Intro to Virus, Lytic, Lysogenic Flashcards

1
Q

ALL viruses rely on host [2 things] and have an ______ and an ______ phase.

A
  1. Metabolic machinery
  2. Protein biosynthesis (NEED HOST RIBOSOMES)
    - intracellular
    - extracellular
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2
Q

Virus taxonomy is _____, meaning that it is based on a collection of individual properties. Name 5 of these properties. Which one is usually used primarily? What is this classification system called?

A
  • polythetic
  • particle type, tissue tropism, disease etiology, serology, genome type** (used the most)
  • Baltimore classification (based on genome type)
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3
Q

____ is an example of an icosahedral, naked virus. _____ is an example of an icosahedral, enveloped virus. ____ is an example of a helical, enveloped virus. Enveloped viruses have _____ proteins under their envelope to provide structure.

A
  • Adenovirus (DNA virus)
  • Herpes Simplex Virus
  • Paramyxovirus (measles)
  • Matrix
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4
Q
Name the following types of genetic material in each Baltimore classification and if the virus uses reverse transcriptase:
Class I
Class II
Class III
Class IV
Class V
Class VI
A

Class I = dsDNA [Parvovirus; HPV]
Class II = +ssDNA [Poxvirus, Herpesvirus]
Class III = dsRNA **have RT [Reovirus–Rotavirus]
Class IV = +ssRNA –> –ssRNA **have RT [Picornavirus, Hepatitis E]
Class V = -ssRNA **have RT; [influenza, Paramyxovirus]
Class VI = +ssRNA –> –ssDNA **have RT [HIV]

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5
Q

Define the following:

  1. Virion
  2. Virus
  3. MOI
  4. CPE
  5. Viremia
  6. Egress
A
  1. viral particle
  2. infectious particle
  3. multiplicity of infection (how many viruses in cell)
  4. cytopathic effect
  5. spread of virus throughout body/bloodstream
  6. viral release from cells
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6
Q

DIAGNOSIS:

  • How are viruses seen?
  • Define the following (a) Plaque assay (b) Focus-forming assay (c) Single-step growth curve
A
  • Electron microscopy
    (a) titration of number of infectious progeny (pfu); count cell DEATH
    (b) for oncology purposes; viruses promoting cell GROWTH
    (c) quantification of burst size (single cell growth curve)
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7
Q

Where does the envelope of enveloped viruses come from?

A

nucleus, ER, golgi, vesicles, PM

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8
Q

Viruses replicate by ______. Viral genome and proteins must be ______, which happens via “zipcodes” on viral components.

A
  • xeroxing

- selectively encapsulated

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9
Q

Naked viruses enter the cell via ______ and exit via ____. Enveloped viruses enter the cell via ___________ or ___________ and exit via _____.

A
  • endocytosis
  • cell lysis
  • inducing fusion of virus and cell membrane (capsid in cytoplasm)
  • endocytosis and fusion with acidic endosome (capsid in endosome)
  • budding
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10
Q

Define the following:

(a) Productive infection
(b) Latent infection
(c) Persistent infection
(d) Abortive infection

A

(a) Productive infection = cytopathic effect due to lysis mostly (acute): form syncytia (RSV), shut off host metabolism, apoptosis, necrosis
(b) Latent infection = no production of infectious virus particles but genetic info remains and can be reactivated
(c) Persistent infection = chronic virus production
(d) Abortive infection = virus life cycle incomplete and virus lost

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11
Q

Name 4 important factors for host tropism for viruses.

A
  1. receptor type (influenza human {2,6} vs avian {2,3})
  2. tissue-specific cellular components (Hep C host miRNAs)
  3. tissue-specific restriction factors (retroviruses)
  4. temperature/pH/activating proteases
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12
Q

Name 3 ways viruses cause disease.

A
  1. destruction of infected cells
  2. modification of cell function/tropism (HPV)
  3. immune and inflammatory responses to infection (Hepatitis, influenza)
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13
Q

Defending the host:

  1. The innate immune response uses _____ and _____
  2. The humoral adaptive immune response uses _____ and _____
  3. The cell-mediated adaptive response use _______
  4. The memory response (B and T cells) use _____
A
  1. soluble mediators (IFNs, chemokines, cytokines for recruitment); apoptosis
  2. neutralizing antibodies; complement-fixing antibodies
  3. MHC presentation of viral peptides
  4. elicit response
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14
Q

What is the eclipse period of viral replication?

A

Post-infection, virus is not detectable; inside the cell and replicating; has not yet elicited an immune response

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15
Q

Picornavirus [LYTIC] properties:

  • Morphology: _____
  • Nucleic acid: _____
  • Tegument? ____
  • Enteroviruses stable at pH ___ whereas Rhinoviruses stable above pH ____
A
  • icosahedral
  • +ssRNA
  • NO
  • 3-9
  • 6
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16
Q

What disease type is associated with each picornavirus [LYTIC]?

(a) Enteroviruses
(b) Rhinoviruses
(c) Hepatoviruses
(d) Parchovirus
(e) Kobuvirus

A

(a) Enteroviruses = paralysis (polio), hand-foot-and-mouth Dz [fecal-oral transmission]
(b) Rhinoviruses = common cold
(c) Hepatoviruses = Hep A
(d) Parchovirus = gastroenteritis, myocarditis
(e) Kobuvirus = gastroenteritis

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17
Q

Polio [LYTIC]:

  • Subclinical (asymptomatic) infections are present in _____% of patients, usually because infection stays in oropharynx/gut.
  • Mild illnesses, like a cole, are present in _____% of patients
  • Aseptic meningitis (nonparalytic polio) is present in _____% of patients and lasts 2-10 days with _____ recovery
  • Paralytic poliomyelitis occurs in ____% of patients; due to asymmetric ___ paralysis, usually more in lower extremities
A
  • 90-95%
  • 4-8%
  • 1-2%; full
  • 0.1-2%; flaccid
18
Q

In poliomyelitis [LYTIC], _____ involves the cranial nerves, medulla and respiratory compromise (think iron lung); this causes a 5% death toll overall. Poliomyelitis has a ___ recovery and usually ____ paralysis.

