9.23 RNA viruses part 2 – Flashcards
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| What family of viruses is influenza a part of? |
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| orthomyxovirus |
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| What's the significance of the name orthomyxovirus? |
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| ortho= straight, myxo= mucus |
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| Describe the genome and protein covering of the influenza virus. |
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| enveloped helical (pleomorphic) virus with RNA SS - with multiple genomic segments |
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| What are the three major types of influenza virus? |
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| A, B, and C |
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| Is influenza prone to zoonoses? |
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| influenza naturally infects a variety of species particularly type A |
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| How many gene segments do influenzas A, B and C have? |
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| A- 8, B- 8, C-7 |
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| Which species do each influenza type infect? |
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| A= humans, swine, avian, equine, marine mammals B= humans only C= humans, swine |
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| List the different major influenza types from most to least severe. |
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| A (often severe)> B (occasionally severe) > C (usually mild) |
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| Describe the epidemic potential of influenza A. |
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| extensive; epidemics and pandemics (antigenic drift and shift) |
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| Describe the epidemic potential of influenza B. |
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| outbreaks; occasional epidemics (antigenic drift only) |
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| Describe the epidemic potential of influenza C. |
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| antigenic drift only |
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| What is the purpose of hemagglutinin? |
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| binds sialic acid for entry of the virus |
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| Describe the structure and different types of hemagglutinin. |
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| trimer; highly variable; H1-9 with 16 HA subtypes |
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| How are the HA subtypes of Hemagglutinin important in the function of the virus? |
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| HAO cleaved into HA1 (used for attachement) and HA2 (used for fusion) |
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| What is the purpose of neuraminidase? |
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| cleaves sialic acid during release |
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| How many different neuraminidase types are there? |
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| N1-N2 in humans (9 NA subtypes in birds) |
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| Neuraminidase is used as a target for which drugs? |
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| tamiFlu and Relenza |
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| Which viral flu protein accumulates mutations in each infection such that the virus out is not the same as the virus in/ |
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| HA protein |
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| T/F Genetic reassortment is easier for flu than other viruses. |
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| true |
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| How does the influenza virus endter the cell? |
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| receptor mediated endocytosis, then acidic environment in endosome allows release of viral particles which go to the nucleus |
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| What is the function of RNA segment 1 for influenza A? |
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| PB2- RNA synthesis ?virulence |
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| What is the function of RNA segment 2 for influenza A? |
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| PB1- RNA synthesis |
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| What is the function of RNA segment 3 for influenza A? |
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| PA- RNA synthesis |
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| What is the function of RNA segment 4 for influenza A? |
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| HA- Attachment |
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| What is the function of RNA segment 5 for influenza A? |
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| NP: RNA synthesis |
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| What is the function of RNA segment 6 for influenza A? |
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| NA- virus released from cell |
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| What is the function of RNA segment 7 for influenza A? |
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| M1, M2- Matrix |
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| What is the function of RNA segment 8 for influenza A? |
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| NS1, NS2- nonstructural (NS1, INF antagonist) |
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| Describe antigenic shift. |
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| Sudden. Emergence of "new" H or N subtype in the human population. Occurs every 10-40 years. Little or no herd immunity to new flu and probably emergence from domestic animals |
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| Describe antigenic drift. |
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| 1) incremental 2) emergence of varient H subtype in humans 3) occurs every 2-3 years 4) accumulation of mutations evades herd immunity 5) probably emergence within humans |
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| Describe influenza nomenclature. |
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| virus type/geographic origin/strain number/year of isolation (virus subtype) |
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| What is the only infectious disease capable in a pandemic year of increasing the world death rate? |
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| influenza via antigenic shift |
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| Name the major flu pandemics in the past century. |
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| 1918 Spanish flu, 1957 Asian Flu, 1968 Hong Kong flu (1977 Russian Flu, and 2009 Swine-origin H1N1) |
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| What modifications must be made to the viral RNA before it is able to be transcribed by host ribosomes? |
