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Immunology 3 > Viral Lifecycles > Flashcards

Viral Lifecycles Flashcards

1
Q

Characteristic of Acute virus infection: ______onset w/ brief period of sypmtoms—eliminate either host or virus
-ex: influenza, norovirus, rhinovirus

A

Rapid

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2
Q

—generate specific adaptive immune response to clear pathogen—establish memory

A

Active virus replication

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3
Q

Overactive immune response may result in ….

A

tissue damage (immunopathology)

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4
Q

Initial steps simular to acute: virus infects a naïve host, replicates, host mounts immune response w/ some difference (3 differences)

A

Virus not cleared (for months to a lifetime)
Start with robust immune response—subdued to prevent immunopath by maintain control on virus
Immune response of host is set to a higher activation state overall (increased systemic cytokine levels)
See 2 types of viral life cycles during chronic infection: Latent and persistent

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5
Q

Viral lifecycle see______ expression of subset of viral genes, absent lytic replication and infectious virion production

A

minimal

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6
Q

herpes virus is a prototype for a……

has both latent and lytic stages

A

latent virus infection

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7
Q

Viral________ degrades host mRNA

A

vhs

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8
Q

Viral transcription factor localizes to nucleus to initiate viral gene transcription

A

VP16

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9
Q

Viral DNA circularizes and HSV ______transcribed by host RNA II polymerase

A

alpha genes

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10
Q

Some alpha gene products transactivate transcription of

A

beta genes

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11
Q

Some beta gene products are necessary for _______

A

viral DNA synthesis

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12
Q

Viral DNA synthesis triggers expression of

A

gamma viral genes

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13
Q

Gamma gene products are

A

structual compoents of the virion

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14
Q

Viral DNA is packaged into a

A

capsid

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15
Q

Filled viral capsid bud through host membranes to form

A

a mature virion that exits the cell

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16
Q

Initial steps are shared btwn lytic and latent:

–viral attachment and entry→ this consists of

A

transport of DNA in the nucleus→ viral DNA circularizes and associates with host nucleosomes

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17
Q

Viral DNA is MAINTAINED ______(episome) to allow viral genome to survive cellular division

A

BY CELL as extra chromosome

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18
Q

Little if any of the viral genes are expresssed (don’t want to tip off immune system) during

A

lytic cylce

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19
Q

Few expressed viral proteins help maintain the viral episome and prevent…..

A

its loss during division

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20
Q

Advantages of lytic cycle

A

a. Stealth: few gene expressed to infected cells are invisible to immune system
b. Virus relies on host cell mechanisms to maintain viral genome—very difficult to design therapeutics that specifically target latently infected cells

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21
Q

few gene expressed to infected cells are invisible to immune system (advantage of lytic cycle)

A

Stealth

22
Q

b. Virus relies on _______ to maintain viral genome—very difficult to design therapeutics that specifically target latently infected cells (advantage of lytic cycle)

A

host cell mechanisms

23
Q

Disadvantages of lytic cycle:

A

a. Spread to naive host is limited bc no production of virions
b. Death of latently infected cell is a dead end for virus—genome is non infectious

24
Q

Death of latently infected cell is a dead end for virus because:

A

genome is non infectious

25
Q

Challnge of latent virus: limited transmission to naïve host

Solution:

A

reactivation-switch from latent→ lytic lifecycle

26
Q

-dangerous for the virus to do this—viral replication during reactivation occurs in the face of a:

A

robuse and highly virus-spcific adaptive immune response that can eliniate reactivating cell b4 infectious virions are made

27
Q

Challenge: Death of a latently infected cell
Solution:

A

viral latency is established in long lived cells
Herpesvirus—neurons, memory T and B cells, hematopoetic stem cells
HIV: memory T cells

28
Q

Protype: Hep C virus

Only has a lytic life cycle and can’t shut itself off

A

Chronic Persistent Virus infection

29
Q

________ continues for duration of chronic virus infection

A

Lytic replication

30
Q
  1. In contrast to latent, during persistent virus replication ________cells are constantly stimulated with high levels of virus antiGs
A

virus-specific T

31
Q

Constant stimulation prevents development of a robust memory T cell population… leads to immunological phenomenon called _______

A

T cell exhaustion

32
Q

-T cells upregulate inhibitor receptors that attenuate signaling downstream of TCR

A

T cell exhaustion

33
Q

T cell exhaustion:

Decreased TCR leads to ……

A

loss of antivirl fnxs and death of T cell

34
Q

HIV is our prototype for:

A

Combinations of latent and persistent virus infection

35
Q

If infected CD4 T cell has a memory T cell phenotype, viral replication

A

becomes very inefficient downstream of viral genome integration

36
Q

__________may lead to undetectable virus loads in the blood—but latent infected T cells persist in tissues

A

HIGH active antiretroviral therapy (HAART)

37
Q

What happens HIV pts discontinue HAART

A

Discontinue HAART in most cases will allow HIV reactivation and persistant replication, leading to disease

38
Q

____ is quiescent, little disease is observed

A

Latent

39
Q

Latent infection: Low level of immune stimulation…latent infections reset baseline of immune response by

A

increaseing systemic cytokine levels and decrease activation threshold of immune system

40
Q

During a latent infection: Disease is primarily generated by

A

reactivation and/or expanded viral gene expression

41
Q

Some Epstein Barr virus (gammaherpesvirus) gene products are part of expanded latency associated gene expression have _______ Continuos expression of these, if not limited by host.. can contribute to cancer

A

oncogenic properties.

42
Q

Overcoming pathogenesis of chronic virus infection: latent infections
Elimination of latent infections is challenge as virus relies on

A

cell machinery to maintain genome—virus specific therapeutic targets are limited if present at all

43
Q
  1. One approach to irradicate and/or limit latent infection is to
A

induce virus reactivation from latency w/ subsequent targeting of lytic virus process (see herpesivirs and HIV blocks for specific therapies)
-tricky as all known stimuli induce reactivation only in very small subset of latently infected cells

44
Q

Vaccine devo is difficult bc latency establishment is

A

extraordinary efficient and often ind of viral replication during initial phase of infection

45
Q

prophylactic tx of susceptible hosts w/ antivirals targeting lytic viral replication is viable alternative because

A

BC pathogenesis is driven by viral reactivation

-ex: gammaherpevirus-induced sarcomas and lymphomas in context of HIV infection

46
Q

Pathogenesis of Chronic virus infection: persistent Pathogeneis of persistent virus infection stems form two primary contributions:

A
  1. tissues and cellular damage associated w/ virus replication
    - depletion of CD4 T cells in Hiv infection
    - hepatocyte death d/t replicating hep C virus
  2. Tissue damage associated with inflammation and excessive immune reponse
47
Q
  1. Chronic inflammation is associated with
A

devo of cancer

-hep B and C infection

48
Q

Overcoming pathogenesis of chronic virus infection: persistent infection
1. Therapies need to target both______

A

viral and host processes that lead to disease

49
Q

Overcoming pathogenesis of chronic virus infection: persistent infection
Viral: therapies specifically target ______

A 
viral replication (like retroviral therapy against HIV)
-often administered as combination (to limit devo of resistance) and for lifetime
50
Q

Overcoming pathogenesis of chronic virus infection: persistent infection
Host: much of tissue damage induced by ________
–mild immunosuppresive therapies can work
-BUT immunosuppresion has to be carefully balanced to maintain _______
-Therapies aim to _____________

A

host immune system
virus-specific immune responses
reverse the T cell exhaustion associated w/ persisten viruses

Immunology 3 (20 decks)

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