Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MII2 > 4. Microorganisms: viruses > Flashcards

4. Microorganisms: viruses Flashcards

(76 cards)

Start Studying
1
Q

Define a virus

A

Virus - nucleoporin (protein + nucelic acid) complex - infects cells and uses their metabolism to replicate itself - smallest known infective agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why are viruses said to be metabolically inert?

A

Metabolically inert - can’t replicate on their own - must enter host cell to perform metabolic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What imaging tools can be used to view viruses?

A
  • Electron microscopy
  • X-ray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the average size of a virus?

A

10 - 400 nm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the common structural components of viruses?

A
  • nucleocapsid
  • envelope (not all have)
  • viral genome: nucleic acids, segmented, DNA / RNA, ss / ds, linear / circular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is viral genome segmented?

A

Segmentation of viral genomes allows exchange of intact genes between related viruses when they coinfect the same cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain why is the capsid needed and what are the possible structures of it

A

Capsid functions:
- protect genome
- aids in viral transfer into host

Capsid structure:
- protein coat - made up of capsomeres (capsid subunits) -> arrangements of capsomeres to compose a capsid: polyhedral, helical, complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why are some viruses naked and others enveloped?

A

Non-enveloped viruses - naked viruses - typically more virulent than enveloped viruses - because usually cause host cell lysis - non-enveloped also more stable, can have broader host range
- Enveloped: ex: poliovirus
- Naked: ex: SARS -CoV-2

Enveloped viruses better protected by envelopes under certain conditions - non-enveloped viruses have evolved more resistant protein capsids to environmental stressors - better suited to survive and persist in a variety of environments

covid naked or enveloped??

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain what are the functions, sources and components of viral envelope

A

Envelope functions:
- protecting the RNA / DNA
- evading immune system recognition
- facilitating virus entry

Envelope sources - acquired when exiting:
- host plasma membrane
- host nuclear membrane
- host ER

Envelope components:
- phospholipids
- proteins
- glycoprotein spikes (+/- could have or not)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the possible variations of ssRNA in viruses?

A

ssRNA in viral genomes can be:
- positive (+) sense: coding - can be directly translated into protein
- negative (-) sense: will need to be copied into pos (+) to be translated into protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the Baltimore classification of viruses?

A

Baltimore classification - classification of viruses into families based on thier structure, genomic and replication properties

(+)ssRNA -> (-)ssRNA -> +mRNA
(-)ssRNA -> +mRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the names of the six Baltimore viral classes?

A

I. Herpesvirus
II. Parvovirus
III. Reovirus
IV. Picornavirus
V. Influenza
VI. Retrovirus

Herpesas Parvaro su Realiu Pico-corn Influenceriu remiu Retro
I Hate Parrots Really, Particularly In Retro glasses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are viruses cultured in labs?

A

Viruses are grown in tissue cultures - tissue cells - their hosts

Ex:
- human fibroblasts
- mouse 3T3 fibroblasts
- human HeLa epithelial cells
- fertilised chicken eggs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What technique is used for virus quantification?

A
  • Plaque assay - if virus forms plaques
  • Cytopathic effect - if virus doesn’t form plaques
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the plaque assay used for?

A

Viral quantification if virus forms plaques:
plaque count * 1/(dilution factor) = plaque forming units (PFU) per unit volume of inoculate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is cytopathic effect (CPE) used for?

A

Viral quantification if virus doesn’t form plaques:
viral invasion induces structural changes in host cells - by observing different dilutions of virus in known cell conc - determine where tissue culture infectious dose is 50% (TCID50) - quantity of virus needed to produce signs of infection in 50% of cultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a one step growth curve?

A

One step growth curve - curve used to make determinations about the life cycle of a virus in a particular host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the general sequence of events in a viral life cycle?

A
  1. Adsorption (attachment)
  2. Entry
  3. Uncoating
  4. Replication and transcription
  5. Synthesis of viral components
  6. Assembly
  7. Release (and maturation)
    Alfonsas Ezys Uzdare Renatos Siuvykla - Atidare Restorana
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do viruses recognise their hosts?

A

They recognise host cell surface components - each virus has specific receptors for their specific host surface components (proteins, glycoproteins, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Explain how viral adsorption to host cell occurs

A

Adsorption:
1) Random collision of virus and host cell
2) Interactions of specific host cell surface components and viral receptors occurs (tropism, host range) - some viruses may use several host cell receptors
3) Not all cells recognised as potential host cells, can be successfully invaded

Most neutralising antibodies are specific for virion attachment points

receptors on viruses or on host cells - or no matter how you call it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the receptors on host cell for Influenza virus?

