7 Evolution and Emergence of New Viruses Flashcards Preview

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Flashcards in 7 Evolution and Emergence of New Viruses Deck (35)
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1
Q

Q: Why do viruses evolve so fast? (3)

A

A: Replicate Fast

Replicate in Large Numbers

High Mutation Rate

2
Q

*Q: What is a quasispecies (in terms of HIV)? (2)

A

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

3
Q

Q: What may a virus encounter during replication? Result?

A

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

4
Q

*Q: What has relative fitness got to do with drug resistance?

A

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

5
Q

*Q: What would monotherapy of HIV result in? How would we prevent this? Today?

A

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

6
Q

*Q: What is antigenic drift? solution for flu virus?

A

A: process of antibodies driving evolutionary change over time

vaccine is updated every year to best represent the circulating strains

7
Q

*Q: Describe antibodies as a selection pressure for evolution. (3)

A

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)

8
Q

*Q: What do rhinoviruses not show? Result?

A

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

9
Q

*Q: How do new viruses emerge? (5)

A

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
10
Q

Q: What are the global influences of emerging infections? (7)

A

A: -Environmental modifications/demographics

  • World population
  • Climate change
  • Travel
  • Farming practices; monocultures
  • Immunosuppressed humans
  • Medical progress
11
Q

*Q: What are arboviruses? Example of virus type? 4 examples. Vector? Concern?

A

A: class of viruses transmitted to humans by arthropods such as mosquitoes and ticks

flaviviruses - single strand positive-sense RNA genomes

  1. Yellow Fever
  2. Dengue
  3. West Nile
  4. Chikingunya
Mosquito host (replicate within the mosquito)
-global warming leads to an increase in the global distribution of mosquitoes
12
Q

*Q: What’s the vector of the West Nile Virus? Host? Type of virus? causes?

A

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

13
Q

Q: What is a dead end host? example?

A

A: With some of these arboviruses, humans and horses are dead end hosts - it doesn’t spread any further

14
Q

*Q: Describe the outbreak of West Nile Virus was found in New York. RT-PCR showed? Why does it still remain today?

A

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

15
Q

Q: What is dengue? Describe the process of being infected with it. Serotypes?

A

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

16
Q

Q: What happens the first time you get dengue viral infection? 2nd? Name?

A

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

17
Q

Q: Why is dengue hemorrhagic fever DHF on the rise?

A

A: correlates with spread in mosquito population

18
Q

Q: What are the risk factors for reported dengue hemorrhagic fever DHF? (4)

A

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
19
Q

Q: What is a serotype?

A

A: serologically distinguishable strain of a microorganism

20
Q

Q: Describe the 2 effects of dengue viral antibodies. Leads to? (2)

A

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

21
Q

Q: What is the zika virus? In unborn babies?

A

A: arbovirus carried by mosquitoes

they have acquired ability to cross placenta and infect foetus-> cause microcephaly (small circumference of head)

22
Q

Q: How did the zika virus gain neurovirulence? (2)

A

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
23
Q

Q: What is chikingunya? Main symptoms. (3)

A

A: alpha virus associated with prolonged arthralgia (joint pain) for months even years

  • muscle aches
  • joint pain
  • back ache
24
Q

*Q: What is zoonosis? Examples. (2) Transmission? examples? (4)

A

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

25
Q

*Q: What are human populations at increased exposure to? result?

A

A: bats to domestic animals to humans -> bats carry lots of disease which can transmit to us inc SARS-CoV

26
Q

Q: What is SARS? Envelope? ability? Evolved from? Transmission.

A

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

27
Q

Q: What amplified SARS infections? Who showed high mortality? Result?

A

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

28
Q

Q: Why were we able to control SARS? (3)

A

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
29
Q

Q: What does MERS cause? in who? (2) Transmission? Method?

A

A: ARDS (acute respiratory distress syndrome) in older people and those who are immunosuppressed

Zoonosis from camels

Uses DPP4 receptor in the lungs

30
Q

*Q: What can recombination of 2 or more viruses give rise to? Example. How? Result? (2)

A

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

31
Q

*Q: Why do you not get antigenic drift in pigs? humans?

A

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

32
Q

Q: What could be the next pandemic? (2) Compare. (3)

A

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
33
Q

*Q: Define host range.

A

A: range of cells that can act as a host to a virus or bacteriophage

34
Q

Q: Why does zoonosis not often happen? explain.

A

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

35
Q

Q: What are noroviruses? occurrence?

A

A: small RNA viruses that cause diarrhoea and vomiting

increase of them in recent years