A
  • bulbar paralysis
  • slow (2 years)
  • residual
19
Q

Polio [LYTIC] is exclusively a _____ disease and is known for its _____ epidemics. Patients that are _____ have a higher incidence of getting paralytic polio; _____ is one invention that has increased our risk for paralytic polio.

A
  • human
  • summer
  • OLDER
  • improved hygiene
20
Q

Picornaviruses (polio) don’t need to cap-snatch like influenza because they have _______ on their 5’ mRNA. When translating, a _____ is made.

A
  • a hydrophobic structure that better “grabs” ribosomes than host mRNAs.
  • polyprotein
21
Q

Picornaviruses [LYTIC] have capsid proteins that bind host PM and convert into an _______ that inject their _____ into the cytoplasm. First ____ are made and then more ____ is made.

A
  • injector (VP1)
  • +ssRNA
  • –ssRNA templates
  • +ssRNA
22
Q

Name the type of antivirals that can inhibit picornaviruses [LYTIC].

A
  1. virus attachment (antibodies–WIN 52035/chemicals)
  2. entry/genome release (Pleconaril)
  3. protease processing (ruprintrivir)
  4. RNA-dependent RNA polymerase inhibitors (ribavirin)
23
Q

____ make the inactivated polio virus vaccine and ___ make the live attenuated polio virus vaccine. New cases of polio are mostly due to ____.

A
  • Salk
  • Sabin
  • live attenuated polio vaccine transformation
24
Q

Viruses with segmented genomes must transcribe each genome separately to produce _____ mRNAs.

A

monocistronic (containing coding sequence for ONE protein)

25
Adenovirus is a complicated ______ and is latent in the _____ and _____. It has ___ serotypes with different disease spectrums, but is most always spread via ____ route. [VERY SIMILAR TO PICORAVIRUSES]
- dsDNA, icosahedral naked virus with penton spikes - adenoids; tonsils - fecal-oral
26
Adenovirus disease is usually severe in ______ patients. It infects the ______ tract and has an incubation period of _____ days. In normal patients (mostly young children), diarrhea lasts _____.
- immunocompromised - upper respiratory - 3 to 10 - 6 to 9 days
27
What is viral surfing?? What virus does this?
It is when spikes of virus grab myosin under the cell surface and "surf" looking for the correct receptor to undergo clathrin-mediated endocytosis (outside PM) then enveloped virus-like fusion of vesicle -Adenovirus
28
How does adenovirus cause diarrhea?
Attaches to apical surface and releases from basal surface; sheds excessive penton spike fibers that disrupt adhesion junctions of GI epithelial cells; adenovirus can then shed into lumen from basal surface
29
In adenoviruses, the DNA + core hexon enters the ____ for replication. ____ allows for this virus to have many different proteins (complex virus).
- host cell nucleus | - alternate splicing
30
There is an adenovirus vaccine. What kind is it?
live, attenuated
31
What is a disadvantage to acute viral infections as compared to latent infections?
- acute = rapid onset and brief infection makes it hard to create immunologic memory (ex. norovirus); overactive immune response can induce tissue damage - chronic = because the virus isn't cleared as quickly, have robust immune response at first, and then subdued response; high immunologic memory
32
In herpesviruses (dsDNA), viral _____ localizes to the nucleus to initiate viral gene transcription; host RNA polymerase II transcribes viral ∂ mRNA to make ∂ proteins, which make _____; ß proteins make _______ and gamma proteins make ______.
- VP16 - proteins that counteract host immune response; TF for ß genes - nuts and bolts proteins for replication of genome/DNA synthesis; TF for gamma genes - proteins to get out of the cell/tegument proteins/structural proteins/etc.
33
In herpesviruses, viral _____ degrades host mRNA
vhs
34
In herpesvirus latent cycle, the viral DNA is maintained as an ______. Very little if any viral genes are expressed because ______. What is the main problem with latent viruses?
- episome - virus doesn't want to elicit immune response - Hard to make vaccines/target those viruses because not many viral proteins made--would be attacking the host!!
35
A switch from latent life cycle to lytic is called ______; it happens when the cell is faced with specific environmental conditions. Because death of a latently infected cell is a dead end, latent viruses infect _____ cells.
- reactivation | - long-lived
36
What is T-cell exhaustion? What type of virus causes this?
- when constant simulation of T cells prevent the development of robust memory T cell populations; eventually this leads to loss of antiviral functions and death of T cells; due to PERSISTENT lytic replication - Hep C
37
___ is an example of a virus that is both latent AND persistent. This is because replication becomes very inefficient downstream of _______. What causes reactivation of this virus?
- HIV - viral genome integration - attenuation of HAART therapy; other environmental factors
38
Why are latent infections a "good workout for the immune system"?
low level of immune stimulation increases the systemic cytokine levels and decreases activation threshold; this is important for vaccines (but can lead to autoimmunity)
39
Name 3 ways to "overcome" latent viral infection pathogenesis. Can you ever get rid of a viral infection?
1. induce viral reactivation and then target (100% of latent viruses won't reactivate = problem) 2. vaccine development for prevention 3. prophylaxis (PEP, in HIV)
40
Persistent chronic infection can cause these 2 things. {That is why therapies must target both virus and host immune system.}
1. tissue/cellular damage (virus) | 2. chronic inflammation (host immune system; Hep B/C)