Intro + Viruses Flashcards

1
Q

What are the barriers to infections?

A

-Stratum corneum: Microbiome barrier, chemical barrier (pH, antimicrobial peptides, lipids, electrolytes, urea, amino ac., lactate)

-Epidermis: Tight junction, adherens junctions, Langerhans and CD8 T cells

-Dermis: Macrophages, Mast cells, ILC, CD4 T cell, DC, NKT cells

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2
Q

What is the Microbiome and how does it effect the immune system?

A

Collection of microbes living in and on our body

-> Commensal: microbes living in and on us and cause no harm (we benefit bc they provide protection against pathogens)
-> Provide homeostasis (metabolic and immune balance)
-> Imbalance or dysbiosis can lead to immune overstimulation and inflammation (dysbiosis due to dietary change, stress, and environmental factors)

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3
Q

What is the first barrier against pathogens?

A

Barrier immunity: physical (Skin), chemical (low pH, antimicrob. agent, lipids, AAs) , biological (microbiome)

Innate immune responses: Phagocytes

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4
Q

How do phagocytes fight pathogens?

A

Engulf and degrade, they use germ-line-encoded recognition molecules
(the adaptive immune system uses gene arrangement of receptors, to identify different pathogens)

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5
Q

What parts of pathogens are different from humans?
(Bacteria, fungi, viruses, parasites)

A

Virus: ds RNA
(ss/ds) DNA in cytoplasm means our nucleus is damaged or there is a virus, but they use our machinery (polymerase, ribosomes)

Bacteria: flagella, peptidoglycan, and LPS for gram neg. bacteria

Fungi: they are commensal fungi in the body
once the microbiota is damaged, they can take over and cause problems

parasites: membrane, proteins, parasitic pathways looks human

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6
Q

What is the adaptive immune system and what are its advantages and disadvantages?

A

Humoral (B-cells), Cell-mediated (primarily T lymphocytes)
Advantage: very specific
Disadvantage: it takes some time to build up the cell number (5-6 days)

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7
Q

How does Cell-mediated immunity respond?

A

-Cytotoxic T cells (T cells) kill infected cells to eliminate pathogens

-Helper T cells (Th cells) produce cytokines to regulate both Tc-cells and B cells

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8
Q

How can adaptive immunity respond to pathogens they have never seen before?

A

Random recombination of the binding site of B and T cell receptors

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9
Q

What is the problem with random recombination?

A

The receptors eventually target to self antigens

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10
Q

Difference between B cell receptors and antibodies?

A

Not a lot of difference, once the B cell gets activated it will generate the same version of B cell receptor but without the transmembrane domain

B cell receptors and antibodies can also be called immunoglobins

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11
Q

How are antibodies produced?

A

Once B-cells are activated they turn into plasma cells, they loose their B cell receptors, they have a lot of ER and ribosome to produce and secrete a lot of antibodies

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12
Q

How are T cell receptors different from B cell receptors?

A

B cell receptors are scanning for small protein pieces that move around in the area

T-cell receptors are binding to even smaller pieces presented by phagocytic cells, so they use MHC-1 (cytotoxic T cells), MHC-2 (T helper cells)

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13
Q

What does Tolerance mean?

A

Early deletion (lymphoid organ) of B and T cells that target self antigens

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14
Q

How is immune memory created?

A

After the primary (first) response the adaptive immune system will leave behind some memory lymphocytes

-> memory lymphocytes are stimulated with the secondary response, resulting in an even greater adaptive immune response

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15
Q

How does the innate and adaptive immune system work together?

A

-innate systems produce signals (often cytokines) -> stimulate and direct adaptive immune system

-Phagocytes present antigens to the adaptive immune system, to stimulate differentation

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16
Q

What are two dysfunctions of the immune system?

A

-Overly active: Allergy, autoimmune disease
-Immunodeficiency: primary (genetic) and secondary (acquired) loss of immune function

17
Q

Difference between viruses and cells?

A

Difference in genetic storage form (DNA and RNA), replication (use host machinery), no metabolism, protein capsid instead of lipid membrane, seen under light microscope

18
Q

What is an example of an enzyme that is viral?

A

Viral reverse transcriptase (HIV-RNA to HIV-DNA to implement into host genome)
Viral RNA-dependent RNA polymerase (RdRP) -> from (-) ssRNA to (+) ssRNA visca versa

19
Q

Why is the mutation rate in viruses higher than in other living infectious agents?

A
  • Because they replicate much faster
  • They are ss, so there is no backup strain
    -they want a huge number of mutations to be able to able to adapt and evade immunity
20
Q

What are the outcomes of genetic changes that benefit or limit infectivity?

A

Beneficial mutations: escape host system and vaccines, more hosts can be infected, increase in infectivity

Changes with lower infectivity: attenuated strain -> can be used in vaccines

21
Q

What does the capsid of viruses look like?

A

-Helical: hollow tube
-Icosahedral: 3-dimensional polygon
-other ones: complex capsids

22
Q

What happens to the genome of bacteriophages after it is injected into target cells?

A

Lysis of the target cell or integration into the host’s genome

23
Q

What is the difference between a viral envelope and capsid?

A

The envelope originates from the infected host cell (budding off) and is lipid-based and surrounds the capsid.

24
Q

How does the attachment of a virion to a target cell work?

A

Through spike proteins for enveloped viruses and capsid proteins in nonenveloped viruses

25
Q

How does the penetration of a virion to a target cell work?

A

Enveloped: Viral envelope and host membrane fuse -> Host enzymes and host cell enzymes break down the capsid -> release

Nonenveloped: entering the cell through endocytic vesicle which has enzymes in it -> break down of capsid

26
Q

What happens to the Genome after it is released from the capsid?

A

If ss DNA or (+) ss RNA, it is turned into ds DNA intermediate -> then converted into mRNA for protein synthesis -> Replication of the genome -> Assembly of new virions

27
Q

How does the release of viruses work?

A

Enveloped: Budding
Nonenveloped: Cell lysis
Exocytosis: for both

28
Q

What are the different disease outcomes for viral infections?

A

Acute infection: infection of the host cell and formation of new virions -> clearance by the immune system
Persistent infections: viruses avoid immune system clearance, Chronic or latent

Chronic infections are characterized by
* Continuous release of virions over time
(e.g., months or years)
* Slow progression of diseases

29
Q

How can persistent viral infections cause cancer?

A

The virus can shut down antiviral stimuli of cell death, causing uncontrolled host cell division
-> Human papilloma viruses (HPV), Epstein-Barr virus (B- and T-cell lymphomas)

30
Q

LO: Size of most viral genomes and what it encodes?

A

ss, ds // RNA or DNA // single or segmented sections // circular or linear

< 5 genes encoding:
-Capsid proteins
-Structural factors
-Enzymes for viral replication
-Proteins to rewrite cells and evade immunity