Lecture Exam 3 Flashcards
Why are viruses non-living?
Viruses are not made out of cells, they can’t keep themselves in a stable state, they don’t grow, and they can’t make their own energy.
Obligate intracellular parasites
Require a living host to multiply
Ex: Viruses
What is the basic structure of a virus?
- Protein coat- capsid
- Nucleic acid (DNA or RNA)
- Enveloped/Naked
- Noncellular
Virus size range
10-400 nm on average.
Range from 20-1000 nm.
Host specificity
Virus particles are commonly very specific about what organisms they attack.
- Lock and Key mechanism (protein spikes)
Ex. Bacteriophage will only attack bacteria.
3 major virus characteristics
a. DNA or RNA
b. Single or double stranded
c. Single molecule or segmented
Virus Particle Structure
a. Isometric: Sides of a triangle
b. Helical: Rod shaped
c. Pleomorphic: Irregular
Presence of Absence of an Envelope
a. Non-enveloped
b. Enveloped
- Advantage: Protection against host’s immune
system (Phagocytosis).
- Disadvantage: Does not survive on objects.
Capsid
Protein coat surrounding a virus. Determines the shape of the virus, made up of capsomeres.
➣ Capsomeres = Subunit of viral protein units.
Genome (virus)
Either RNA or DNA.
➣ Can be single or double stranded, enzymes may be packaged with it.
Nucleocapsid
The capsid together with the nucleic acid.
Virion
A complete virus particle that has not yet attached to a host cell.
Viroid
A virus that infects plant cells.
Helical capsid
Consists of a ribbonlike protein that forms a spiral around the nucleic acid.
- Appears as a rod
Isometric capsid
- Capsomeres arrange a shell around nucleic acid.
- Each side of the shell is an equilateral triangle.
Protein Spikes
Projections of the envelope or capsid
- Use glycoproteins to attach to cell
- Illicit immune responses in the host.
Bacteriophages replication
➣ Lytic Replication - Bacterial cell is destroyed through release of the virus.
➣ Lysogeny - Bacterial cell is not destroyed. Incorporation into the bacterial DNA.
Lytic Replication Steps
- Attachment/penetration
- Synthesis
- Maturation
- Release of new phage
by lysis of host cell
Lysogenic Replication Steps
- Attachment/penetration
- Incorporation of phage DNA
into DNA of bacterial host
Prophages
Inactive phages
Provirus
Viral DNA that inserts into a host genome.
▻ Causes latency in human host.
▻ Retrovirus: A retrovirus is a type of virus that
inserts a copy of its RNA genome into
the DNA of a host cell that it invades,
thus changing the genome of that cell.
Viruses that produce latent infections in humans
▻ Herpes simplex virus
▻ Varicellovirus
Attachment to host cell
Virus:
▻ The virus must have protein spikes.
——————————————————
Host:
▻ Needs receptors that bind with the Viral spikes.
▻ Specific
Penetrating the host cell
▻ Direct Penetration (RARE) - Naked virions inject their genomes into a cell.
▻ Endocytosis - Naked or enveloped virus is engulfed by the host cell.
▻ Membrane Fusion - The viral envelope becomes one with the host’s cell membrane.
Uncoating
The separation of viral nucleic acid from its protein coat
Synthesis in the host cell
▻ ds DNA Virus: Viral dsDNA ➙ RNA ➙ Protein
▻ ss DNA Virus: Creates the complement of viral
ssDNA and combines them to
create dsDNA. dsDNA is then used
to make mRNA, and then translated
into a protein. ----- ▻ (+) sense ssRNA Virus: Acts directly as mRNA ▻ (-) sense ssRNA Virus: Must convert (-) sense to a complement (+) sense in order to be used as mRNA.What does a virus need to do
to make new viruses?
▻ Copy its genome (DNA or RNA)
▻ Make new viral protein coats
▻ Make new spike proteins
▻ Get an envelope if it needs one
Release of Viruses
➣ Enveloped viruses are released through budding.
➣ Naked viruses are released by exocytosis or lysis of the host cell.
Latent Viruses
➣ Different forms
➣ Some viruses remain dormant inside host
cell
➣ Others incorporate genetic material into
chromosome of host cell
How does a virus like Influenza escape the immune system?
Antigenic drift.
Influenza develops a series of mutations that allow it to escape recognition.
Antigenic drift
A kind of genetic variation in viruses, arising by the accumulation of mutations in the virus genes that code for virus-surface proteins that host antibodies recognize.
Host Range
Most viruses are limited to a few hosts.
➣ With the exception of rabies
Persistent Viruses
Viruses that can reactivate periodically.
➣ Typically seen in enveloped viruses that exit
the host cell by budding.
➣ Varicella-zoster virus, measles virus, HIV-1, and human cytomegalovirus are examples of viruses that cause typical persistent infections.
Cytopathic effect (CPE)
Structural changes in host cells that are caused by viral invasion.
➣ Can be used to determine type of viral infection.
ex: Virus may cause cell to swell or burst. This may be unique to the
virus.
More examples:
➣ Rabies: Negri Bodies (clusters of virus) within the cells.
