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MMI > Lecture 5 - Viruses > Flashcards

Lecture 5 - Viruses Flashcards

1
Q

What kind of parasites are viruses?

A

obligate intracellular

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2
Q

Virion

A

complete infectious viral particle with nucleic acid surrounded by protein coat

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3
Q

Capsid

A

protein coat that wraps around the virus

composed of individual capsomeres (protein molecules)

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4
Q

nucleocapsid

A

RNA/DNA (single or double stranded) + capsid

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5
Q

what are lipid envelopes

A

layer of plasma membrane from the host that surrounds the nucleocapsid

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6
Q

what kind of viruses have lipid envelopes

A

influenza, herpes virus, HBV and HIV

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7
Q

what are glycoproteins/spikes?

A

inserted in the envelopes or capsid –> help the virus attach to the host cell

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8
Q

Two types of protein spikes on influenza virus?

A

HA (haemagglutinin) [H1] –> attaches to the sialic acid receptors on the red blood cells and cells lining the mucous membranes

NA (neuraminidase) [N1] –> helps virus exit the host cell after replication

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9
Q

Zoonotic infections

A

infections that can be passed across species i.e. rabies virus (virus of canines that can also infect moose and humans) and West-Nile Virus

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10
Q

What are bacteriophages?

A
  • viruses that infect bacteria
  • they can transfer new genes from one bacteria to another
  • bacteriophages cannot infect humans
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11
Q

How can bacteriophages be used in scientific labs?

A
  • can be used in genetic engineering
  • i.e. producing large amounts of insulin from E.coli
  • splice the human gene that makes insulin and then put it into the genome of a bacteriophage (bacteria virus); then have the virus infect e.coli and give it the insulin gene. E.coli will then make mass amounts of insulin for a low cost
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12
Q

What is the negative side effect of bacteriophages?

A

they can transfer genes across bacteria for production of toxin

i.e. a bacterophage that infects Corynebacterium diphtheriae (causes diptheria) can transfer its virulence factors across multiple bacteria

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13
Q

How do we classify viruses?

A

grouped into families on the basis of DNA/RNA composition and structure
i.e. we have a group of DNA viruses and a group of RNA viruses

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14
Q

Why are RNA viruses known for their ability to mutate quickly?

A

Because they require RNA polymerase that the virus brings with itself; this RNA polymerase can convert viral RNA straight into protein (positive) or into mRNA (negative) and by-passes the proof reading ability that DNA polymerase has; therefore it introduces much more mutation than DNA viruses

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15
Q

What are the 6 DNA viruses?

A
  1. Papillomaviridae (HPV)
  2. Adenoviridae (Adenovirus)
  3. Hepadnaviridae (Hepatitis B virus)
  4. Herpesviridae (HSV-1, HSV-2, HSV-3…)
  5. Poxviridae (small pox, monkeypox, chicken pox etc..)
  6. Parvoviridae (B-19)
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16
Q

How big are viruses compared to bacteria?

A

viruses are 10-500 nm while bacteria are 500 - 2000nm

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17
Q

What are the three steps that occur in viral infection?

A
  1. attachment and penetration into host cell
  2. Replication of viral genome
  3. Assembly and Release of New virus
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18
Q

Explain the attachment process of virus to host cell

A

viruses attach to the host cell usually to their receptors with the help of their glycoproteins/spikes

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19
Q

What are the two processes of penetration of the virus into host cell?

A
  1. fusion –> fusion of viral envelope into the host cell and the release of its genome into cytoplasm of host cell
  2. Pinocytosis –> virus attaches into the receptors and then gets engulfed into the host cell; it then breaks out of its vacoule and releases its genome
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20
Q

How do DNA viruses transcribe in the host cell?

A

A DNA Virus will hijack the host cell DNA polymerase to produce viral DNA, the viral DNA will then transcribe using the host cell’s RNA polymerase to make mRNA (messener RNA) and leaves the nucleus to the ribosomes to make amino acids to begin protein synthesis

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21
Q

How do RNA viruses transcribe in the host cell?

A

RNA viruses must bring their own RNA polymerase so they can create mRNA in the host cell [humans do not have this];

22
Q

What is the difference between positive and negative RNA viruses?

A

positive rna viruses can translate straight into making protein (they are essentially mRNA)

negative rna viruses must transcribe into positive rna first (mRNA) before translating to make viral proteins

23
Q

How do retroviruses transcribe?

A

retroviruses are RNA viruses that bring their own enzyme called reverse transcriptase;

reverse transcriptase makes DNA out of viralRNA and that viral DNA can go to make viral mRNA which can go to translate into viral proteins

the viral DNA that is made is integrated into the chromosome of the host cell and can be replicated whenever the virus wants to reproduce

24
Q

How are viruses assembled?

A

newly replicated RNA or DNA with newly made viral proteins results in new nucleocapsids

if the virus is enveloped, then the enveloped components are produced and inserted into the host cell plasma membrane; the viral particle then attaches to the plasma membrane and buds through it

25
Q

Fuzeon

A

antiviral drug that stops entry (fusion) of HIV into cells

26
Q

Acyclovir

A

antiviral drug that stops replication of herpes viruses by interfering with the viral DNA polymerase

27
Q

HAART

A

a cocktail of antiviral drugs
Highly Active AntiRetroviral Therapy –> used to stop replication of HIV and helps prevent virus from becoming resistant to the antiviral drug

28
Q

TamiFlu (oseltamivir)

A

an antiviral drug that stops the budding/release of influenza virus from host cell

29
Q

3 host-virus interactions?

