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IIH > Intro to viruses > Flashcards

Intro to viruses Flashcards

1
Q

Why are viruses considered to be intracelluar obligate parasites

A
  • They depend on the host cell for raw materials and energy.
  • They can only replciateom host cell
  • They exist as either an extracellular virion containing DNA or RNA virus genome
  • or as nucleic acid inside the host cell.
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2
Q

What is the general structure of viruses

A
  • always contained in capsid: protects nucleic acid
  • some viruses have an envelope: take part of the cells plasma membrane (smart things)
    • makes it easier for it to infiltrate a human cell
    • a bit like a trojan horse
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3
Q

How do we classify viruses

A

Hard to do so,
but we use baltimore’s classification (this is based on nucleic acids and how they transcribe mRNA

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4
Q

What are the steps of virus lifecycles

pssst there’s 12

A

2.Adsorption

  • have specific glycoprotiens, which interact with specific proteins on the cell
  • for example EBV is only specific for b cells
  1. Entry
  • can directly fuse with plasma membrane
  • or via endocytosis
  1. Capsid transport to the nucleus
  2. Transcription
  3. Translation
  4. Replication
  • needs to replicate new viral proteins, like capsid proteins, so new nucleic acids can be encapsulated for new virions
  1. Capsid assembly
  2. Glycosylation
  3. Glycoprotein export to the cell surface
  4. Endocytosis of glycoprotein-containing plasma membrane
  5. Envelopment
  6. Virus release
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5
Q

Influenxa

Describe the structure of influenza

A
  • it’s a segmented negative sense single stranded RNA virus
  • its a segmented virus
    • it has 8 segments
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6
Q

Influenza

How does being segmented help influenza

A
  • gives it an advantage
    -Why?
  • each segment codes for 1 or 2 proteins

  • for example RNA polymerase which will help turn the negative sense genome into a positive sense to make proteins
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7
Q

Influenza

What are the three types of influenza

not really like scientfic names, think broad

A

A
The one that causes pandemics (infects humans, pigs, birds, horses)

B
the one that causes easonal epidemics (only infects humans)

C
The one that causes mild resiportiry illness (only humans and pigs)

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8
Q

Influenza

How do we divide influenza

it;s based on viral proteins

A
  • Haemagglutinin (H1 – H18)
  • Neuraminidase (N1 – N11)

we can class them as avain, swine or other types of influenza

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9
Q

Influenza

How does influenza get into target cells

A
  • influenza interacts with the cell surface to help the virus enter the cell
  • in humans the virus can interact with alpha 2,6 sialic acid which is found in the airway epithelium
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10
Q

Influenza

Influenza is a acute virus
what does this mean?

A

-once you get it, you make antibodies
-these neutrailsing antibodies block the interaction between the haemagglutinin and the cell surface

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11
Q

Influenza

Why do we get infected a lot with influenza

A

-its because its an RNA virus
-RNA viruses really unstable,
-can get mutations really quickly

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12
Q

What is meant by antigenic drift

A
  • Everytime influenza replicates,
  • there’s no proofreading
  • so it will accumulate mutations
  • the mutations can make be meh, great or bad
  • small changes happen in the genes over time, as the virus replicates
  • These mutaions accumulate over time.
    • Eventually this will generate proteins no longer recognised by the immune system
    • so the mutations alter epitomes in haemagglutinin so that neutralsing antivodies no longer binds
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13
Q

Influenza

Why does influenza mutate so much

A
  • RNA viruses must replicate their genomes using RNA polymerase
  • RNA polymerase lacks the proofreading ability (DNA polymerase does have this ablity thoughO
  • RNA viruses mutate more than DNA viruses
  • RNA viruses can alter antigenic epitopes targeted by the immune system.
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14
Q

How does antigenic drift result from replication errors

A
  • In vitro, a single cell infected with poliovirus can yield 10 to the power of 5 virus particles
  • In vivo, an HIV-infected person may produce 10 to power of 9 virus particles/day