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| "cap snatching"- PB1 protein takes 5' cap and about 10 nucleotides from host mRNA and puts it on viral RNA |
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| Which protein is responsible for making + ssRNA from influenza genomic - ssRNA? |
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| RNA polymerase activity of PB1 protein |
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| Which enzyme is responsible for making new copies of influenza viral genome from +ssRNA? |
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| PB1 protein |
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| How do influenza progeny leave the host cell? |
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| budding from the host cell |
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| In a hemagglutination Inhibition Assay, what happens to RBCs not bound by the influenza virus? |
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| they sink to the bottom of the well to form a button |
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| Where/when was the first case 2009 novel H1N1? When was it pandemic and when did the pandemic officially end? |
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| April 2009 in Veracruz Mexico. Pandemic peaked in Nov 2009 and officially ended in August 2010 |
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| How many deaths, hospitilizations, and infected people were there in the 2009 H1N1 pandemic in the US? What population had the highest number of cases? |
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| 20,000 deaths, 270,000 hospitlizations, 43-89 million infected people, highest number of cases in 18-65 year olds |
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| What is swine origin influenza H3N2? |
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| virus resulting from genetic re-assortment of 2009 H1N1. 4 cases in children in Indiana and Pennsylvania (3 had contact with swine). All recovered and no person to person transmission noted |
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| T/F Influenza is limited to the respiratory tract. |
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| true! tracheitis! |
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| How does influenza damage the host? |
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| multiplies in ciliated respiratory epithelium cells which causes cell damage which elicits an acute inflammatory response and impairs mechanical and cellular host responses. This damage renders the host highly suceptible to invasive bacterial superinfection |
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| How does influenza pave the way for secondary bacterial infection? |
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| damages host cells/defenses and bacteria actually adhere more redily to the surfaces of influenza virus infected cells |
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| Production of what cytokine begins recovery from influenza infection? |
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| interferon |
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| A rare complication can occur in young children with influenza who are treated with salicylates that is called.... |
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| Reye's syndrome |
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| What percent of the US population gets the flu each year? |
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| 5-20% (more than 200,000 people hospitalized) |
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| How many people die of the flu each year? |
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| annual flu associtaed deaths range from 3,000 to 49,000 |
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| Why was the 1918 flu so devastating? |
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| rapid dissemination from the URT to the LRT inducing a cytokine storm that causes inflammation and increased mortality |
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| What is the "high dose" flu vaccine? |
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| for people 65 and older, IM, has 4x antigen, first available last year |
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| What is the intradermal flu vaccine? |
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| inactivated flu vaccine for people between 18 and 64 that is injected into the dermis |
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| Describe the live attenuated flu vaccine. |
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| a nasal spray recommended for "healthy" people aged 2 through 49 years of age who are not pregnant |
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| What's in this years flu vaccine? |
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| A/California/7/2009 (H1N1) A/Perth/16/2009 (H3N2) B/Brisbane/60/2008 |
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| Describe the drug Amantidine/Rimanditine. |
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| antiviral for influenza A that targets the M2 ion channel and blocks fusion. It is adminstered orally and resistant strains are emerging |
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| How does Relinza/Zanamivir work? |
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| its a influenza A and B antiviral that targets virus release by inhibiting NA. It is inhaled and resistent strains are emerging |
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| Describe Tamiflu/Oseltamivir. |
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| influenza A and B antiviral that targets virus release by inhibiting NA. It is administered orally and resistant strains are emerging |
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| What is the mortality rate of bird flu? |
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| 58% |
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| How is avian flu transmitted? |
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| bird to human transfer (which is rare) with limited human to human transmission |
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| What will cause Bird Flu to become a human pandemic virus? |
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| better binding to human configuration of receptor neuraminic acid by HA, better replication and enhanced production of progeny virus in humans (diverse genes), better processing of viral RNAs and proteins (diverse genes ), Can be achieved either by mutation or recombination with current cirvulating human strains of H1N1 or H3N2 |
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| Contrast human alpha 2,6 tropism and alpha 2,3 tropism. |
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| 2,6= high transmission, low virulence 2,3= low transmission and high virulence |
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| Describe the genome and protein covering of arena viruses. |