A

Influenza virus ligands bind to sialic acid - receptor on host cell surface

Viruses bind with ligands to host cell surface receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the natural species barriers in viral infections?

A

Natural species barriers - pathogens specific to species - infectious to one but not other - genetic resistance

Ex: avian and human influenza viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Explain viral entry into hosts cells

A

Entry mechanisms:
- endocytosis
- fusion of virus envelope with cell memebrane

  • also injection of genetic material - ex bacteriophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Explain how viral uncoating occurs in host cells

A

Uncoating - release of viral genome - cell lysosomes strip off virus protein coat - virion can no longer be detected - eclipse period

  • uncoating at plasma membrane
  • uncoating within endosomes
  • uncoating at nuclear membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Explain HIV processes of attachment and entry into a host cell
Attachment: - **SU (gp120) protein attaches to CD4** expressed on host CD4+ T-lymphocyte (Th) - co-receptors required - chemokine receptors
26
Explain Influenza virus processes of entry and uncoating
1. **Attachment**: **hemagglutinin (HA)** protein on the surface of the influenza virus (ligand) **attaches to sialic acid receptors** on the surface of host cells 2. **Internalization**: virus is internalized into host cell by **receptor-mediated endocytosis** - virus is taken up into a vesicle called an **endosome** 3. **Fusion**: endosome acidic environment causes conformational change in the HA protein - triggers **fusion of the viral envelope with endosomal membrane** - **viral RNA + protein release** into host cell cytoplasm 4. **Uncoating**: viral RNA and associated proteins must be uncoated to initiate replication - first RNA transcribed into **complementary RNA (cRNA)** because (-)RNA can't be read by host machienry - viral broight reverse transcriptase used - cRNA - a template to produce more viral RNA + proteins
27
Explain SARS Cov processes of attachment and entry into a host cell
1. **Spike protein** binding to **ACE2** 2. Internalization through **endocytosis** 3. **Fusion** of the **viral and endosome membranes** 4. **Release** of the **viral genome** into the host cell cytoplasm 5. **Replication** and production of **new virus particles** 6. **Release** from the host cell to infect new cells
28
Explain processes of poliovirus entry and uncoating in a host cell
1. Poliovirus enters host cells through **receptor-mediated endocytosis** 2.**Uncoating** and **releases viral genome** into the host cell cytoplasm 3. Viral genome is **translated, replicated**, and assembled into new virus particles 4. Virus particles **released** from the host cell to infect new cells
29
Explain adenovirus entry into a host cell
1. Adenovirus enters host cells through **receptor-mediated endocytosis** - **escapes endosome** into the host cell cytoplasm 2. Transported to the nucleus for **replication and assembly** of new virus particles 3. **Released** from the host cell to infect new cells
30
Where does viral assembly take place in a host cell?
- cell nucleus - cytoplasm - plasma membrane Assembly may occur together with viral release
31
Explain the process of viral release form host cells
Release: - **sudden rupture** of host cell (non-enveloped viruses) - **gradual budding** through cell membrane (enevloped viruses) Release may occur together with viral assembly
32
What is special about Influenza virus RNA packing into virions?
2 theories to packing: - **random** - **specific** - recent data suggests specific
33
What is HIV maturation?
**Viral maturation** - transition process from an initial, **non-infectious**, **assembly** product **to an infectious virion**
34
Explain herpes virus assembly and release
1. Herpesviruses enter host cells through **receptor-mediated endocytosis** 2. **Replicate their DNA** genome in the **host cell nucleus**, assemble their capsids and envelopes 3. **Released by budding** from the host cell surface
35
Herpes virus smth read what is that axon
36
Explain SARS Cov assembly and release
37
What is the possible variation in viral genome?
Viral genomes can be: - dsDNA / ssDNA / dsRNA / ssRNA - circular / linear - non-segmented / segmented
38
What is the possible variation in all existing polymerases? What are their functions?
- DNA dependent DNA polymerase - DNA dependent RNA polymerase - RNA dependent RNA polymerase - RNA dependent DNA polymerase
39
Why do all RNA viruses encode an RNA dependent RNA polymerase?
RNA viruses themselves must encode **RNA dependent RNA pol** (**RdRP**) because **host cells** only code for DNA pol - **can't provide** RNA pol
40
How do the processes of mRNA generation differ in +ve / -ve strand viruses?
**+ve strand** (coding) RNA: - genomic RNA **can act as mRNA** on cell entry - translated to produce the pol **-ve strand** (non-coding) RNA: - **need to carry pol** in virion - to c**onvert -ve strand** into mRNA after entry
41
Explain how do DNA viruses produce proteins inside host cell
