WEEK 4 Flashcards
(92 cards)
1
Q
Describe neutrophils
A
Are the most common polymorphs & circulate in the blood
- they form the bulk of the early acute inflammatory response.
- infiltrate at the site of damage & generally arrive before monocytes
- in response to chemotactic agents, they adhere to the endothelium of local capillaries & venules & their pseudopodia squeeze between the endothelial cells & dissolve the basement membrane in order to move into the tissue space
2
Q
Describe eosinophils.
A
Have a bi-lobed nucleus & lots of granules in the cytoplasm.
- are also phagocytic & involved in the control of allergy
- also have a role in the removal of fibrin deposited as part of the inflammatory response
3
Q
Describe basophils.
A
Move into tissues during inflammation
- found in the blood
- are rich in granules that contain histamine, this is why it can be hard to identify a nucleus in a micrograph
- contain heparin for clotting prevention
4
Q
What 3 types of leukocytes are granulocytes?
A
neutrophils
eosinophils
basophils
5
Q
What are monocytes?
A
circulating WBCs derived from precursors in bone marrow becoming macrophages when they leave the circulation
6
Q
What are macrophages?
A
versatile cells & act as the main scavengers for old cells & debris
7
Q
What are the 3 types of phagocytic cells?
A
eosinophils
neutrophils
macrophages
8
Q
What is chemotaxis?
A
The movement of a motile cell/organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration.
Cells “stick” to the walls of the BVs & “push” their way through the gaps between the cells
9
Q
What is the differential count?
A
It gives the proportions of the different leukocytes in the blood
This is determined by creating a blood film from a sample of blood & counting the number of each cells
10
Q
What happens during an allergic reaction?
A
IgE Ab binds to the Fc receptor on a mast cell & allergen can bind to the IgE Ab which causes the release of histamine & vasoactive amines
11
Q
Describe the (i) humoral response (ii) cell-mediated repsonse
A
(i) Plasma cells (B cells) secrete Ab’s. Vaccinations stimulate the immune response
(ii) Cytotoxic (T cells) kill virally infected cells WITHOUT damaging healthy cells. They are in the blood stream
12
Q
What are (i) Erythrocytes (ii) Reticuloctyes?
A
(i) responsible for oxygen & carbon dioxide transport
(ii) newly formed erythrocytes with a short lifespan
13
Q
What is the reticulocyte count? What does an increase in this value indicate?
A
It gives information on the activity of bone marrow
- an increased count indicates that erythrocyte production has increased
14
Q
What happens to the reticulocyte count in response to the treatment of a patient with a B12 deficiency? Why is this the case?
A
Reticulocyte count peaks, as a boost of activity in the bone marrow occurs
15
Q
How long do reticulocytes retain RNA when in the blood? Why is this useful?
A
For 24-48 hours
- it can be stained by specific dyes (cresyl violet, methylene blue)
16
Q
What is the (i) PCV (ii) MCV (iii) MCH (iv) MCHC
A
(i) PACKED CELL VOLUME - the volume of RBCs in a sample after centrifugation (haematocrit)
(ii) MEAN CORPUSCULAR VOLUME - average volume of 1 RBC
= vol. of x RBCs / x RBCs
(iii) MEAN CORPUSCULAR Hb - average amount of Hb in 1 RBC
= amount Hb in x RBCs / x RBCs
(iv) MEAN CORPUSCULAR Hb CONC - average concentration of Hb in 1 RBC
= amount Hb in x RBCs / volume x RBCs = MCH / MCV
17
Q
Describing platelets, state their lifespan, where they are derived from, what they are involved in & how they are destroyed.
A
Lifespan = 5-9 days
Derived from megakaryocytes
Involved in clot formation (coagulation cascade)
Destroyed by phagocytosis in spleen & kupffer cells in liver
18
Q
Define (i) Haemostasis (ii) Anaemia.
A
(i) process by which haemostasis is arrested following vascular injury. This can go wrong if it occurs at the wrong place or wrong time. A mass can be formed in the BVs due to the aggregation of platelets
(ii) Reduction in Hb or Red cell conc in the blood. Therefore a reduced supply of oxygen to tissues (tissue hypoxia). Can be due to cells not being manufactured OR loss of cells.