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| enveloped helical (pleomorphic) with segmented RNA genome (1 large negative RNA segment, one small ambisense strand), Two seperate nucleocapsids surrounding the L and S RNA. |
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| WHat gives arena viruses a "sandy" appearance? |
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| virion contains host cell ribosomes |
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| Arenaviruses are transfered to humans zoonotically from... |
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| rodents |
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| What are some examples of Arena viruses? |
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| lymphocytic choriomeningitis virus, hemorrhagic fevers (lass fever virus, Junin, machupo) |
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| Where from the host are arena viruses shed? |
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| urine or droppings |
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| How do humans get arena viruses? |
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| contact with excretions of an infected rodent (ingestion, direct contact of abraded skin, aerosol transmission from rodent urine or saliva |
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| Which arena viruses are associated with secondary person-to-person and nosocomial transmission? How does this occur? |
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| lassa and Machupo; direct contact with blood or other excretions containing virus particles, airborne transmission from contaiminated material (medical equipment) |
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| How does lymphocytic choriomenigitis present? |
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| most are asymptomatic or mild febrile illness. biphasic febrile illness: 1)fever malaise, lack of appetite, muscle aches, headache, nausea for a week; 2) meningitis or encephalitis |
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| What congenital issues occur with transplacental infection of LCM? |
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| hydrocephalus, chorioretinitis, and mental retardation |
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| How long after exposure do symptoms of LCM occur? |
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| 8-13 days |
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| What is the primary host of LCM? |
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| mus musculus (common house mouse) 5% of mice in US infected without sings of illness. |
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| Can you get LCM from your pet hamster? |
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| possibly but rodents other than the mice are not natural reservoirs for the disease. However other rodents can be infected via breeding colonies like in a pet store |
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| Are humans more likely to get LCMV from their pets or from a house mouse? |
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| house mouse but infectious from pet rodents have also been reported |
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| Can LCM be transmitted from person to person? |
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| only "vertically" (through placenta) possible transmission via organ transplantation |
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| What is the prognosis of LCM? |
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| most recover completely, mortality is less than 1% |
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| What is the tx for LCM? |
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| hospitilization and supportive tx (corticosteroids and other anti-inflammatory drugs) for those with meningitis or encephalitis |
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| What disease does Lassa virus cause? |
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| lassa fever (African hemorrhagic fever) |
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| What diseaes does Junin virus cause? |
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| Argentine hemorrhagic fever |
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| What disease does machupovirus cause? |
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| bolivian hemorrhagic fever |
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| What disease does guanarito virus cause? |
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| venezuelan hemorrhagic fever |
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| What disease does Sabia cause? |
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| brazilian hemorrhagic fever |
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| What are the symptoms of arenavirus hemorrhagic fevers? |
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| fever, hemorrhagic manifestations, shock, neurologic manifestations, hepatitis, acute deafness |
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| How long does viremia and viral shedding occur in arenavirus hemorhhagic fevers? |
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| viremia for > 1 month, viral shedding in urine for > 2 months |
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| What is the prognosis of patients with Lassa fever? |
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| 15-20% of patients hospitalized for Lassa fever die from it. Only 1% of infections result in death |
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| Death rates from Lassa fever/arenavirus hemorrhagic fevers are particularly high for what population? |
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| women in the third trimester of pregnancy--approx 95% of fetuses die in utero |
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| How do you treat arena virus hemorrhagic fevers? |
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| supportive care, IV rabavirin may be helpful |
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| How do you diagnose arenavirus hemorrhagic fever? |
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| travel history, serology (ELISA) for IgM or IgG |
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| Describe the genome and capsid of rabdovirus. |
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| enveloped RNA ss- with helical capsid that is bullet shaped. RNA polymerase and genome are enclosed in matrix protein |
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| Surface glycoproteins of rhabdoviruses are important because... |
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| they allow the virus to attach to host cells and are also the targets of neutralizing antibodies |
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| Give two examples of rhabdoviruses. |
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| rabies and vesicular stomatitis virus |
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| What are the three phases of rabies virus? |
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| prodome, neurologic and comatose |
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| Describe the prodom phase of rabies virus. |
