7 Evolution and Emergence of New Viruses Flashcards
Q: Why do viruses evolve so fast? (3)
A: Replicate Fast
Replicate in Large Numbers
High Mutation Rate
*Q: What is a quasispecies (in terms of HIV)? (2)
A: Within a single infected person, you will get HIV genomes which are slightly different because they evolve while they are in the host
=group of viruses related by similar mutations competing within a highly mutagenic environment
Q: What may a virus encounter during replication? Result?
A: Bottlenecks (limiting conditions)-> only one or two of the quasispecies genomes will make it through -> create a whole new quasispecies in another host
Some mutations will improve viral replication and some will emerge to be more predominant than others
*Q: What has relative fitness got to do with drug resistance?
A: could gain a mutation which makes it resistant to a certain drug -> but in doing so could become crippled and no longer be able to replicate and therefore not pass on resistance gene
*Q: What would monotherapy of HIV result in? How would we prevent this? Today?
A: proliferation of a resistant population of HIV (just needs a single mutation to do this)
give a combination of antiviral drugs that target different parts of the HIV life cycle eg protease inhibitors
for a virus to be resistant, it would need 5 or so simultaneous mutations which is unlikely
use HAART
*Q: What is antigenic drift? solution for flu virus?
A: process of antibodies driving evolutionary change over time
vaccine is updated every year to best represent the circulating strains
*Q: Describe antibodies as a selection pressure for evolution. (3)
A: If a person is infected with a virus for which the patient already has antibodies for HA, then the person is immune and protected
BUT, if the person infected has a subneutralising amount of antibody - the virus will replicate in that person and only the fittest viruses survive - ones which change their spike proteins
(antibodies target specific aa sequence on virus so if that sequence were to change-> resistant and become the dominant strain)
*Q: What do rhinoviruses not show? Result?
A: don’t show antigenic drift -> undergo evolutionary expansion but all continue to circulate at the same time
likely to catch many of them in your lifetime = difficult to treat
*Q: How do new viruses emerge? (5)
A: Zoonosis = from animals (adapted to become human viruses)
- Genetic Variation (would require some level of)
- Increased Exposure - travel or world population (often caused by)
- Increased Exposure - spread of vector
- New Discoveries
Q: What are the global influences of emerging infections? (7)
A: -Environmental modifications/demographics
- World population
- Climate change
- Travel
- Farming practices; monocultures
- Immunosuppressed humans
- Medical progress
*Q: What are arboviruses? Example of virus type? 4 examples. Vector? Concern?
A: class of viruses transmitted to humans by arthropods such as mosquitoes and ticks
flaviviruses - single strand positive-sense RNA genomes
- Yellow Fever
- Dengue
- West Nile
- Chikingunya
Mosquito host (replicate within the mosquito) -global warming leads to an increase in the global distribution of mosquitoes
*Q: What’s the vector of the West Nile Virus? Host? Type of virus? causes?
A: Culex tarsalis (mosquito)
bird and mosquito virus that can occasionally affect humans and horses (replicate in us and cause death)
Belongs to Japanese encephalitis group of flaviviruses - cause disease by going to the brain
Q: What is a dead end host? example?
A: With some of these arboviruses, humans and horses are dead end hosts - it doesn’t spread any further
*Q: Describe the outbreak of West Nile Virus was found in New York. RT-PCR showed? Why does it still remain today?
A: hot summers day with lots of mosquitoes in NY
Some elderly people succumbed to a brain disease - crows and birds at the zoo became ill
RT-PCR showed that the virus originated from Israel
in wild bird resevoirs
Q: What is dengue? Describe the process of being infected with it. Serotypes?
A: arbovirus that causes aches and pains usually (first time)
vector= Aedes aegypti mosquito that bites infected human and spreads to someone that’s not (replicates inside mosquito)
4 for dengue virus
Q: What happens the first time you get dengue viral infection? 2nd? Name?
A: you are sick but not that sick (aches and pains)
If, the second time you get infected, you get infected by a different serotype - then the antibodies you developed the first time will make you MORE sick = Dengue Haemorrhagic Fever
This is called Antibody Dependent Enhancement of the Infection
Q: Why is dengue hemorrhagic fever DHF on the rise?