A
  1. Acute/Productive infection
  2. Latent infection
  3. Chronic infection
30
Q

acute/productive infection

A

virus replicates and produces many virions in a short time span

the host cell is killed and causes a lytic infection

then you recover and the virus is gone out of your system

examples: adenovirus, and poliovirus

31
Q

latent infection

A

viral genome persists in host cell but does not replicate and is called a provirus

it stays in the host cell even after the infection and symptoms are done; this is because the genome of the virus is likely spliced into the host cell’s chromosomes and replicates proteins later on in life

examples: herpesviruses (HHV-3) and HIV

32
Q

chronic infection

A

virus replicates without causing host cell lysis (doesn’t kill host cell) and can persist for a long period of time (slow and long lasting); it can cause long term damage

i.e. hepatitis C virus and hepatitis B virus

33
Q

What is chicken pox / Varicella / HHV-3?

A
  • enveloped DNA virus

- starts off as an acute infection and then becomes latent

34
Q

What are the acute symptoms of Chicken pox/HHV-3?

A
  • the acute part causes fevers and itching
  • the rash is spread on trunk and head
  • virus particles can escape from the rash and infect via airborne
  • skin vesicles are always present in different stages of lesion formation (some vesicles are erupting, while some are healing all at the same time)
  • when the lesion heals completely, it signifies the end of the acute infection; however, the virus travels up the trigeminal nerve and makes home in the peripheral nerve ganglion where it remains latent
35
Q

What are the latent symptoms of Chicken pox/HHV-3?

A

virus is present in the peripheral nerve ganglion but is nt replicating until it is triggered by some external factors

  • then it travels down the skin and reactivates
  • it is still spread by the airborne route
  • When it comes back from latency, it is called shingles/Zoster
36
Q

Shingles/zoster

A
  • reactivation of the chicken pox virus
  • begins as a local skin rash
  • described as rash and pain
  • untreated rash lasts 2-5 weeks
  • it is infectious to people who have not had chicken pox
37
Q

Post Herpetic Neuralgia (PHN)

A

most common complication of shingles/zoster

  • affects 20-50% of patients over 50 years of age
  • it is pain that persists for months or years
  • can cause permanent nerve damage
  • occurs to shingles patients who did not get Acylovir within 48-72 hours of symptoms appearing (the rash)
38
Q

What is the complication of chicken pox in immunocompromised?

A

secondary bacterial infections from scratching skin

and CNS diseases like encephalitis, meningitis and myelitis as well as hemorrhagic complications and primary varicella pneumonia (last two are very rare)

39
Q

two ways of preventing chickenpox (HHV-3)

A
  • Active imunization

- Passive immunization

40
Q

what is the difference between active and passive immunization

A

active immunization –> live attenuated vaccine, highly protective and produces memory cells for the host to have
- is included with MMR (MMRV) vaccine now

passive immunization: effective 3 days after exposure to HHV-3

  • includes VZIG: varicella-zoster immunoglobulin (anitbodies to the virus)
  • normally used for immunocompromised exposed children and neonates born to mothers with varicella
41
Q

What is the difference between chicken pox and small pox?

A

chicken pox has lesions that are in different stages of development

small pox has all the lesions at the same stage of development

42
Q

Oncogenic viruses

A

viruses that can transform normal host cells into cancer cells

they can be RNA or DNA viruses

43
Q

Examples of oncogenic viruses?

A

i.e. HPV (human papilloma virus) can cause vagina, cervical and oral cancer

i. e. Ebstein-Barr Virus (EBV) causes mononucleosis (mono) and can be linked to burkitt’s lymphoma in immunocompromised people and people who live in malaria prone areas
- EBV lives in B-cells and is latent for all ur life

44
Q

What are two common ways to obtain a viral diagnosis?

A
  1. Culture –> culturing (growing) the virus in the lab and observing it for cytopathic effects [slow and labou intensive]
  2. PCR —> polymerase chain reaction –> used in molecular biology to detect genes in an organism
45
Q

what are cytopathic effects?

A

they are characteristic changes to the cells that a virus infects on a cultured plate –> we can use CPE’s to check for the effects of the virus on the host cell and use it to determine which viral infection it is

46
Q

Syncytia - why is it so bad?

A
  • type of cytopathic effect observed while culturing a virus
  • is is a group of multiple nucleated cells that are fused together by near by cell membranes –> often called a “virus producing factory”
  • these are abnormal cells that cannot function as they should and keep producing viruses
  • after all the viruses are produced and the nucleic acid precursors of the virus are depleted, this giant cell dies and causes inflammation in the tissues leading to scarring tissue damage
  • the organ will NOT be functional like it was before the infection and other organisms like bacteria can take advantage of this scarred area and reproduce to cause secondary infection
47
Q

What are prions?

A
  • protein misfolding disease
  • identified by Stanley Prusiner in 1982
  • causes our natural proteins to become changed and unfunctional
  • prions are already misfolded proteins that act as infectious agents
  • prions will disrupt the function of quaternary proteins and will not allow enzyme binding
  • human prion disease is always fatal and someone with it can die in 4 months
48
Q

examples of prions?

A
  • Mad Cow Disease
  • Scrapie in sheep
  • Kuru in N.Guinea (transmitted by cannibalism)
  • CJD, or vCJD (creutzfeld jacob disease) –> occurs to people who eat the meat of a cow that has mad cow disease
  • fatal familial insomnia (prion disease of the brain that results in inabilit to sleep)
49
Q

What are some signs of prion disease?

A
  • ataxia (loss of limb control)
  • cortical visual symptoms
  • progressive dementia
  • myoclonus (shaking)
  • akinetic mutism (unable to talk)
50
Q

Why is mad cow disease called spongiform encephalitis?

A

because a microscopic picture of Mad Cow Disease shows holes in the brain of the cow that look like spongy brain tissue

MMI (18 decks)

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