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| 2-7 days: headache malaise |
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| Describe the neurologic phase of rabies virus. |
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| few days: difficulty swallowing, CNS effects |
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| Describe the comatose phase of rabies virus. |
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| upt to 2 months, fatal convulsions |
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| What is the rabies vaccine called? |
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| HDCV (human diploid cell vaccine) |
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| How is rabies infection treated? |
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| passive and active immunization. |
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| T/F Post-exposure vaccination for Rabies virus is possible. |
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| true |
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| How does rabies spread throughout your body? |
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| 1)replicates in muscle, 2)enters periphearl nervous system, 3) passive ascent via sensory fibers, 4)replication in dorsal ganglion, 5) rapid ascent in spinal cord, 6)infection of spinal cord, brainstem, cerebellum etc 7) descending infection via nervous system to eye, salivary glands, skin and other organs |
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| What is happening during the incubation period of rabies and how long does it last? |
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| virus is traveling to the brain within nerves; may last weeks to months |
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| How long does it take after virus has multiplied in the brain for an animal to show signs of rabies? |
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| 3-5 days signs are evident |
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| T/F Besides being bitten by an infected animal, Rabies is also often spread via other routes such as contamination of mucous membranes, aerosol transmission, and corneal and organ transplanatation. |
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| false, although documented, spread of infection in those ways is very rare |
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| Which animal is responsible for most transmission of rabies to humans in the US? |
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| bats |
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| What histological finding is diagnostic for rabies infection? |
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| negri bodies in the brain |
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| How do you diagnose Rabies in a live humna patient? |
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| several tests needed 1) viral isolation or RT-PCR in saliva 2) antibodies to rabies virus in serum or spinal fluid 3) detection of rabies antigen in cutaneous nerves at the base of hair follicles from nape of neck |
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| Who came up with the first rabies vaccine? |
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| pasteur |
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| How do you treat rabies post exposure? |
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| regimen of one dose of immune globulin and four doses of rabies vaccine over a 14 day period (3,7,14) |
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| How is HDCV made? |
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| in tissue culture usuing hormal WI-38 fibroblasts. The rabies virus is then inactivated |
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| Describe the rabies virus used for animals. |
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| live attenuated vaccine (flury strain) grown in chick embryos |
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| What is VRG or Raboral? |
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| recombinant anti-rabies vaccine made by inserting the gene for the surface glycoprotein of rabies into vaccinia virus (used for treating wild animals since it can give herd immunity because its a live virus) |
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| What are the different types of Bunyaviruses? |
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| arboviruses and hantaviruses |
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| Name 3 different arboviruses. |
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| California and LaCrosse encephalitis virus, Rift valley fever |
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| Name two hantaviruses. |
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| Hemorrhagic fever with renal syndrome (HFRS), and Hantavirus pulmonary syndrome (HPS) |
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| Describe the genome and capsid of a hantavirus. |
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| ss RNA - with 3 segments envelope with glycoproteins G1 and G2 |
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| Where is HFRS? |
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| observed in Hantaan, Korea; china Japan, Russia, first described in the 1950s in the Korean War |
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| What do you call the mild version of HFRS? |
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| nephropathia epidemica (NE) (puumala hantavirus) |
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| Which hantavirus is old world? new world? |
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| old: HFRS, new: HPS |
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| What're different types of HPS? |
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| sin nombre virus "four corners virus" or "navajo flu" |
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| Where do you find HPS? |
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| first identified in humans in the US in 1993, western US. Bayou virus in Monroe. BLack Creek Canal VIrus in FL. |
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| HOw do you get hantaviruses? |
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| found in urine and feces of infected rodents but it does not make the animal sick. Transmitted thru aeorsolized rodent excreta. |
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| What population has the majority of HPS mortalities? |
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| 10-60 years old |
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| What is the rodent reservoir of Sin nombre virus? |
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| deer mouse. Has an epizootic cycle |
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| What is the major target organ, first phase, second phase and mortality of HFRS? |
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| Kidney, febrile, shock, 1-15% |
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| What is the major targe organ, first phase, second phase and mortality of HPS? |
