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IAHI Block 3 > Intro to Virus, Lytic, Lysogenic > Flashcards

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
Q

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]

A
  • dsDNA, icosahedral naked virus with penton spikes
  • adenoids; tonsils
  • fecal-oral
26
Q

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 _____.

A
  • immunocompromised
  • upper respiratory
  • 3 to 10
  • 6 to 9 days
27
Q

What is viral surfing?? What virus does this?

A

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
Q

How does adenovirus cause diarrhea?

A

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
Q

In adenoviruses, the DNA + core hexon enters the ____ for replication. ____ allows for this virus to have many different proteins (complex virus).

A
  • host cell nucleus

- alternate splicing

30
Q

There is an adenovirus vaccine. What kind is it?

A

live, attenuated

31
Q

What is a disadvantage to acute viral infections as compared to latent infections?

A
  • 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
Q

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 ______.

A
  • VP16
  • proteins that counteract host immune response; TF for ßgenes
  • 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
Q

In herpesviruses, viral _____ degrades host mRNA

A

vhs

34
Q

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?

A
  • 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
Q

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.

A
  • reactivation

- long-lived

36
Q

What is T-cell exhaustion? What type of virus causes this?

A
  • 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
Q

___ 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?

A
  • HIV
  • viral genome integration
  • attenuation of HAART therapy; other environmental factors
38
Q

Why are latent infections a “good workout for the immune system”?

A

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
Q

Name 3 ways to “overcome” latent viral infection pathogenesis. Can you ever get rid of a viral infection?

A
  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
Q

Persistent chronic infection can cause these 2 things. {That is why therapies must target both virus and host immune system.}

A
  1. tissue/cellular damage (virus)

2. chronic inflammation (host immune system; Hep B/C)

IAHI Block 3 (5 decks)

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