Intro + Viruses Flashcards
(30 cards)
What are the barriers to infections?
-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
What is the Microbiome and how does it effect the immune system?
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)
What is the first barrier against pathogens?
Barrier immunity: physical (Skin), chemical (low pH, antimicrob. agent, lipids, AAs) , biological (microbiome)
Innate immune responses: Phagocytes
How do phagocytes fight pathogens?
Engulf and degrade, they use germ-line-encoded recognition molecules
(the adaptive immune system uses gene arrangement of receptors, to identify different pathogens)
What parts of pathogens are different from humans?
(Bacteria, fungi, viruses, parasites)
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
What is the adaptive immune system and what are its advantages and disadvantages?
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)
How does Cell-mediated immunity respond?
-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
How can adaptive immunity respond to pathogens they have never seen before?
Random recombination of the binding site of B and T cell receptors
What is the problem with random recombination?
The receptors eventually target to self antigens
Difference between B cell receptors and antibodies?
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
How are antibodies produced?
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
How are T cell receptors different from B cell receptors?
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)
What does Tolerance mean?
Early deletion (lymphoid organ) of B and T cells that target self antigens
How is immune memory created?
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
How does the innate and adaptive immune system work together?
-innate systems produce signals (often cytokines) -> stimulate and direct adaptive immune system
-Phagocytes present antigens to the adaptive immune system, to stimulate differentation
What are two dysfunctions of the immune system?
-Overly active: Allergy, autoimmune disease
-Immunodeficiency: primary (genetic) and secondary (acquired) loss of immune function
Difference between viruses and cells?
Difference in genetic storage form (DNA and RNA), replication (use host machinery), no metabolism, protein capsid instead of lipid membrane, seen under light microscope
What is an example of an enzyme that is viral?
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
Why is the mutation rate in viruses higher than in other living infectious agents?
- 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
What are the outcomes of genetic changes that benefit or limit infectivity?
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
What does the capsid of viruses look like?
-Helical: hollow tube
-Icosahedral: 3-dimensional polygon
-other ones: complex capsids
What happens to the genome of bacteriophages after it is injected into target cells?
Lysis of the target cell or integration into the host’s genome
What is the difference between a viral envelope and capsid?
The envelope originates from the infected host cell (budding off) and is lipid-based and surrounds the capsid.
How does the attachment of a virion to a target cell work?
Through spike proteins for enveloped viruses and capsid proteins in nonenveloped viruses