1. enter the host cell, **DNA molecule** - **transported to nucleus** -> replication + **transcription into mRNA** 2. mRNA into cytoplasm - **translated** into viral protein 3. Viral assembly in host cytoplasm Same info flow as the cell: DNA -> RNA -> protein
42
What are the different possible viral genomes?
- dsDNA - ssDNA - dsRNA - ssRNA (+) - ssRNA (-) - ssRNA with DNA intermediate
43
Explain how do RNA viruses produce proteins inside host cell
1. eukaryotic host cells don't have RNA dep RNA pol - need to make themselves 2. **(+)RNA** - **as mRNA** - into cytoplasm to be translated + into nucleus for replication **(-)RNA** + **RNA dep RNA pol** -> mRNA -> into cytoplasm -> protein (-)RNA -> (+)RNA - template for transcription 3. Viral assembly in cytoplasm
44
Explain how do RNA viruses with DNA intermediate produce proteins inside host cells
Produce proteins inside host cells by **reverse transcribing** their RNA genome into a **DNA intermediate** -> **integrated into the host cell genome** -> serves as a **template** for transcription and translation of viral mRNA -> used to produce viral proteins
45
What are the problems that must be overcome by an RNA virus inside eukaryotic host cell?
1. Eukaryotic cells don't have **RNA dep RNA pol** -> need to make themselves to replicate genome 2. Eukaryotic cells **don't encode for 1+ protein from one mRNA** - **transcriptiona and translation decoupled** by the nucleus -> **virus has to adapt** to produce multiple proteins from single mRNA
46
What is the strategy employed by poliovirus to produce more than one protein from one RNA?
Poliovirus: **polyprotein** - single large protein - produced by poliovirus - **cutting** it to produce different **smaller proteins** => **mRNA used once but many proteins produced**
47
What is the strategy employed by coronavirus to produce more than one protein from one RNA?
Coronavirus: original genomic **+ve RNA** -> **-ve RNA template** produced -> Gene I for **RNA dep RNA pol** + **multiple transcripts** produced for each protein
48
What are the possible strategies used by viruses to produce multiple proteins froma a single RNA molecule?
- Produce a **polyprotein** - cut it (poliovirus) - Produce **multiple -ve RNA transcripts** from original RNA for each protein (coronavirus) - Have a **segmented genome** (influenza virus) - **Splice mRNA** into different transcripts -> different proteins (HIV)
49
What is the strategy employed by influenza virus to produce more than one protein from one RNA?
Influenza: **segmented genome** (several molecules instead of one compose the genome) + **re-assortment** (re-assortment of genomic sequences between different viruses -> zoonotic emergence when non-human virus gets human infection sequence) + **alternative splicing** (host cell's machinery used for splicing of single sequences)
50
What potential problem can occur by genome re-assortment in segmented genome viruses?
Segmented genome can **produce new pathogenic strains** by re-assortment of viral sequences -> ex: **pigs great host for new strain emergence** - can be infected by both avian and human viruses - avian virus acquires human infection sequence in re-assortment => new strain of human virus - human contact with pigs -> new virus spread in humans
51
What is the strategy employed by HIV to produce more than one protein from one RNA?
HIV: retroviruses **splice their mRNA transcripts** to produce different proteins form same RNA
52
What are the unique aspects of viruses that are targeted by anti-viral drugs?
Anti-viral drugs can **target unique aspects of viral replication** - host cells not affected: - **attachment** -> drugs - attachment antagonists - **uncoating** -> drugs - inhibiting viral uncoating - **DNA / RNA synthesis** -> drugs - inhibit DNA / RNA synthesis - **viral maturation** -> drugs inhibit viral maturation
53
What are the specific drug targets of HIV life cycle?
HIV life cycle targets: - inhibit **fusion** / **entry** / **uncoating** - **reverse transcriptase action** - inhibit HIV DNA production - viral **integrase action** - inhibit HIV DNA integration in host genome - viral **protease action** - inhibit viral maturation inside host cell Highly active antiretroviral therapy (**HAART**) - use more than one anti-viral drug to reduce probability of virus acquiring drug resistant mutations for all used drugs
54
What are the factors affecting viral epidemiologies?
Factors affecting viral epidemiologies: - mode of transmission - age - gender - ethnic background / country of origin - travel history - occupation - season - underlying medical conditions (ex: immune sppression)
55
What are the types of viral transmission routes?
- **Horizontal transmission**: direct contact / respiratory / contaminated inanimate objects / faecal/oral / insect vector / zoonosis - **Vertical transmission**: mother to fetus (ex: HIV)
56
What can be the results of a viral infection?
- primary infection - disease (symptomatic / asymptomatic) - secondary disease (+/-)
57
What are the main factors influencing the development and outcome of an infection?