A: correlates with spread in mosquito population
Q: What are the risk factors for reported dengue hemorrhagic fever DHF? (4)
A: -Virus strain
- Age
- Higher risk in secondary infections (Pre-existing anti-dengue antibody (from previous infection/maternal antibodies in infants))
- Higher risk in areas where there are two or more serotypes circulating simultaneously at high levels (hyperendemic transmission) -> needs at least 2 serotypes to get DHF
Q: What is a serotype?
A: serologically distinguishable strain of a microorganism
Q: Describe the 2 effects of dengue viral antibodies. Leads to? (2)
A: can either neutralise infection or enhance infection
neutralise: become infected with one serotype-> produce homologous antibody for it-> bind the antibodies TIGHTLY and stop it from entering the cell
enhance infection: infected with a different serotype-> antibodies bind to it but don’t neutralise-> instead viruses are given another way of getting into the cells
Q: What is the zika virus? In unborn babies?
A: arbovirus carried by mosquitoes
they have acquired ability to cross placenta and infect foetus-> cause microcephaly (small circumference of head)
Q: How did the zika virus gain neurovirulence? (2)
A: mutations
- may have changed outer parts-> given ability to enter neuronal cells (acquired tropism)
- could have mutation in non coding region of RNA-> interferes with protein in neuroprogenitor cells called MS1 which has function of expressing MCPH1 which allows development of mature neurons
Q: What is chikingunya? Main symptoms. (3)
A: alpha virus associated with prolonged arthralgia (joint pain) for months even years
- muscle aches
- joint pain
- back ache
*Q: What is zoonosis? Examples. (2) Transmission? examples? (4)
A: a disease which can be transmitted from animals to humans (viruses from animals transform in humans such that it becomes a real human virus)
- HIV used to be a primate virus but now it is very much a human virus
- SARS-CoV from bats
Some zoonoses have potential to start a pandemic but they do not transmit efficiently
-SARS, Ebola, Hendra and Nipah do not transmit efficiently
*Q: What are human populations at increased exposure to? result?
A: bats to domestic animals to humans -> bats carry lots of disease which can transmit to us inc SARS-CoV
Q: What is SARS? Envelope? ability? Evolved from? Transmission.
A: Severe Acute Respiratory Syndrome
-large CORONAVIRUS - positive-sense RNA genome
Enveloped spike protein
-attach to receptor ACE-2 (human lung)
evolved from bats to civic cats to humans
It was transmitted via respiratory droplets
Q: What amplified SARS infections? Who showed high mortality? Result?
A: Nebulizers in hospitals brought up virus from deep down in the lungs
Elderly people showed high mortality
destruction of lung tissue from overexuberant immune response
Q: Why were we able to control SARS? (3)
A: -can identify who has it and isolate them
- Patients did not become contagious until quite late into the infection once they had become symptomatic
- emergency response was coordinated and rapid
Q: What does MERS cause? in who? (2) Transmission? Method?
A: ARDS (acute respiratory distress syndrome) in older people and those who are immunosuppressed
Zoonosis from camels
Uses DPP4 receptor in the lungs
*Q: What can recombination of 2 or more viruses give rise to? Example. How? Result? (2)
A: new virus with new properties
influenza: lots of serotypes in birds and some have crossed into pigs and humans
method that bird virus (avian) crossed into humans = recombination event called reassortment
-> genome of influenza virus is segmented so if 2 serologically different viruses find themselves replicated in same cell (eg a human one and avian one) -> can get a cross of both viruses -> antigenic shift-> PANDEMIC VIRUS
*Q: Why do you not get antigenic drift in pigs? humans?
A: because pigs don’t live long enough to be re-infected by the virus so the virus stays the same
Humans live long enough to be re-infected so their antibodies can drive evolution
Q: What could be the next pandemic? (2) Compare. (3)
A: MERS
- limited transmission
- civerse clinical signs
- no vaccine, no antiviral
H7N9
- limited transmission
- no vaccine but technology to make one = known
- antivirals but resistance tolerated
*Q: Define host range.
A: range of cells that can act as a host to a virus or bacteriophage
Q: Why does zoonosis not often happen? explain.
A: there is a host range barrier
means that most viruses are compromised in their ability to replicate and spread in humans due to the genetic differences between host factors the virus needs
Q: What are noroviruses? occurrence?
A: small RNA viruses that cause diarrhoea and vomiting
increase of them in recent years