➣ Respiratory Syncytial Virus (RSV): Syncytia (cause cells to merge)
Teratogenic
Acronym TORCH:
TO: Toxoplasma (protozoa)
R: Rubella virus
C: Cytomegalovirus
H: Herpes virus
Other: Hepatitis B, Varicellovirus
Oncogenic
Viruses that can cause cells to become cancerous.
ex: Epstein Barr virus - Burkitt’s lymphoma, Papilloma virus, Hepatitis B,
Retroviridae
Acute Infections
Acute infections are of relatively short duration with rapid recovery.
Immunity
Resistance to an infection by microorganisms
Adaptive Immunity (specific)
Immunity against a particular microorganism after having been exposed to it.
Innate Immunity (non-specific)
Immunity against any invader, born with it.
Non-specific Mechanisms
➣ Anatomical barriers
➣ Secretory Chemicals
➣ Cellular Mechanisms
Anatomical Barriers
➣ Skin (Epithelium) - Layers of protection.
• Two layers: Epidermis, and Dermis
• KERATIN protects Dermis
- Keeps moisture out, create salty
environment on skin
➣ Mucus Membranes - Contain antibodies (Iga)
• Ciliary Escalator: Traps particles
➣ Lacrimal Apparatus - Glands that produce tears
• Dilute particles that get into the eyes.
• Natural antibiotic: Lysozymes (protects from
gram +)
➣ Cerumen - EARWAX!
• Fatty acid composition. (acidic)
• Lysozyme: Break down Gram positive cell
walls
Cells
⓵ Neutrophils ⓶ Monocytes (prophage) ⓷ NK Cells ⓸ Basophils ⓹ Eosinophils
Neutrophils (PMNs)
➣ Nuclei contain 2 or 5 lobes.
➣ Highly phagocytic
➣ Active during the 1st phase of infection
➣ Exit through the blood to enter infected tissue, destroy microbes.
FIRST RESPONDERS
Monocytes
➣ Nuclei in the shape of a horseshoe
Phagocytosis Steps
⓵ Chemotaxis:
• Recruitment of phagocytes to an infected area
⓶ Attachment:
• Microbe is tagged to inform WBCs that it must be phagocytosed (Opsonization).
• Opsonins: Antibodies and Compliment proteins
⓷ Injestion:
• Macrophage morphs membrane into a psuedopod (False Feet), begins to engulf the microbe. Traps microbe in a phagosome.
⓸ Digestion:
• Phagosomes are fused with lysozomes (Phagolysozomes).
• RESULT: Microbe is murdered eheheheh >:D
• Secrete parts of microbe through exocytosis
Macrophage
Destroys microbes in the body.
• Once microbe is destroyed the Macrophage signals to the white blood cells what it encountered.
- Display the antigen on it’s surface, “Y’all kill this thang”
Basophils
Not as abundant in the body.
• Release Histamine - Causes inflammation.
- Dilate blood vessels, capillaries more permeable, recruit WBCs to infected site.
• Stain purple
Eosinophils
Destroy helminths (parasitic worms). • Aid in allergic response • Stain red/orange
NK Cell
Destroy any abnormal cell in the body.
• Punch membranes (perforins). “Surprise motherfker!”
Interferons
Proteins made when a virus infects a cell.
• Binds to adjacent cells, protects other cells from viral replication.
Complement
Series of proteins in the plasma.
a. Increase inflammation
b. opsonization
c. MAC (membrane-attack-complex): Punch holes in microbe, kill it.
Classical pathway
Complement is activated through the binding of a specific antigen to an antibody
Alternate pathway
Complement is activated through surface proteins of the invading microorganism.
Inflammation
Body's response to an infection, caused by an increase in histamines. ------------ Four Cardinal Signs (Increase bloodflow) 1) Redness (Erythema) 2) Heat 3) Swelling (edema) 4) PAIN (That's what this class is fr) OTHER SIGNS: - Pus: dead bacteria - Abscess: Pus accumulation - Granuloma: Chronic inflammation
Inflammation Mediators
- Histamines - Cause vasodilation (edema)
- Kinins - Cause vasodilation, and chemotaxis
- Prostaglandins - Intensify histamine and kinin response ( Aspirin and Ibuprofen )
- Leukotrienes - increased permeability of the blood vessels
Inflammation Steps
1) Vasodilation
2) Chemotaxis
3) Tissue Repair
Fever
Caused by PYROGENS ( fever causing chemicals).
- Cytokines are released by macrophages
- Body’s way of getting rid of microbes by increasing temperature.
- Increased phagocyte activity and metabolism.
Specific Immunity Mechanisms
a. Humoral: (Antibody-mediated)
- For bacteria, and viruses outside of cells.
b. Cell-mediated: (T-lymphocytes)
- For viruses, cancers, fungi, worms, and transplants.
Antigen
A protein that produce immune responses.
- Epitope: Part where antibody will bind
1. Exogenous antigen - on surface (flagella, walls, etc.)
2. Endogenous antigen - antigens within the body cell.
Antibody
Made in response to antigen (activated B-lymphocyte)
- Antibody attaches to antigen so it can be phagocytized
Adaptive immunity characteristics
- Recognize self/non-self
- Antigen specific
- Diversity: recognize antigens but only respond to 1
- Rapid production of cells that react to an antigen
- Memory
B-cells
Make up 15% of lymphocytes.
- Become plasma cells when stimulated. - Secrete antibodies
T-cells
Classified into subgroups CD (cluster differentiation)
- T-Helper Cells (CD4): Humoral and cellular responses. - T-Cytotoxic Cells (CD8): Cellular response.