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| lung, febrile "prodrome"; shock/pulmonary edema, 50% mortality |
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| Name two filoviruses. |
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| ebola virus and marburg virus |
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| Describe the filoviruses. |
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| cause african hemorrhagic fever, enveloped, helical (filamentous/pleomorphic), SS RNA -, viral GP surface protein mediates entry |
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| Where do you get African hemorrhagic fever (ebola, marburg) from? |
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| zoonoses from bats |
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| What is the disease process of african hemorrhagic fever (ebola, marburg)? |
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| infect endothelial cells with cytopathic effects, blood loss |
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| How do you die of African hemorrhagic fever? What percent of patients die? |
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| hypovolemic shock, > 65% mortality |
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| Name the subtypes of Ebola. |
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| Zaire, Sudan, Reston |
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| Describe the paramyxoviruses. |
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| ss RNA - genome, enveloped, helical capsid |
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| Name the different paramyxoviruses. |
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| respiratory disease (RSV, parainfluenza, metapnuemovirus) mumps and exanthems (measles, mumps) zoonoses (nipah and hendra) |
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| What populations are affected by ReSV? |
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| infants and the elderly |
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| What disease do parainfluenza viruses cause? |
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| croup or acute respiratory disease in young children, 4 serotypes |
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| Describe the envelope of parainfluenza virus. |
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| hemagglutinin and neuraminidase on the same spike |
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| Which parainfluenza serotypes particularly can cause serious disease in infants and young children? |
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| 1 and 3 |
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| What is the course of illness of infection with parainfluenza virus? |
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| mild URI with variable progression over 1-3 days to involvement of middle or lower respiratory tract. Duration of acute illness varies from 4 to 21 days |
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| How do you diagnose parainfluenza viruses? |
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| isolation or antigen detection |
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| How do you treat croup? |
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| no specific treatment |
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| Describe the virion structure of RSV. |
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| similar to parainfluenza virus except that the envelope glycoproteins are an attachment (G) protein and a fusion (F) protein |
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| What are the glycoprotiens on the RSV virus used for? |
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| G glycoprotein mediates attachment; F or fusion glycoprotein induces fusion of viral envelope with host cell surface |
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| What are the different types of RSV? |
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| there are two antigenic subgroups (A and B). Dimorphism is due primarily to differences in the G glycoprotein |
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| What is the major cause of bronchiolitis and pneumonia among infants under 1 year of age? |
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| RSV |
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| How do you detect RSV? |
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| virus isolation, PCR, immunoflouresence, and immunoassays |
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| What parts of the respiratory tract does RSV infect? |
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| bronchi, bronchioles, alveoli (clinically categorized as croup, bronchitis, bronchiolitis or pneumonia) *confined to respiratory epithelium |
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| Who is at risk for contracting RSV besides infants? |
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| elderly and immunocompromised |
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| What is the rate of pts with secondary infection of pts with RSV? |
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| 50% |
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| How long is the RSV virus shed? |
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| 5-7 days; young infants may shed virus for 9 to 20 days |
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| Why is RSV so severe? |
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| TH2 stimulated cytokines cause injury |
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| What are the pathological findings of RSV? |
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| necrosis of epithelial cells; interstitial mononuclear inflammatory infiltrates |
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| What drug is used in severe cases of RSV? |
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| ribavirin |
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| Describe the RSV vaccine. |
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| there isn't one |
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| What is the second leading cause of bronchiolitis in infants and young children? |
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| human metapneumovirus |
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| T/F Reoviruses are ubiquitous and have been found in humans, simians, rodents, cattle and a variety of other hosts. |
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| true |
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| What nucleic acid is found in adenoviruses/bocavirus? |
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| DNA |
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| What type of virus is rubella? |
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| togavirus + ssRNA |
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| How is mumps, measles and rubella spread? |
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| aerosol |
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| Describe the disease caused by the measles virus? |