19
Q
What are the SIGNS and SYMPTOMS of anaemia? (HINT: 4 signs, 5 symptoms)
A
SIGNS - pallor face - glossitis - angular stomatitis - koilonychia SYMPTOMS - fatigue - weakness - headaches - breathlessness - palpitations
20
Q
What is the function of enzymes? How do they do this?
A
Enzymes lower the activation energy required for a chemical reaction by stabilising the transition state
21
Q
What is the equation for calculating rate enhancement?
A
Catalysed rate / uncatalysed rate
22
Q
WHY is product accumulation not linear? (HINT: there’s 4 reasons)
A
- Substrate concentration falls
- Product may inhibit the enzyme
- Enzyme may denature
- Reverse reaction becomes favourable
23
Q
How is enzyme activity (Vo) measured?
A
By increasing the substrate concentration & measuring the accumulation of products over time
24
Q
The maximal velocity (Vmax) is hard to achieve, how can it be calculated?
A
By plotting a double reciprocal of the data, creating a Lineweaver-Burke Plot
25
What is the Km? What is the Michaelis-Menten equation?
Km = the substrate concentration required for half the maximum velocity
Michaelis menten eqn measures the activity of an enzyme:
= Vmax * [S] / Km +[S]
26
What is irreversible inhibition? Give an example.
Inhibitors react with the enzyme & form a covalent adduct with the protein
E.g. ORGANOPHOSPHATES
The primary mechanism of action of diisopropyl fluorophosphate (DIPF), an organophosphate pesticide, is inhibition of AChE. AChE degrade ACh into acetic acid & choline. Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group (located at active site of AChE) Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of receptors
27
What is reversible competitive inhibition? Give an example.
Competes with the substrate for the active site of the enzyme as it has a similar structure to that of the normal substrate. The drug occupies the active site & leaves it unchanged => the activity of an enzyme is slowed down
E.g. BACTERIA cannot use readily made folic acid, but must synthesise it from 4-aminobenzoic acid. Sulphonamides are similar in structure to 4-aminobenzoic acid are are therefore effective Ab as they starve bacteria of essential folic acid.
When a competitive inhibitor is present, an increased concentration of substrate is needed to reach Vmax => increase in Km (Vmax is constant)
28
What is reversible allosteric inhibition? What is the difference between mixed & non-competitive inhibition? Give an example
Can bind to the enzyme at the SAME TIME as the substrate as they don't bind to the active site. They render the enzyme substrate complex inactive because the inhibitor cannot be driven from the enzyme by increasing substrate conc.
The difference between mixed & non-competitive inhibition is that the latter affects activity ONLY, but the former affects activity & substrate binding
MIXED: Vmax dec, Km inc
NON-COMP: Vmax dec, Km unchanged
E.g. PFK catalyses the transfer of phosphate from ATP to fructose-6-P
- PFK bindds to ATP at 2 sites (active & inhib site). In increased levels of ATP, the inhibitory site is occupied & fructose-6-P binding is affected
29
What are the 3 causes of acute inflammation?
microbial infections
hypersensitivity
physical & chemical agents
30
What are the 5 key points to recognising inflammation?
1. Redness (RUBOR) - dilation of BVs
2. Heat (CALOR) - increase in peripheral temp due to hyperaemia
3. Swelling (TUMOR) - mainly oedema
4. Pain (DOLAR) - stimulation of nerve endings
5. Loss of function
31
What are the 2 stages of acute inflammation?
1. VASCULAR phase - dilation & increased permeability of local BVs
2. EXUDATIVE phase - fluid & cells escape from permeable venules
32
What is an exudate? What are the features of an exudate?
```
Defined as a mass of cells & fluid that has seeped out of BVs OR an organ
Features:
- high protein content
- increased vascular permeability
- net flow OUT
```
33
What are the features of a transudate?
Low protein content
Normal vascular permeability
Net flow OUT
34
How does an increase in vascular permeability come about?
