Tolu cahill Flashcards

1
Q

Innate immune response to virus

A
  1. Interferons: Infected cells release interferons (INF-alpha and beta), which act in an autocrine and paracrine manner to stimulate the production of antiviral peptides in nearby uninfected cells. These interferons also activate natural killer (NK) cells.
  2. Natural Killer Cells: NK cells detect the absence of MHC-1 receptors on infected cells and release perforins and granzymes to induce apoptosis in these cells. NK cells also release INF-gamma, which activates and attracts macrophages and dendritic cells.
  3. Macrophages: Activated macrophages target and phagocytose opsonized viral particles in the blood, contributing to the clearance of the virus.
  4. Dendritic Cells: Dendritic cells phagocytose viral particles and present viral peptides on MHC-II receptors. This antigen presentation is crucial for the activation of CD4+ T cells, bridging the innate and adaptive immune responses.
  5. Complement System: The complement system is activated via pathways such as the classical, alternative, and lectin pathways. Components of the complement system, such as C3b, opsonize viral particles, enhancing their recognition and phagocytosis by macrophages. The formation of the membrane attack complex (MAC) can also directly lyse viral particles or infected cells.
  6. Pattern Recognition Receptors (PRRs): PRRs, such as toll-like receptors (TLRs), on innate immune cells recognize viral components, triggering cytokine production and further enhancing the antiviral response
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2
Q

Adaptive immune response

A

The naive in the lymph nodes are activated by APCs that present viral peptides on MHC molecules.

CD4+ T cells are activated by MHC-II, while CD8+ T cells are activated by MHC-I. The T cell receptor (TCR) binds to MHC-II or MHC-I (activation), and CD28 binds with CD80/86 (costimulation).

Differentiation is determined by the cytokines released. IL-12 results in Th1 differentiation, and IL-4 results in Th2 differentiation.

Th1 cells enhance the cell-mediated cytotoxic response by producing cytokines like IFN-γ, which activate macrophages and support the activation and proliferation of CD8+ T cells.

Th2 cells enhance the humoral response through the activation of B cells, which can then proliferate and become plasma cells producing antibodies against the virus.

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3
Q

describe herpes simplex virus. Name 2 other shapes and example of each

A

Double stranded DNA, enveloped, icosahedral - capsid composed of capsomeres arranged into multiple equilateral triangle shapes surrounding nucleic acid

Helical - tobacco mosaic virus
Mixed - bacteriophage

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4
Q

Distinguish between the 2 phases/cycles of HSV infection

A

Lytic cycle
-The lytic cycle involves active replication within the host cell.
-The production of immediate, early and late proteins takes place
-The new virions are assembled, shed from the host cell resulting in cell lysis.
-This results in symptomatic viral infection such as cold sores, fever, temperature.

The lysogenic/latent cycle
- This is when the virus lays dormant within the dorsal root ganglia.
-The virus gets here via retrograde axonal transport using Dyenin.
-In this stage, the virus remains episomal in the nucleus but is not integrated into DNA and so protein synthesis does not take place.
-This is achieved through production of LATs (non-coding RNA) which inhibits protein synthesis and thereby prevents progression to lytic cycle.
-Stimuli such as fever, stress, exposure to UV light and pregnancy can result in viral replication, anterograde axonal transport via Kinesin and the lytic cycle begins.

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5
Q

4 ways that herpes viruses can evade immune system

A
  1. Produces INF homologues to prevent binding of IFN to nearby un-infected cells/ activation of NK cells.
  2. Can inhibit loading of viral peptides onto MHC-1 receptors.
  3. Can make analogues of MHC-1 receptors to avoid detection by NK cells which respond to absence of MHC.
  4. The dorsal root ganglia/nerves in general are immunologically priveledged and so residing here in latency allows for evasion of immune response.
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6
Q

Distinguish between antigenic shift and drift

A

Antigenic Shift:

Antigenic shift refers to a major change in the surface receptors of a virus, often caused by reassortment of genes within doubly infected cells. This process can result in the emergence of a new viral subtype to which the human population has little or no preexisting immunity.
This significant genetic change can lead to pandemics because the adaptive immune response is not effective against the new virus strain.

Antigenic Drift:

Antigenic drift involves minor changes in the surface receptors of a virus, primarily due to point mutations within the genes encoding these proteins. These small changes accumulate over time and can alter the virus enough that preexisting immunity in the population is less effective.
Antigenic drift can result in epidemics, as the humoral immune response may still recognize the virus to some extent, but not fully prevent infection. This partial recognition allows for some degree of cross-protection.

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7
Q

3 modes of viral shedding

A
  1. Budding - can cause lysis eventually
  2. Apoptosis - lysis
  3. Exocytosis - no lysis
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8
Q

4 cytopathic effects of viral infections

A
  1. Blister/ulcer formation due to focal damage causing epithelial detachment.
  2. Acantholysis due to degradation of desmosomes.
  3. Proliferation of epithelial cells (warts)
  4. Dysplasia (cervical cancer)
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