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| "rubeola" 7 day measles, maculopapular, erythematous rash, Koplik spots, buccal mucosa; largely disappeared in the US |
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| Describe the disease caused by the mumps virus? |
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| epidemic parotitis; once the principle cause of aseptic meningitis; largely disappeared in the US |
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| What populations were susceptible to measles? |
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| 5-10 year old children in old world; unknown to new world and caused death of native adults |
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| Where is the virus located in measles? |
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| initial replication in the URT, proceeding to the respiratory mucosal epithelium, followed by dissemination to distant sites; and T and B cells (resulting in transient immunosuppression). |
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| T/F Measles is highly contagious. |
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| true |
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| How long is the incubation and acute phase of measles? |
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| 1-2 weeks incubation; acute phase < 1 week |
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| What are the symptoms of the measles? |
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| fever, cough, Koplik's spots on the buccal mucosa |
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| What are complications of the measles? |
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| bacterial superinfection, encephalitis, keratitis, orchitis, oophoritis; VERY RARELY will have subacute sclerosing panencephalitis (progressiv neurological and intellectual deterioration) |
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| Where in the body is the Mumps virus located? |
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| initial replication in the respiratory tract and local lymph nodes followed by dissemination to the salivary glands and CNS. Secondary viremia may cause spread to other organs |
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| How long is the incubation period and acute phase of mumps? |
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| incubation: 2-4 weeks acute: 1 week |
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| What are the symptoms of Mumps? |
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| fever, parotitis |
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| What are the complications of mumps? |
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| meningitis and encephalitis, pancreatitis, orchitis, and oophoritis |
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| What virus causes the german measles? |
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| rubella |
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| Where in the body is the rubella virus? |
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| replication in the URT, followed by dissemination to lymphoid tissue, skin and organs |
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| Why is it important to vaccinate against rubella? |
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| can cause fetal damage (cardiac defects, CNS defects, eye defects, deafness, hyperplasia of the liver and spleen) |
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| T/F There is no treatment mumps, measles, or rubella. |
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| true |
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| What is the MMRV vaccine? |
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| measles, mumps, rubella, varicella virus vaccine |
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| What types of viruses are the henipavirus (nipah/hendra)? |
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| zoonotic paramyxoviruses |
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| Where do zoonotic paramyxoviruses come from? |
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| from bats to domesticated animals (pigs and horses) |
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| What are the symptoms of henipavirus (nipah/hendra)? |
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| fever, respiratory distress with pulmonary edema, severe abdominal pain, difficulty swallowing that rapidly progresses to meningitis. >50% of patients become comatose. >60% mortality rate |
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| Describe the coronavirus genome and virion. |
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| enveloped SS + RNA virus. Spike-like glycoprotein projections are petal shaped; give "crown or solar corona" appearance |
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| What virus replicates via "nested" RNAs? |
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| coronaviruses |
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| Neutralizing antibodies and cell-mediated responses for coronaviruses are directed against... |
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| spike-like glycoprotein projections |
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| What kind of diseae do coronaviruses cuase? |
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| URI in humans; very common; usually mild with no severe infection except in pulmonary compromise |
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| How many serotypes of coronaviruses are there? |
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| we don't know |
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| What percent of colds are caused by coronaviruses? |
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| 5-10% of common cold overall 35% in an outbreak epidemics in winter and springtime |
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| Where did SARS began/spread? |
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| Nov 2002 in Guangdong PRC; officially discovered in Feb/mar 2003, exported to Hong Kong and Toronto in major outbreaks. Resolved by quarantine methods |
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| How many cases of SARS have there been worldwide? |
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| >8,000 |
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| What is the mortality rate of SARS? |
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| 10% |
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| T/F SARS-causing corona virus evolved from avirulent human coronaviruses that cause the common cold. |
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| FALSE!!! probs from a very closely related coronavirus found in civet cats |
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| Pathogenicity of RNA viruses is frequently associated with .... |
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| cross species jump |
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| T/F Mumps and exanthem viruses' sole reservoir is humans |
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| true |