Produced by chemical mediators such as histamine & bradykinin & involves the stimulation of endothelial cell cytoskeleton by chemical mediators.
It is confined to post capillary venules & does NOT damage them
35
During inflammation, what happens to lymphatics & antigens?
Lymphatics are dilated & they drain fluid from the exudate
Antigens are carried to the lymph nodes where they are recognised by lymphocytes
36
What is the difference between lymphangitis & lymphadenitis?
LymphANGITIS is inflammation of lymphatic vessel
| LymphADENITIS is inflammation of the local lymph nodes
37
What is the function of neutrophils? (HINT: there's 4) How do they do this? (HINT: there's 4)
They : kill organisms, degrade necrotic tissue, ingest offending agents & produce chemical mediators
They do this by: movement (chemotaxis), recognition & adhesion to micro-organisms, phagocytosis, intracellular killing of micro-organisms
38
How does acute inflammation vary in its nature? (HINT: there's 7)
1. SEROUS e.g. peritonitis
- protein rich fluid exudate
2. CATARRHAL e.g. cold
- mucus hypersecretion
3. FIBRINOUS e.g. pericarditis
- exudate contains plentiful fibrin
4. HAEMORRHAGIC e.g. pancreatitis
- severe vascular injury
5. SUPPURATIVE
- production of pus
6. MEMBRANOUS
- epithelium coated by fibrin
7. PSEUDOMEMBRANOUS
- superficial mucosal slough
39
What are the BENEFICIAL effects of acute inflammation? (HINT; there's 6)
1. Dilution of toxins
- allows them to be carried away by lymphatics
2. Entry of Ab
- due to increased vascular permeability
3. Fibrin formation
- impedes movement of microorganisms
4. Transport of drugs
- e.g. antibiotics
5. Delivery of nutrients & O2
- aided by an increase in vascular permeability
6. Stimulation of the immune response
- fluid exudate containing antigens reaches local lymph nodes
40
What are the HARMFUL effects of acute inflammation? (HINT: there's 3)
1. Digestion of normal tissues
2. Swelling e.g. laryngeal oedema, brain swelling
3. Inappropriate inflammation response e.g. type I hypersensitivity
41
What are the systemic effects of acute inflammation? (HINT: there's 4)
1. Constitutional symptoms
- including malaise, anorexia & nausea
2. Weight loss
- due to negative nitrogen balance, particularly when there's extensive chronic inflammation
3. Reactive hyperplasia
- of the reticuloendothelial system
4. Haematological changes
- e.g. increase in erythrocyte sedimentation rate, anaemia, leukocytosis
42
What is respiration?
Provides oxygen to the body & removes CO2 through inhalation & exhalation
43
How is (i) INHALATION (ii) EXHALATION achieved?
(i) by increasing the size of the thorax via contraction (&lowering) of the diaphragm & raising the ribs, also by creating a -ve intrathoracic pressure that sucks air through the conductive passages & down into the lungs, but this air must be warmed, filtered & humidified
(ii) by decreasing the size of the thorax, generally a passive process
44
What structures are a part of the (i) Conducting tract (ii) Respiratory tract?
(i) nose, pharynx, larynx, trachea, bronchi & bronchioles
(ii) respiratory bronchioles, alveolar ducts, alveolar saccules & alveoli
45
What is the nasal cavity? Where is it located in relation to surrounding structures & what is its function?
A 'box' of bone & cartilage & is the start of the respiratory tract
- found posterior to the nose, anterior to the nasopharynx, above the oral cavity & between the 2 orbits
Its function is for warming, filtering & humidifying the inhaled air
46
What is the function of the turbinates (conchae)? Describe its mucous membrane
Increase the surface area & create turbulence
- the mucous membrane is highly vascular & lined with respiratory epithelium i.e. pseudostratified, ciliated, columnar, interspersed with goblet cells that secrete mucus
47
What is the nasal septum? What are they made of anteriorly & posteriorly?
A midline structure that separates the L & R nasal cavities
- anteriorly, the septum is made of septal cartilage
- posteriorly, the septum is made of bone
48
Where are the meati located? What is their function?