Basically you make bare viruses each day

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15
Q

What is antigenic shift

A

-causes a major change in influenza A viruses
-makes new haemagglutinin/or new neuraminidase proteins
-this makes new influenza A subtype
-influenza A has a segemnted genome, so if you get an infection of one cell with two different virusese,
-there can be swap RNA segements between the different viral strains
-results in creation of new virus with new proteins
-therefore you have no cross protective immunity to the virus
-which can cause a pandemic

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16
Q

How does antigenic shifts happen

A

-there’s a less chance that birds will pass on influneza to humans because of the different places the alpha 2,3 SA recpetor are (humans at base of lungs, birds high up respiratory tract)

Pigs however,

this flashacrds needs helppp

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17
Q

Hepatitis B virus

How many peopel around the world have a HBV infection

A

2 billion people have HBV infection

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18
Q

Hepatitis B virus

Describe the structure of hepatitis B virus

A
  • tiny virus
  • genome partly DNA and RNA
  • there are 8 genotypes
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19
Q

Hep B

How is Hep B transmitted

A
  • Perinatal transmission (mother to child at birth)
  • Parenteral transmission (blood, blood products)
  • Needlestick injury, tattooing, piercing
  • Sexual
  • Infected body fluids (saliva, menstrual, vaginal, seminal fluids)
  • Medical/surgical/dental instrument
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20
Q

Hep B

Who is most at risk of contracting Hep B

A
  • Health care workers
  • Men who have sex with men/people who have multiple sex partners/sex workers
  • Blood transfusion recipients
  • I.V. drug users
  • Infants of HBV carrier mothers
  • Recipients of solid organ transplants
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21
Q

Hep B

Describe the Hep B virus incubation period, severity, chronic infection

A

the incubation period
-is between 30-180 days (av is 75 days)
Acute
-usually mild, but 30-50% of adults can present with jaundice and hepatitis
Chronic
can be chronic
Severity
-can be asympotamatic to fatal

22
Q

Hep B

Acute hepatitis

A
23
Q

Chronic Hep B

A
24
Q

Hepatitis C

Is there a cure for Hep C

A

-there’s a cure for hep C
-but there’s no vaccine

25
Q

Hep C

Describe Hep C and how it infects our cells

A
  • small virus
  • their envelope glycoproteins are small, so not efficient enough to interact with the cell surface
  • so a small virus like this needs to overcome electrostatic forces to get to the cell
  • but hep c isn’t great at that
  • so hep c said WHERE THERE IS A WILL THERE IS A WAY
  • and that WILL was these low-density lipoproteins
  • these proteins can overcome the electrostatic forces of the cell
  • which allows hep c to be in close contact with the cell, so that it can get in
26
Q

Hep C

How is Hep C transmitted

A

it’s bloodborne
- Injecting drug use/sharing injection equipment
- Reuse or inadequate sterilization of medical/surgical/dental equipment (esp syringes/needles)
- Transfusion of unscreened blood and blood products
- Sexual practices that lead to exposure to blood
- Perinatal transmission (mother to child at birth) → less common

27
Q

What is the incubation for Hep C

A

2 weeks to 6 months

28
Q

What symtoms of an acute infection

A

80% are asymptomatic
20% have
-fever
-fatigue
-decreased appetite
-nausea
-vomiting
-abdominal pain
-dark urine
-joint pain
-jaundice

29
Q

Hep C

How severe is Hep C

A

it can be asymptomatic to fatal

30
Q

Hep C

How does the chronic infection affect people with Hep C

A

some people chronically imfected will develop cirrhosis and/or liver cancer

this happens to about 20-30% of people

31
Q

How do we test/diagnose hep C

A
  1. You can do antibody testing (for historical infection)
  2. Viral nucleic acid testing (it can tell you there’s a current infection)

  • At the beginning there’s lots of virus replication
  • if they are reactive, then the hep C virus is present → this means there is HCV
  • once it reaches threshold, symptoms will begin
  • but it takes long for antibodies to develop
  • if they are then there is no HCV infection, cant see RNA
32
Q

