Types of Vaccines

 

I have text (bottom, using tabs to look through the different types) and I have a pre-recorded lecture (17 min but you can speed me up). Please choose whichever method works better for your learning.

There are many ways to make a vaccine

We use many strategies to induce a "primary response" of the immune system in order to train the immune system to recognize antigens from a pathogen. Creating cellular & humoral memory is what underlies "immunity" to a pathogen.

The key part of designing a vaccine is to expose the body to antigen that won't cause disease, but will provoke an immune response that can block or kill the pathogen if a person becomes infected with the real pathogen later. After a vaccine shot, some people will feel soreness or heat around the injection site. Others might even develop a slight fever and headache in the next day or so. These are all very normal reactions that indicate the vaccine is stimulating an immune response! This is not to be confused with getting sick or developing disease. Remember that it's the immune response that generates inflammation and fever symptoms and signs in people.

The material I show here illustrates the idea using a virus but please keep in mind that the same guidelines apply to bacteria and eukaryotic pathogens as well.

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Review:  The Immune Response to Viral Pathogens

The figure below does a pretty great job of summarizing the basic steps that the immune system takes to generate an immune response and immunological memory to an invading viral pathogen.  The rest of this mini-lecture will focus on how the virus enters or is processed to be presented on the antigen presenting cell (APC).  After that, activation of the helper T cell (CD4), cytotoxic T cell (CD8) and B cells happen as we've discussed in lecture (or as summarized, in MUCH less detail on this figure).

Week 9-10study guide

 

Weeks 9-10 Study Guide

Innate Immunity Study Guide

Terms you should know:

Innate immunity	Adaptive immunity	Chemical immune mechanisms	Physical immune mechanisms	Cellular immune mechanisms	Skin
Mucous membranes	Ciliated epithelium	Microbiome	Antimicrobial peptides (AMPs)	defensins	lysozyme
sebum	oleic acid	lactoferrin	bacteriocins	histamine	cytokine
chemokine	interferon	interleukin	complement system	Alternative pathway	Lectin Pathway
Classical pathway	C3	Lectin	Mannose	C3a	C5a
C6, 7, 8, 9	Membrane attack complex (MAC)	opsonization	inflammation	autocrine	endocrine
paracrine	leukocytes	erthrocyte	granulocyte	phagocyte	monocyte
basophil	eosinophil	neutrophil	macrophage	dendritic cell	natural killer cell
mast cell	Pathogen recognition receptor (PRR)	Pathogen-associated molecular pattern (PAMP)	phagocytosis	apoptosis	fever

 

Be able to describe/explain in your own words or draw out the process:

• Describe &  provide examples of the three lines of defense of our immune system.
• Draw a sample of the skin. Identify the dermis, epidermis and describe how skin acts in the first line of defense. 
• Where are mucous membranes located? Give some examples of secretions and their chemical components that protect the skin and mucosal surfaces. 
• Explain how the normal microbiota serves a protective role against microbial invasion.
• Explain how the innate immune cells can detect extracellular pathogens (that live outside of host cells) and intracellular pathogens (those that are inside host cells).
• What are the phagocytic cells that participate in the second line of defense? 
• What is chemotaxis and why is it important in an innate immune response? What molecules are used for chemotaxis? 
• How do phagocytes recognize pathogens? Describe the mechanism of phagocytosis. 
  • Describe some strategies that some microbes use to evade phagocytosis (think of virulence factors we've learned this quarter)
• Describe, in general terms, how the complement system tags microbial cells and products as foreign.  
  • How does fragmentation of C3 lead to the activation of complement?  
  • What are the three outcomes of complement activation? 
  • What are the three ways of activating complement?
• Explain the difference between intracellular PRRs and PRRs in the membrane of the cell. What purpose do each of them serve? 
• Describe how viruses and intracellular bacteria trigger the production of interferons. 
  • How do interferons help to defend the host against the spread of the infection. 
• What are the targets of natural killer cells? How do they kill their target cells?
• What are the four signs and symptoms of inflammation? What are the functions of inflammation? 
• Describe the steps of inflammation: Be sure to use the terms vasodilation, phagocyte migration, histamines, cytokines. 
  • What are the first types of phagocytes that migrate to the site of infection? Which come later?
• How does fever help fight pathogens? How can fever be detrimental to hosts?
  

Study guide

 

Viruses Study Guide

Viruses (parts 1 & 2; I highlighted what was relevant in Week 6)

Virus	Prion	Obligatory intracellular pathogen	Virion	Capsid	Envelop virus
DNA virus	RNA virus	----	Non-enveloped virus	Spike	Bacteriophage
Lytic cycle	Lysogenic cycle	Multiplication cycle		Eclipse period	Assembly
Release	Recombination	Latent virus	Phage/lysogenic conversion	Induction	---
Animal viruses	Retrovirus	Reverse transcriptase	Integrase	Provirus	SARS-CoV-2
COVID-19	Spike	ACE2	Variants	Influenza A virus	Hemagglutinin
Neuraminidase	Antigenic shift	Antigenic Drift	Oncogene	Tumor suppressor	Cancer
Oncogenic virus	HPV	Prion

 You can refer to the lectures and pre-class activities (videos & textbook chapters linked there). 

