genome Polio virus uses IRES Cap independent translation Polio is highly cytopathic kills cells Eif4g cleaved Neg strand RNA is a replicative intermediate 1) Translation of viral proteins (before this remove protein primer) 2) Self assembly mechanism Polio Treatment Neurons do not divide in culture Attenuated- weaked and permissive in non host More closely resembles actual particle. Your immune system is continuously exposed Eradication: 2 very effective vaccines, no animal reservoir (other than non human primates) 95% of polio infection are asymptomatic so a lot of infected animals are shedding virus even though we don’t see symptoms Roadblocks: Highly contagious Afghanistan, Pakistan, and Nigeria endemic because refusal to get vaccine 11.11 Other Enteroviruses you can make viruses using synthetic material dual use research- biology of virus or agents of bioterrorism influenza 8 genomic segments negative strand orientation single stranded lipid bilayer 2 main proteins: Ha and N hemoglutinin, neurominidase specific viral infection: the flu seasonal epidemic and pandemic throughout history only vaccinate major subtypes, so if segment exchange occurs and there is recombinance, not protected against during vaccination ability of avian or swine flu to replicate in ferrits closely resembles that of humans quick symptom onset (unlike SARS- very long) respiratory and droplet spread up to a million particles symptomatic people tend not to stay at home lack of herd immunity mostly weakened immune system: children and elderly: more susceptible to infection Spanish flu infected healthy people who are usually very healthy Infections of one time doesn’t protect u against the others Shift- different species exchange Drift- same species mutation Cellular atruism- ei inate cell enore it causes further infection Cytokine storm kills infected cells Laboratory adapted strains don’t resembleit in the interview Pleomorphic particles spiral 8 genomic segments  bigger Conformational change activating fusion peptide from the endosome fusion more pulling lipid bylayers together Aidificaiton of edndosome, activated fusion peptide Replicates in the nucleus of the cell * 80/20 more hemagglutinin than neuraminidase M2 ion channel, H+ pump Bring RNA dependent RNA POL Ha synthesyses as a Ho precursor Naming of influenza virus** Type A, B, C Species that it is isolated from (if humans- it is left blank) Place of isolation Strain designation Year isolation H#N# subtypes Avian influenza outbreaks- where most viruses originate: allow genetic shift and recombination Neuominidaes prevents clumping of virus particles NS2 carrys virus out of the nucleus and into the cytoplasm- chaperone Lower pH, comofrmational change, activates fusion peptdes, uncoats virus parti Important in fusion and uncoating Cap snatching- taken from cellular RNA to use on viral RNA cytopathic effects because no more cellular transcription Concentration of nucleocapsid determines replication PB2 snaches cellular caps and PB1 binds to viral transcrips so that the viral transcripts are not suceptibl to cleavage HTLV EBV Immune pressure, immune selectivity- very homogenous Lab adapted strains 1) Cellular altruism- infected cell and surrounding cell 2) Morbitity-severity/symptoms of disease/mortality 3) Triad model of disease 4) Zoonozooinosis 5) What cells transformed in Burkits lymphoba- B cells 6) ATL caused by HTLV March 29, 2016 Influenza Virus has ability to modulate splicing to produce different protein products NS1: evading interferon response Binds to sialic acid receptor Endosome gets acidified by M2 protein * NS2 chaperone protein that exports RNP out of the nucleus Cleaving sailic acid from cells prevents clumping (neuominidase removes sailic acid) HA would otherwise bind and cause viral clumping Duplex RNA during influenza infection ** The genome is negatively stranded make a plus strand intermediate double stranded intermediate activates PKR Infectious viral particle: at least one copy Tamiflu inhibits the function of Neurominidates, cant remove salic acid, clumps RNA viruses undergo mutation with very high frequency: no proofreading Genetic Drift occurs due to mutations made because of the RNA dependent RNA polymerase which doesn’t have proofreading Therefore because segmented and RNA virus with genetic drift, there is not necessarily herd immunity against influenza virus Antigenic shift: segment exchange by two different viruses hybrid virus (can alter tropism) Responsible for pandemic strains – more than one country – crosses boundries, viral reassortment- every form of influenza can replicalte in water fowl 2009 outbreak- less pathogenic than normal flu- killed less people Antigenic drift: subtle changes in plasticity (HA protein)  responsible for seasonal influenza strains Both can change properties and Epidemic- larger than normal outbreak 2009 H1N1 Swine influenza Genetics avian, human, and porcine viruses coinfected a host porcine of 4 different hybrids  proteins from all four strains, originated in mexico. But not as pathogenic as normal seasonal flu segment reassortment taken place Timeline of pandemic strains Can never completely eradicate a virus because there are multiple hosts it can infect China May be an incubator for flu virus Dense population of humans and animals Close association of humans with animals and birds- slaughter in marketplace, allows spread of disease. Why is influenza seasonal: Aerosol spread is dependent on humididty and temperature. unknown humidity and low temperature Whether prevents dessication of virus Spanish flu, major pandemic outbreak Able to regenerate pandemic strains we don’t vaccinate against therefore we are able to predict there will be another flu outbreak that wont be vaccinated against. H1N1 >20million Spanish Flu High mortality: killed more people than AIDS in 25 years, and than middle age plauges 20-50 million deaths 7X WW1 true estimates will never be known Characterizing feature: infected young, healthy adults (20-40yoa) Killed in 2-3 days Those infected suffered from hemorrhagic symptoms Could not be isolated because wasn’t stable from temp and dessication Sequencing was done on the virus and regenerated It was an AVIAN strain- not swine Highly pathogenic 2007- Yoshihiro Kawaoka BSL4 lab infecting macaque with reconstructed 1918 influenza cirus Died of SIRS- cytokine storm – infliltrate the lungs cytokines massive tissue damage 1968 Hong King Flu flu scare 2009 H1N1 Swine Flu infected young, healthy individuals older people not infected so younger people had no immunity. Older people may have been around for older pendemics that has made H1N1 antibodies to neutralize before 189-57 10-19 years of age


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