Why is there not a vaccine that is immune against Hep V

A

there are many genotypes that are in different parts of the world

33
Q

Herpesviruses

How would we describe the structure herpesviruses

A

DNA virus in envelope

there’s 8 herpes viruses

34
Q

How do herpes viruses infect people

herpes viruses are masters of invading the immune system

A
  • they have proteins that inactive the inate immune system
  • this allows for enough time to get into the cell, go to the neuclus , reprogramme and then replicate
35
Q

How do herpes viruses transmit

A

-Herpes infections are most contagious when symptoms are present
-can be transmitted oral to oral contact (HSV-1)
- genital to genital contact (HSV-2);
- oral to genital (HSV-1/2)
- via sores, saliva, surfaces in or around the mouth/genitals

36
Q

Are herpesviruses symoptamatic, asymptomatic

A

Most oral and genital herpes infections are asymptomatic.

37
Q

What’s the lifecycle of a herpes simplex 1 virus

A

Lytic virus
-infect mucoepithelial cells
-they replicate in the cells
-they then release the virus

But then they become latent
-this is immunological silent infection
-they then re-activate
-they replicate in the cells
-and then release

when a virus is latent it means they will stay with us forever

38
Q

Where do simplex viruses go latent

A
  • they go latent in trigeminal ganglion
  • and HSV 2 goes in the sacral ganglia
39
Q

What does neurovirulence mean

A
  • Invade and replicate in the CNS
  • Profound disease
  • Severe neurologic devastation
  • Meningitis/encephalitis
40
Q

How does the virus spread when latent

A

when the immune system is preoccupied, they take their chance

41
Q

Who does VZV effect

A
  • Infants
  • Adolescents
  • Adults
  • Pregnant women
  • People with HIV/AIDS or cancer
  • Patients who have had transplants
  • People on chemotherapy, immunosuppression, long-term steroids.
42
Q

What are the complications of VZV

aka chickenpox

A

Serious complications from chickenpox include:

  • Bacterial infections of the skin and soft tissues, including Group A

streptococcal infections (Necrotising faciitis)

  • Pneumonia
  • Encephalitis, cerebellar ataxia
  • Haemorrhagic complications
  • Sepsis
43
Q

is there a cure of VZV

A

there’s a vaccine

44
Q

Cytomegalovirus infection

How do we transmit cytomegalovirus infection

A

via body fluids, urine, breast milk sexual, blood proudcts, organ donations, bone marrow

45
Q

Cytomegalovirus infection

Is the infection symptomatic

A

usually its asymptomatic
but it can sometimes be symptomatic: can cause fevers, mononucleosis, hepatitis

46
Q

Cytomegalovirus infection

What can happen in utero

A

You can get infections in mutiple body systems
like pneumonia, hepatitis, encephalitis

47
Q

Epistein Barr virus

How is it transmitted

A

Salvia (via kissing)

48
Q

Epistein Barr virus

Tell me about the primary and secondary infection

incubation peroid, sympyoms, where it replicates, who it affects

A

usually asymptomatic
has a 4-7 week incubation period
replicates in oropharengeal epithelial cells and B cells
happens during childhood
about 95% of people have it during adulthood

Symptoms, delayed infection can cuase glandular fever
-fever, pharyngitis, swollen lymph nodes, hepatitis

49
Q

Epistein Barr virus

Where does it become latent

A

In B cells

expresses viral proteims, non codingmRNA,

50
Q

Epistein Barr virus

EBV has a complication, what is it

A

EBV can cause a whole bunch of virus associated maligances
-B cell maligances (hodgkins lymphoma)
-epithelilal cells malaginices
T and NK cell maligancies

51
Q

Epistein Barr virus

What is EBV complaications are associated with those that are immunocomprimised

A

Hodgekins lymphoma (post transplant)
-pneumonia, hepatitis (post transplant disease)
-Burkitt lymphoma, diffuse large B cell lymphoma (EVB and HIV related lymphoas)

52
Q

What type of sarcima is associated with herpesviruses

not mentioned in lecture, but on slides

A

Kaposi sarcoma

latenxy in B cells and endoletjlail cells

IIH (7 decks)

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