You should be able to explain in your own words (yellow stuff is mostly covered in pre-class of this week)

• What does it mean for a virus to be an obligate intracellular parasite?
• How is the host range of a virus determined?
• Differentiate bacteriophages from animal viruses
• How big is a viral genome compared to a bacterial genome? What kind of genes are found in a viral genome?
• Compare and contrast a capsid from a viral envelope. Do all viruses have envelops? What about capsids?
• During viral replication, what two types of molecules must the virus make? How and where do viruses replicate? What do viruses provide & what does the host cell provide? What is the fate of the virus-infected host cell?
• Describe the stages and what happens in each stage of the lysogenic cycle of bacteriophage λ.
• What is phage conversion & when does it happen?
• How could bacteriophages be used to treat bacterial infections in humans?
• Describe how attachment in animal viruses to the host cell determines the host range, and the type of cell that is infected. Why are the adhesins on a virus considered a virulence factor? Describe the process of entry of animal viruses to the host cell and release from the host cell.
• How is the genome of DNA viruses replicated? What enzymes are used & what is their origin (host or viral)?
  • How are structural proteins for DNA viruses made and assembled? What enzymes are used & what is their origin (host or viral)?
• List the four classes of RNA viruses & describe their genomes.
  • What is a sense (+) strand of RNA? What about antisense (-) strand of RNA?
  • What is the function of RNA-dependent RNA polymerase and is it viral or host?
    • How is a DNA-dependent RNA polymerase different?
  • Why do RNA viruses tend to accumulate more mutations than DNA viruses? Why does this make RNA viruses harder to treat?
  • Describe how the genomes for the following types of viruses are copied & how the structural proteins are made/assembled. Name the enzymes involved and whether they are host or viral:
    • ssRNA viruses with a + strand
    • ssRNA viruses with a – strand
    • ds RNA viruses
    • retrovirus
  • Depending on the viral structure and type (genetic material), can you identify if an antiviral target will work on the virus you are interested in?
    • Why don't antivirals work on bacteria? Why don't antibacterials work on viruses? Why should neither antibacterials nor antivirals target us (humans) in theory?
  • What is a retrovirus? What is the function of the different components of a retrovirus?
    • What is the biosynthesis of retroviruses (use terms: reverse transcriptase, viral integrase, provirus)?
    • How does a retrovirus cause a latent viral infection and why are these hard to treat?
  • Describe the structure and genetic material of SARS-CoV-2. What are the portals of entry & exit?
    • Describe the interaction b/w the spike protein & ACE2. Where are each of these proteins found? Why is this interaction important?
  • Explain the origin of the variants of SARS-CoV-2. How and why have these variants become more or less prevalent over time?
  • Describe the structure and type of influenza A virus. What are the portals of entry/exit?
    • What are the two major surface proteins in the envelope of influenza A? How many different types are there? How do they determine severity fo the influenza virus?
    • Why do you need to get a new flu shot every year?
    • Why does the immune system have some memory for seasonal flu but not when an antigenic shift happens.
  • Differentiate antigenic drift from antigenic shift. Why do antigenic shifts cause more severe diseases & pandemics?
  • Regarding the Varicella-Zoster virus:
    
    • Distinguish between varicella and herpes zoster.
• Describe how viruses are involved in cancer.

• What is a prion and what is the outcome of a prion infection? 
  
  • Discuss the model for prion infectivity we discussed in class. Be sure to state how a normal cellular protein can be converted to an infectious prion form.
  • Didn't get to this stuff this quarter for Unit 2!!!! (crossed out)

 

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Final- notes

  

🔬 Step 1: Draw the 4 Cells

1. Prokaryotic Cell (Bacterium)
   Label:
   
• Cell wall (peptidoglycan)
• Plasma membrane
• Cytoplasm
• DNA (circular, no nucleus)
• Ribosomes (small)
• Flagella or pili (optional)
2. 
   
3. Eukaryotic Cell 1: Human Skin Cell
   Label:
   
• Nucleus (with DNA inside)
• Plasma membrane (no cell wall)
• Cytoplasm
• Mitochondria
• Ribosomes
• Endoplasmic reticulum
• Golgi apparatus
4. 
   
5. Eukaryotic Cell 2: Plant Cell
   Label:
   
• Nucleus
• Cell wall (cellulose)
• Plasma membrane
• Chloroplasts
• Large central vacuole
• Mitochondria
• Ribosomes
6. 
   
7. Eukaryotic Cell 3: Yeast Cell (Baker’s Yeast)
   Label:
   
• Nucleus
• Cell wall (made of chitin)
• Plasma membrane
• Mitochondria
• Vacuole
• Ribosomes
8. 
   

🔍 Step 2: Highlight Key Differences

Between Bacteria (Prokaryote) and Eukaryotic Cells:

4. RNA viruses use an enzyme called RNA-dependent RNA polymerase (RdRp) to copy their genes.

🦠 Microbiology Summary: Pathogens, Immunity & Microbial Relationships

🔬 1. Types of Microbial Relationships

• Mutualism: Both the human and the microbe benefit.
  → Example: Gut bacteria make vitamins.

• Commensalism: Microbe benefits, human is not affected.
  → Example: Skin bacteria.

• Parasitism: Microbe benefits, human is harmed.
  → Example: Tapeworm or malaria parasite.

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🧫 2. Types of Pathogens

• Opportunistic pathogens: Already in the body (normal microbiota) but can cause disease when:

  • They enter the wrong place (e.g., bloodstream).

  • The immune system is weak.

  • Antibiotics disturb the balance.

• Exogenous pathogens: Come from outside the body and enter through:

  • Air (inhalation)

  • Food or water

  • Cuts or wounds

  • Insect bites

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🛡️ 3. Types of Immunity

• Natural active immunity: You get sick, and your body makes memory cells (long-lasting protection).

• Artificial active immunity: You get a vaccine, and your body makes memory cells.

• Natural passive immunity: Antibodies passed from mother to baby (short-term protection).

• Artificial passive immunity: You receive ready-made antibodies from a shot (e.g., rabies antibody injection).

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🧬 4. Immune System Defenses

• NK cells (natural killer): Destroy infected or abnormal cells.

• Plasma cells: Make antibodies.

• Macrophages: Eat invaders (phagocytosis).

• Helper T cells: Help start the immune response.

• Antibodies: Proteins that bind to pathogens and mark them for destruction.

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💊 5. Disrupting Normal Microbiota

• Antibiotics can kill good bacteria.

• This can lead to overgrowth of harmful ones like Clostridium difficile (C. diff).

• Normal Gut → Antibiotics → Kill Good Bacteria → Dysbiosis → C. diff Overgrowth → Toxin Release → Infection & Symptoms

• 
  

• This causes infections, especially in the intestines.

Virus is not living cell; they hide in the host cell. It is hard to target because hidden in the host cell could hurt the host cell. 

Type	Cell or Not?	Living?	Example
Bacteria	✅ Unicellular (1 cell)	✅ Living	E. coli, Staph
Archaea	✅ Unicellular (1 cell)	✅ Living	Extremophiles
Protists	✅ Unicellular (usually)	✅ Living	Amoeba, Paramecium
Viruses	❌ Not a cell at all	❌ Not truly living	Flu virus, COVID-19

 viruses so hard to treat?

• Viruses are not living cells — they hide inside our own cells.

• They use our own machinery to copy themselves → hard to target without hurting our own cells.

• Antibiotics don’t work against viruses.

• Only specific antivirals or vaccines can help.

3. How to identify different types of microbes under the microscope

• Bacteria: Tiny, usually seen with oil immersion lens (1000x); shape (round, rod, spiral); Gram stain helps

• Fungi: Larger, can see yeast buds or mold hyphae at 400x

• Parasites: Usually bigger, can see whole structures (like worm eggs)

• Viruses: Too small for light microscope — need electron microscope or detect with molecular tests (PCR)

Microbe	Features	How to Identify
Bacteria	Prokaryotic cells, cell wall, single-celled	Shape (cocci, bacilli, spirilla), Gram stain, culture
Fungi	Eukaryotic, have nuclei, can be yeast or mold	Seen under light microscope; culture shows fuzzy or budding
Viruses	Not living, DNA or RNA in protein shell	Need electron microscope or PCR; can’t grow on plates, only in living cells

 

Fungi, protozoa, and parasites are eukaryotic

prion protein

 Above is a visual representation of a prion protein, often illustrated to show its normal cellular form (PrPᴄ) and its misfolded disease-causing form (PrPˢᶜ).

🧬 What You're Seeing:

• Normal prion (PrPᴄ): Typically shown in an alpha-helical structure, which is the healthy version found in cells.

• Pathogenic prion (PrPˢᶜ): Characterized by a change in its structure—more beta-sheet content—which leads to aggregates and disease.

Why Prion Structure Matters:

• The shift from alpha-helix to beta-sheet allows the misfolded prion to induce healthy prions to misfold in the same harmful way.

• These aggregates form amyloid plaques, which are associated with neurodegenerative diseases like Creutzfeldt-Jakob disease and Mad Cow disease.