Interaction between the host and pathogen affects development + outcome of infection (disease): - primary host **physical barriers** - host's i**mmunulogical ability** to control + eliminate the pathogen - pathogen's ability for **immune evasion** - pathogen's **virulence factors** - **ability** of the pathogen to **spread** in the host
58
What is the cycle of infection?
Cycle of infection (not viral life cycle): 1. Entry 2. Primary site of replication 3. Spread within the host 4. Secondary site of replication 5. Shedding 6. Transmission
59
What is the site of entry in the cycle of infection
Entry: physical barriers - mucous membranes / skin: - respiratory tract - oral - GI tract - sexual - ocular - percutaneous (infected needles / wounds / animal bites / insect bites)
60
Explain replication process in the cycle of infection
Replication: replicating itself -> shedding
61
Explain what is the course of infection of mousepox
1. invasion 2. Replication in LN 3. Spread in bloodstream - primary viremia 4. Replication in other organs 5. Further spread in bloodstream - secondary viremia 6. Skin infection - focal infection -> ulceration
62
What are the three types of infection?
Categories fo types: - acute - chronic - latent
63
Explain acute infections
**Acute infection**: **rapid onset** of disease - **resolved /killed quickly** by robust innate immune responses exerted by the host or, instead, may kill the host
64
Explain chronic infections
**Chronic infection**: **continued presence** of infectious virus after primary infection - may include **chronic / recurrent** disease - **prolonged incubation period** followed by progressive disease
65
Explain latent infections
**Latent infection**: **lack of demonstrable** infectious virus between **episodes of recurrent** disease
66
What are the possible effects of infection to the infected cells?
Infection effects on infected cells: - **abortive infection**: restrictive factors block / limit viral replication - **cytopathic effect** (cpe): morphological changes of cells - **translation switch off**: host cell's proteins not produced - only viral - **apoptosis** - **transformation**: immortalisation of cell -> tumours (cancer) - **immune response**: PRRs - innate immune response, immune evasion, interferons
67
How do the cells change in cytopathic effect?
**Morphological** cell changes in **cytopathic effect** (cpe): - cells **round up** -> **detach** from grown surface - cell **fusion** -> **multinucleate syncytia** formed - **plaques** - necrotic cells - **inclusion bodies** formed (virus factories)
68
How do virus shut off host cell protein translation?
Ways how viruses shut off host cell protein synthesis: - **cleavage of 'cap-binding complex'** (CBC) -> needed at translation initiation -> no translation of uncapped host -> **viral RNA contain IRES** -> translated - **host mRNA cap stealing** -> viral endonucleases cut off cap - reduced host protein expression -> **attach to own mRNA** -> translated | IRES - sequence only on viral RNA - allows uncapped translation
69
Explain what is IRES
**Internal ribosome entry site** (IRES) - **viral sequences** that can **recruit ribosomes** - allow **cap-independent translation** - used by viruses to exploit host cell machinery
70
What are the possible mechanisms of apoptosis as an effect of viral infection?
Apoptosis mechanisms: - **intrinsic** - mitochondrial pathway: cell injury - **extrinsic** - death receptor pathway: receptor-ligand interaction
71
Explain what is the effect of HPV on host cells
Human papillomavirus (HPV) - **disrupts the cell cycle**: cancer-causing HPV genes mediate **destruction of tumour surpressing proteins**: E6 gene -> p53, E7 gene -> pRB => cell cycle uncontrolled - **cell division increases** - **HPV replicates more efficiently**
72
How does the HPV vaccine work?
HPV vaccine: - **recombinant** virus-like particles based on **HPV capsid protein** - quadravalent (4 strains) / nonavalent (9 strains) vaccines available
73
At which points of the viral lifecycle can PRRs recognise the virus?
At all stages of the life cycle: - Entry - Uncoating - Replication, transcription - Assembly, release
74
What are interferons?
**Interferons** (IFN) - small molecules - produced as a response to viral infection - major role in inhibiting infection - **activate the adaptive immune system** + **induce neighbouring** uninfected cells - **anti-viral state**
75
Explain what is a cytokine storm
**Cytokine storm** - severe immune reaction - body releases too many cytokines into the blood too quickly - **overproduction of cytokines**
76
What are the ways in which viruses try to limit the immune response?
**Immune modulation strategies** used by viruses: - secrete **modulators**: cytokine / chemokine mimics and binders, mimics / antagonists of immune signalling - **stealth / latency**: express few / no proteins - hard to detect - **Ag hypervariability**: adapts and changes to avoid adaptive response - **block adaptive immunity receptors** - inhibit **Complement System** - interfere with **PRRs** - Block **interferons / inflammatory cytokines**

MII2 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions