Lecture 1: the microbial world

Full Coverage Summary: Lecture 1 – The Microbial World

I. Fundamentals of Microorganisms
Microorganisms (microbes) are life forms too small to be seen by the unaided
eye, existing as single cells or clusters of cells,,. They are the oldest form of
life on Earth and constitute a major fraction of the planet's biomass,,. In nature,
they live in microbial communities, interacting with their environment and
other organisms,,.
Microbes have a profound impact on human society:
 Pathogens: A small percentage (about 5%) are agents of disease,.
 Agriculture: Nitrogen-fixing bacteria (e.g., Azotobacter) provide essential
nutrients for plants,,.
 Human Nutrition: The gut microbiome helps digest complex
carbohydrates and synthesizes vitamins,,.
 Industry: Used in wastewater treatment, bioremediation, and the
production of biofuels (like ethanol and methane) and food (cheese, beer,
yogurt),,,-.
II. Cell Structure: Prokaryotes vs. Eukaryotes
All living cells share four essential components: a cytoplasmic membrane (the
most important barrier), cytoplasm (aqueous mixture of macromolecules and
ions), ribosomes (protein synthesis), and a DNA genome,,,.
Key Differences:
 Prokaryotes (Bacteria and Archaea): Lack a nucleus and membrane-
enclosed organelles,,. Their DNA is typically a single circular
chromosome aggregated in the nucleoid,,. They often possess
plasmids, which are extrachromosomal DNA providing special traits like
antibiotic resistance,,.
 Eukaryotes (Plants, Animals, Fungi, Algae, Protozoa): Contain a
membrane-bound nucleus and specialized organelles like mitochondria
and chloroplasts,,. Their DNA consists of multiple linear chromosomes
containing non-coding introns, making their genomes much larger than
those of prokaryotes,,,.
III. Microbial Metabolism
Metabolism is the sum of all chemical reactions in a cell,,.
 Catabolism: Reactions that produce energy (ATP),,.
 Anabolism: Reactions that use energy to build biomass,,.
Classification by Energy and Carbon Source:
 Energy Sources: Phototrophs use light; Chemotrophs use chemicals,,.
Chemotrophs are further divided into chemoorganotrophs (organic
compounds) and chemolithotrophs (inorganic compounds, a process
unique to prokaryotes),,,.
 Carbon Sources: Autotrophs use $CO_2$ (primary producers);
Heterotrophs require organic compounds,,,.
IV. Cell Size, Morphology, and the S/V Ratio
Common bacterial shapes (morphology) include coccus (round), rod
(cylindrical), spirillum (spiral), and spirochete,,,.
The Surface-to-Volume (S/V) Ratio: Small cells have a higher S/V ratio than
large cells,,. This makes them more efficient at exchanging nutrients and wastes,
allowing them to grow faster than larger cells,,. The lower limit for a cell is
approximately 0.15 µm, as it must house essential proteins, nucleic acids, and
ribosomes,,.
V. History and the Discovery of Microbes
 Robert Hooke (1665): First to describe microbes (specifically molds),,.
 Antoni van Leeuwenhoek (1676): First to describe bacteria using a self-
made microscope,,.
 Louis Pasteur: Disproved spontaneous generation using swan-necked
flasks, proving that life does not arise from non-living matter,,-. He also
discovered that life discriminates between optical isomers and
developed vaccines for rabies and anthrax,,,.
 Robert Koch: Established Koch’s Postulates, a set of criteria to prove a
specific microbe causes a specific disease,,,. He developed pure culture
techniques using solid media like agar,,,. Teacher's Note: Postulate 1 is
limited because pathogens can be present in healthy animals without
causing disease until the immune system is compromised.
 Martinus Beijerinck: Developed the enrichment culture technique to
isolate specific microbes from environmental samples,,,.
 Sergei Winogradsky: Discovered chemolithotrophy and linked
microbes to biogeochemical cycles (nitrogen and sulfur),,,.
VI. Microscopy and Resolution
 Light Microscopy: Resolution is limited to 0.2 µm,,. Contrast is
improved by staining,.
o Gram Stain: A differential stain separating bacteria into Gram-
positive (purple, thick peptidoglycan) and Gram-negative (pink,
thin peptidoglycan plus an outer membrane),,,,.
 Electron Microscopy: Uses electrons instead of light, reaching a
resolution of 0.2 nm,,,.
o Transmission (TEM): For viewing internal molecular structures
(requires thin sections),,.
o Scanning (SEM): For viewing the cell surface (coated in heavy
metal),,.
VII. The Tree of Life
Carl Woese pioneered the use of ribosomal RNA (rRNA) sequences as an
"evolutionary clock" to determine relationships between all life,,. This led to the
discovery of the Archaea domain,,. All life descended from the Last Universal
Common Ancestor (LUCA),,.

Analogy for Microbial Growth: Imagine a music festival. In the Lag Phase,
organizers are setting up the stage (enzymes preparing for growth). During the
Exponential Phase, the crowd doubles rapidly as more fans arrive (maximum
growth rate). At the Stationary Phase, the food trucks run out of supplies
(nutrients exhausted), and the number of people entering equals those leaving.
Finally, in the Decline Phase, the festival ends, and the population disappears
as the site is cleaned up.
Full Coverage Summary: Lecture 2 – Microbial Cell Structure and
Function
I. The Cell Envelope: Cytoplasmic Membrane and Transport
The cell envelope consists of layered structures surrounding the cytoplasm,
including the cytoplasmic membrane, cell wall, and sometimes an outer
membrane or S-layer.
 Cytoplasmic Membrane: This is the most essential structure; if it is
broken, the cell dies. In Bacteria, it is an 8–10 nm phospholipid bilayer
containing hydrophobic fatty acids and hydrophilic glycerol phosphates
linked by ester bonds. Archaeal membranes contain ether linkages
and isoprenes (not fatty acids); they can form lipid monolayers (e.g.,
diglycerol tetraethers), which are more rigid and stable in extreme heat.
 Functions: It acts as a permeability barrier, a protein anchor, and a site
for energy conservation via the Proton Motive Force (PMF), where a
proton gradient drives ATP synthesis.
 Transport Systems:
o Simple Transport: Driven by the PMF; includes symport (solute
and $H^+$ move together) and antiport (solute and $H^+$ move
in opposite directions).
o Group Translocation: The substance is chemically modified
during transport, driven by energy-rich organic compounds like
phosphoenolpyruvate (PEP).
o ABC Systems: Highly specific systems that use substrate-binding
proteins and ATP to drive uptake.
II. Cell Walls: Bacteria vs. Archaea
Bacterial cell walls are primarily distinguished by the Gram stain.
 Peptidoglycan (Murein): A rigid layer found only in Bacteria, composed
of alternating N-acetylglucosamine (G) and N-acetylmuramic acid (M)
sugars with $\beta$-1,4 linkages. It is destroyed by lysozyme (found in
human tears and saliva) and inhibited by penicillin.
 Gram-Positive: Features a thick peptidoglycan layer (up to 90%) and
teichoic acids (or lipoteichoic acids) that bind divalent metal ions and
provide protection.
 Gram-Negative: Features a thin peptidoglycan layer and an outer
membrane. The outer membrane contains Lipopolysaccharide (LPS)—
which includes the Lipid A endotoxin—and porins, which are selective
channels for solutes.
 Archaeal Walls: Lack peptidoglycan. Some use pseudomurein
(composed of G and T sugars), which is insensitive to lysozyme because
it uses $\beta$-1,3 bonds.
  S-Layers: Paracrystalline surface protein layers found in many bacteria
and nearly all archaea; they are always the outermost layer and provide
structural strength.
 Wall-less Prokaryotes: Some pathogens, like Mycoplasmas, lack cell
walls and survive in osmotically protected environments by having tough
membranes containing sterols.
III. Surface Structures and Cell Inclusions
 Capsules and Slime Layers: Polysaccharide layers used for
attachment, biofilm formation, and protection from the immune system
(phagocytosis).
 Fimbriae and Pili: Filamentous proteins; fimbriae stick to surfaces, while
pili are longer and facilitate genetic exchange (conjugation) or
twitching motility (Type IV pili).
 Hami: Archaeal "grappling hooks" used for surface attachment.
 Cell Inclusions: Function as energy or carbon reserves (e.g., PHB,
glycogen, polyphosphate, and sulfur globules) or for specialized tasks
like magnetosomes (orienting in magnetic fields) and gas vesicles
(buoyancy for phototrophs).
 Endospores: Highly resistant, dormant structures formed by Bacillus and
Clostridium to survive heat, radiation, and chemicals. They contain
dipicolinic acid (DPA) and Small Acid-Soluble Proteins (SASPs) to
protect DNA.
IV. Locomotion and Taxis
 Swimming Motility: Flagella (Bacteria) rotate like tiny machines and
are powered by the PMF. Archaella (Archaea) are thinner and powered
by ATP.
 Surface Motility: Includes twitching (crawling using Type IV pili and
ATP) and gliding (smooth movement along a surface powered by PMF).
 Taxis: Directed movement toward or away from stimuli, such as
chemotaxis (chemicals) or phototaxis (light). Peritrichous bacteria like
E. coli use a "run and tumble" mechanism governed by chemoreceptors.
V. Eukaryotic Microbial Cells
 Organelles: Contain a membrane-bound nucleus (DNA wound around
histones), mitochondria (aerobic respiration), and chloroplasts
(photosynthesis, containing RubisCO).
 Endosymbiosis: Mitochondria and chloroplasts likely descended from
respiratory and phototrophic bacteria that lived inside a host cell.
 Cytoskeleton: Composed of microtubules (tubulin), microfilaments
(actin), and intermediate filaments (keratin) to maintain shape and
move cargo.
 Motility: Eukaryotic flagella and cilia move with a whiplike motion
(they do not rotate) and are powered by ATP and dynein.

Analogy for the Microbial Cell: Think of the microbial cell as a highly
secured mobile fortress. The cytoplasmic membrane is the inner
gatekeeper (the "ID checkpoint"), while the cell wall is the outer stone wall
providing shape and strength. To move, the fortress might use a flagellum (an
outboard motor) or Type IV pili (grappling hooks for "twitching" forward). When
resources are scarce, it packs essentials into inclusions (storage bunkers), and
in extreme danger, it can collapse into an endospore (an indestructible survival
pod) until the environment is safe again.

Full Coverage Summary: Lecture 3 – Microbial Growth and Its Control

I. Microbial Nutrition and Culture Media
Microorganisms require a supply of elements to support growth, categorized into
macronutrients (required in large amounts) and micronutrients (trace metals
and growth factors).
 Essential Elements: H, C, N, O, P, and S are required by all cells.
o Carbon (C): The major element in all macromolecules; a typical cell
is ~50% carbon by dry weight. Heterotrophs use organic carbon,
while autotrophs use $CO_2$.
o Nitrogen (N): Found in proteins and nucleic acids. Most microbes
use Ammonia ($NH_3$) as their primary nitrogen source.
 Micronutrients:
o Trace Elements: Inorganic ions (e.g., Iron, Copper, Zinc) acting as
enzyme cofactors.
o Growth Factors: Organic compounds like vitamins and specific
amino acids.
 Culture Media Classes:
o Defined Media: The exact chemical composition is known.
o Complex Media: Composed of digests of microbial, animal, or plant
products (e.g., yeast extract); the exact composition is unknown.
o Selective vs. Differential: Selective media inhibit the growth of
some microbes while allowing others to thrive; differential media
use an indicator (dye) to detect specific metabolic reactions.
o Teacher's Note: Specialized media are essential for enriching non-
fast-growing microbes to prevent faster species from overgrowing
them.
II. Measuring Microbial Growth
Growth in microbiology refers to an increase in the number of cells, not the
size of an individual cell.
 Total Cell Count: Performed microscopically using counting chambers.
Limitations: It cannot easily distinguish between live and dead cells
without special stains, and small cells or debris can cause errors.
 Viable (Plate) Counts: Measures only the living, reproducing population.
Samples must be diluted to achieve 30–300 colonies per plate.
o The Great Plate Count Anomaly: Microscopic counts of natural
samples reveal significantly more organisms than those recoverable
on plates because different organisms have vastly different growth
requirements.
 Turbidimetric Measures: A spectrophotometer measures Optical
Density (OD). This is the fastest, non-destructive method, but cells must
grow planktonically (as single cells in suspension) to be accurate.
III. Growth Dynamics and Life Cycles
  Binary Fission: The most common division process where a cell enlarges
and divides into two identical daughter cells via a septum.
 Generation Time: The time required for a population to double. E. coli
can double in 20 minutes in a lab environment, whereas environmental
microbes may take days.
 Batch Culture Growth Cycle: A closed system with four distinct phases:
1. Lag Phase: Interval for synthesizing enzymes and metabolites
before growth starts.
2. Exponential Phase: Healthiest state where cell numbers double at
a constant rate.
3. Stationary Phase: Growth rate is zero; nutrients are exhausted or
waste products accumulate.
4. Decline/Death Phase: Cells eventually die at an exponential rate.
 Continuous Culture (Chemostat): An open system where fresh medium
is added and spent medium is removed at the same rate to maintain a
steady state.
 Biofilms: Most microbes in nature grow in attached polysaccharide
matrices rather than as planktonic cells. Biofilms offer protection against
antibiotics, grazing, and desiccation.
IV. Environmental Effects on Growth
 Temperature: Microbes have cardinal temperatures (minimum,
optimum, maximum).
o Psychrophiles: Optima $\le 15^\circ C$. Adapted with $\alpha$-
helices (flexibility) and unsaturated/short-chain fatty acids to
keep membranes fluid in the cold.
o Thermophiles/Hyperthermophiles: Optima $>45^\circ C$ or
$>80^\circ C$. Adapted with saturated fatty acids (Bacteria) or
lipid monolayers (Archaea) to maintain membrane integrity in the
heat.
 pH: Most microbes grow between pH 3–9, but intracellular pH must stay
near neutral ($\sim 7$) to protect macromolecules.
o Teacher's Note: Extreme external pH can mess up the Proton
Motive Force used for ATP synthesis; alkaliphiles often use a
sodium ($Na^+$) motive force instead.
 Osmolarity: Cells maintain a positive water balance using compatible
solutes (e.g., sugars, alcohols) to prevent water loss in high-solute
environments.
 Oxygen Relationship:
o Obligate Aerobes: Require $O_2$; Obligate Anaerobes: $O_2$
is lethal.
o Facultative Anaerobes: Can grow without $O_2$ but grow better
with it.
o Toxicity: Molecular $O_2$ is not toxic, but its byproducts
(Superoxide, Hydrogen peroxide, Hydroxyl radical) are. Enzymes like
catalase neutralize these.
V. Controlling Microbial Growth
 Heat: The most common method. The Autoclave uses steam under
pressure to reach $121^\circ C$, which is necessary to kill endospores.
Pasteurization reduces the microbial load but is not sterilization.
  Radiation: UV is used for surfaces but has poor penetration; ionizing
radiation is used for surgical supplies and food.
 Filtration: Used for heat-sensitive liquids. HEPA filters remove particles
$\ge 0.3 \mu m$ from the air.
 Chemical Agents:
o -static: Inhibits growth; -cidal: Kills without lysis; -lytic: Kills by
bursting the cell.
o MIC (Minimum Inhibitory Concentration): The smallest amount
of an agent needed to inhibit growth.

Analogy for Microbial Growth (The Pop-Up Festival): Imagine a batch

culture is like a weekend music festival in a remote field.
1. Lag Phase: The roadies are setting up the stage and sound system
(enzymes being synthesized). No music is playing yet.
2. Exponential Phase: The gates open, and the crowd doubles rapidly as
word spreads. This is the peak of the party.
3. Stationary Phase: The food trucks run out of supplies and the trash
starts piling up. For every person arriving, one person leaves (growth rate
is zero).
4. Decline Phase: The festival is over. Everyone leaves because there is no
food or water left, and the site becomes empty again.

Full Coverage Summary: Lecture 5 – Molecular Aspects of Microbial

Growth
I. Visualizing Molecular Growth
To study growth at a molecular level, researchers use advanced techniques that
go beyond standard light microscopy.
 Super-resolution microscopy: Resolves structures as small as 5–50 nm
in living cells, allowing scientists to watch individual molecules move in
real-time.
 Fluorescent Tagging: Reporter genes, such as Green Fluorescent
Protein (GFP), are fused to genes of interest to localize specific proteins
or genetic elements (like chromosomes vs. plasmids) under a microscope.
 Photoactivated probes: These probes switch between bright and dark
states, helping map the movement of individual molecules, such as MukB,
which assists in unknotting chromosomes after replication.
II. Chromosome Replication and Segregation
The bacterial cell cycle requires precise temporal (timing) and spatial (location)
control.
  Initiation at oriC: DNA replication begins at the origin of replication
(oriC). The protein DnaA-ATP binds to oriC to unwind the DNA and load
the replisome (a complex of ~13 proteins).
 Inactivation Mechanisms: To prevent over-replication, DnaA-ATP must
be deactivated via:
1. SeqA binding: SeqA binds to hemimethylated DNA at oriC, blocking
DnaA and repressing dnaA gene expression.
2. HdaA activity: This ATPase hydrolyzes DnaA-ATP into the less
active DnaA-ADP.
 Fast-Growing Cells: In E. coli, replication takes 40 minutes, but the cell
can double in 20 minutes. This is possible because multiple replication
forks form; a new round of replication begins before the previous one
finishes.
 Segregation (Par System): In many bacteria, the Par system
distributes chromosomes. PopZ localizes at the poles, and ParB binds to
the parS sequence near the origin to pull the chromosomes to opposite
ends.
III. Cell Division and the Divisome
 The Divisome: A protein complex (~10 proteins) that orchestrates cell
division.
 FtsZ Ring: Crucial for division, FtsZ forms a ring around the center of the
cell, defining the division plane.
 Anchor Proteins: ZipA connects the FtsZ ring to the cytoplasmic
membrane, while FtsA helps recruit other divisome proteins.
 Septum Formation: FtsI (a penicillin-binding protein) is essential for
peptidoglycan synthesis at the septum.
 Min Proteins (Finding the Center): To ensure FtsZ forms exactly in the
middle, MinC and MinD inhibit FtsZ at the poles, while MinE oscillates to
repel them, leaving the center open for the FtsZ ring to form.

IV. Determinants of Cell Morphology

Bacteria utilize a dynamic protein cytoskeleton to maintain shape, which
resembles eukaryotic systems.
 MreB (Rods): Forms patchlike filaments below the membrane that direct
local peptidoglycan synthesis. If MreB is inactivated, rod-shaped cells
become cocci.
 Crescentin (Vibrios): Found in curved cells like Caulobacter; it localizes
to the concave face of the cell to impart curvature.
 Evolutionary Links: MreB is a homolog of eukaryotic actin, FtsZ is a
homolog of tubulin, and crescentin is a homolog of keratin.
V. Peptidoglycan Biosynthesis
To grow, the cell must cut the existing wall and insert new material without
bursting.
 Cutting: Autolysins create small gaps by breaking the $\beta$-1,4
glycosidic bonds in the peptidoglycan backbone.
  Transport (Lipid II): Bactoprenol, a hydrophobic C55 alcohol, carries
peptidoglycan precursors across the cytoplasmic membrane.
 Insertion: Transglycosylases insert the precursors and reform the
glycosidic bonds.
 Transpeptidation: The final step where transpeptidases (like FtsI) form
peptide cross-links between glycan chains. Penicillin inhibits this step,
leading to cell lysis by autolysins.
VI. Biofilm Formation and Social Behavior
Biofilms are protective matrices of exopolysaccharides.
 Four Stages: 1. Attachment (using flagella/pili), 2. Colonization
(extracellular polysaccharide production), 3. Development, and 4. Active
Dispersal.
 c-di-GMP: The "master switch" regulatory molecule that triggers the
transition from swimming to biofilm growth.
 Quorum Sensing: In P. aeruginosa, the accumulation of acyl
homoserine lactones (AHLs) signals that the population is growing,
triggering matrix production.
 Polymicrobial Biofilms: Different species interact via metabolic crosstalk
or DNA sharing. Example: In cystic fibrosis, P. aeruginosa can kill and
scavenge nutrients from S. aureus, increasing infection virulence.
VII. Antibiotics: Resistance and Persistence
 Targets: Antibiotics target essential processes like DNA replication, RNA
synthesis, protein synthesis (ribosomes), and cell wall synthesis.
 Resistance Mechanisms:
1. Metabolic bypass: Producing more of the target enzyme than the
drug can bind.
2. Enzymatic inactivation: For example, $\beta$-lactamase
destroying penicillin.
3. Efflux pumps: Removing the drug from the cell.
4. Target modification: In MRSA, the MecA protein provides an
alternative penicillin-binding protein that the drug does not
recognize.
 Persistence and Dormancy: Unlike resistant mutants, persister cells
are genetically identical but enter a dormant state (non-growing). This is
often controlled by toxin-antitoxin modules (like HipAB); because they
aren't growing, antibiotics cannot kill them, leading to recurring infections.

Analogy" for Microbial Growth: Bacterial growth is like a construction crew

building a skyscraper from the inside while it is occupied.
 DnaA is the lead architect starting the blueprints (replication).
 Min proteins are the surveyors ensuring new walls are placed exactly in
the middle.
 MreB acts as the internal scaffolding that determines the building's shape.
 Autolysins are the demolition crew carefully removing old bricks so
bactoprenol delivery trucks can bring in new ones.
 If antibiotic inspectors (drugs) arrive, the crew uses efflux pumps to
throw them out or simply goes on dormancy (a long coffee break) until
the inspectors leave.
Full Coverage Summary: Lecture 6 – Viruses and Their Multiplication
This summary integrates all topics from the Lecture 6 slides, the teacher’s
preprepared summary, the word document notes, and the study book to
provide a complete overview for your exam.
I. Fundamentals of Virology
 Definition: A virus is a genetic element that can multiply only inside a
living host cell. They are obligate intracellular parasites, relying
entirely on the host for energy, protein synthesis, and metabolic
intermediates.
 The Virion: This is the extracellular form of a virus that facilitates
transmission between host cells. Replication only begins once the virus
infects a permissive host cell.
 History: Viruses were discovered late because they passed through filters
designed to trap bacteria. Martinus Beijerinck described them as
"contagium vivum fluidum" (soluble living germs).
 Strength in Numbers: Viruses are the most abundant "microorganisms"
on Earth, with an estimated $10^{31}$ particles.
 Ecological Impact of Marine Viruses: In the ocean, virion concentration
is as high as $10^8$ per mL. They kill 5% to 50% of seawater
bacteria daily, which is a vital factor in the elemental carbon and
nutrient cycles because it releases organic matter back into the water.
II. Structure of the Virion
 Capsid: The protein shell surrounding the genome, composed of individual
protein molecules called capsomeres.
 Nucleocapsid: The combination of the nucleic acid genome and the
capsid.
 Naked vs. Enveloped Viruses:
o Naked viruses (most bacterial and plant viruses) consist only of
the nucleocapsid.
o Enveloped viruses (common in animals) have an outer
phospholipid bilayer derived from the host cell membrane,
embedded with viral glycoproteins. They exit the host more easily
via budding.
 Symmetry:
o Helical: Rod-shaped (e.g., Tobacco Mosaic Virus); the length is
determined by the nucleic acid length.
o Icosahedral: Spherical (e.g., HPV); the most efficient arrangement
requiring the fewest capsomeres.
 Enzymes in Virions: Some carry specialized enzymes like lysozyme (to
bore holes in bacterial walls), neuraminidases (to release influenza from
host cells), or RNA replicases/Reverse transcriptase for genome
replication.
III. Viral Genomes and the Baltimore Classification
Viruses are classified by the relationship between their genome and their mRNA
(which is always "plus-strand" or +).
 The 7 Baltimore Classes:
o Class I (dsDNA): Classical semiconservative replication (e.g., T4).
 o Class II (ssDNA+): Must make a minus-strand DNA intermediate
(replicative form) before making mRNA.
o Class III (dsRNA): Requires RNA replicase to make +mRNA from
the minus strand.
o Class IV (ssRNA+): Genome can be used directly as mRNA.
o Class V (ssRNA-): Must transcribe the minus strand to make
+mRNA using RNA replicase.
o Class VI (ssRNA+ Retroviruses): Replicate through a dsDNA
intermediate using reverse transcriptase (e.g., HIV).
o Class VII (dsDNA): Replicate through an RNA intermediate using
reverse transcriptase.
IV. Quantification and Culture
 Titer: The number of infectious units per volume of fluid.
 Plaque Assay: Method where viruses are mixed with host cells on agar.
Clear zones of cell lysis, called plaques, represent one initial infectious
virion.
 Plating Efficiency: The number of plaque-forming units (PFU) is always
lower than the actual number of particles seen under an electron
microscope.
o The Reason: This is due to defective virions or environmental
conditions that are not perfectly "permissive" for every particle.
V. The Viral Replication Cycle
1. Attachment (Adsorption): Highly specific; viruses bind to host
receptors (like LPS, flagella, or transport proteins).
2. Penetration: In prokaryotes, only the nucleic acid is injected (capsid
stays outside). In eukaryotes, the entire virion typically enters via
endocytosis or fusion.
3. Synthesis: Host machinery is redirected to replicate the viral genome and
produce proteins.
o Viroplasms: Some eukaryotic cells form membrane-bound "viral
factories" to increase the assembly rate and protect the virus from
host defenses.
4. Assembly: Capsids are formed and genomes are packaged (e.g., using
ATP to pump DNA into a T4 head).
5. Release: New virions exit via cell lysis (lytic viruses) or budding
(enveloped viruses).
Growth Curve: Viruses show a one-step growth curve. There is a latent
period (eclipse + maturation phases) where no infectious viruses are found
outside the cell, followed by a sudden burst as cells lyse.
VI. Life Cycles: Lytic vs. Lysogenic
 Virulent (Lytic): The virus always lyses and kills the host (e.g.,
Bacteriophage T4).
 Temperate: The virus can choose between the lytic pathway or
lysogeny.
o Lysogeny: The viral genome integrates into the host chromosome
as a prophage.
o Induction: Stress (like DNA damage) triggers the prophage to exit
the genome and enter the lytic cycle.
VII. Animal Virus Outcomes
Animal viruses often replicate in the nucleus. Outcomes include:
 Virulent infection: Cell lysis.
 Latent infection: Viral DNA (provirus) remains dormant until triggered.
 Persistent infection: Virions are released slowly by budding without
killing the host.
 Transformation: Conversion of a normal cell into a tumor cell (cancer).

VIII. The Host-Virus "Arms Race"

 Bacterial Defenses:
o Restriction Endonucleases: Cleave foreign DNA at specific sites.
o CRISPR-Cas: An adaptive immune system. It stores "memory" of
past infections in spacers; if the same DNA enters again, Cas
proteins destroy it.
o Toxin-Antitoxin Modules: These can slow down host cell
growth or trigger "abortive infection" (cell suicide) to prevent the
virus from spreading to the rest of the colony.
 Viral Counter-Defenses: Viruses may modify their DNA (e.g.,
glycosylation or methylation) or produce proteins that inhibit host
restriction systems.
IX. Specific Human Viruses
 Influenza: An enveloped ssRNA(-) virus with a segmented genome (8
pieces).
o Hemagglutinin (H): For attachment.
o Neuraminidase (N): For release.
o Antigenic Drift: Minor mutations leading to seasonal outbreaks.
o Antigenic Shift: Major reassortment of segments when two
different strains infect one host, leading to pandemics.
 Ebola: A filamentous (filovirus), ssRNA(-) virus transmitted via direct
contact with body fluids; it is zoonotic, originating in bats.
 SARS-CoV2: An enveloped ssRNA(+) virus that attaches specifically to
the ACE2 receptor. Most vaccines are directed at its Spike protein.

Analogy for Plating Efficiency and Defective Virions: Imagine a vending

machine (the host cell). You have 100 tokens (virions). If you direct-count them
with a microscope, you see 100 tokens. However, when you try to get a snack
(successful infection/plaque), only 10 snacks come out. This is because 90 of the
tokens were dented or the wrong size (defective virions), or the machine was
jammed (non-permissive environment). This is why the "Plaque-Forming Units"
count is always lower than the "Direct Particle" count.

(The lecturer also has his own summary up in Brightspace!)