Located linear/lateral to each concha
| - adjacent air sinuses open up into the meati, communicating between the sinuses & the nasal cavity
49
What are the 3 types of para-nasal air sinuses? What is the importance of them?
Frontal, maxillary & sphenoidal
| - the mucous from the sinuses & the tears from the eye (via the nasolacrimal duct) empty into the meati
50
What is the clearance of mucus dependent upon? What can this be compromised by/ what can this lead to?
Dependant upon ciliary action which can be compromised by infection, possibly leading to sinusitis
51
What is the pharynx? Name the 3 parts of the pharynx & their function.
Tube of fibrous & muscular tissue
1. NASOPHARYNX: transports air, divided from the oropharynx by soft palate
2. OROPHARYNX: transports air PLUS food & fluid, but these must be separated so air passes into the larynx while food & fluid continue into the laryngopharynx
3. LARYNGOPHARYNX: transports food & fluid to the start of the oesophagus
52
What is the larynx? Why can its laryngeal diameters be altered?
A membranous tube suspended between cartilages, the positions of which are controlled by muscles
- laryngeal diameters may be altered to allow the passage of air only, & control air flow for speech & raising instra-abdominal pressure
53
Where is the (i) Aryepiglottic fold (ii) Vestibular fold (iii) Vocal fold located within the body?
(i) at the upper edge of the quadrangular membrane
(ii) formed at the lower edge of the quadrangular space
(iii) at the upper endge of the cricovocal/cricothyroid membrane
54
What do the aryepiglottic folds form?
Laryngeal inlet
55
What is the laryngeal inlet? How & when is it closed? What do muscles within the folds aid?
The protective sphincter
- closure is by elevation of the larynx which is lifted UP & FORWARD during swallowing
- muscles within these folds aid both closure & widening of the laryngeal inlet
56
The vocal cords control laryngeal diameter for what? (HINT: there's 4)
speech
coughing
sneezing
raising intra-abdominal pressure
57
What are the 3 main actions of the laryngeal muscles?
1. Close/open the inlet (aryepiglottic folds)
2. Close/open the rima glottidis
3. Shorten/lengthen the vocal folds
58
Where is the trachea located?
Infront of the oesophagus
- medial to the carotid arteries & internal jugular veins
- inferior to the larynx
- thyroid gland surrounds the upper portion
- divides into R & L main bronchii
59
What is a clinical condition which affects the upper respiratory tract?
Laryngeal cancer
60
How many lobes do the right and left lungs have? How do their main bronchi vary?
The left lung has 2 lobes & the right lung has 3 lobes
The right main bronchus is slightly more vertical, shorter & wider than the left, therefore foreign bodies are more likely to enter the R lung
61
What is the difference between the left & right lungs costal surface? Why is this the case?
The left lungs costal surface is slightly longer & narrower than the rights due to the deviation of the heart to the left & the liver sitting below the right lung
62
What does the trachea divide into, state up to the segmental bronchi. The bronchus & trachea are similar in structure BUT what makes the bronchus different from the trachea?
Into the L&R main bronchi, which divides into the lobar bronchi, which then subdivide into segmental bronchi
- it branches into the lungs & the C-shaped cartilage rings are replaced by plates, its epithelium is still pseudostratified ciliated columnar BUT its height decreases
63
In the lungs, what does the bronchi divide into?
terminal bronchioles, respiratory bronchioles, alveoli
64
What causes asthma?
The smooth muscle in the wall can excessively narrow the lumen
65
In the terminal & respiratory bronchioles, what does the epithelium become?
Non-ciliated cuboidal & goblet cells dissapear
66
What are the respiratory alveoli? What is their function?
They are the functional unit of the lung.
They are out-pocketings of bronchioles, alveolar ducts & alveolar sacs
- where gaseous exchange takes place
67
Describe the pleural membrane & its cavities.
Each lung lies within its own lubricated potential space/pleural cavity (as the heart lies within the pericardium)
- the L & R pleural cavities have visceral & parietal layers which are continuous with each other
68
What are the surfaces of the lungs?
costal surface
mediastinal surface
diaphragmatic surface
69
What do lymph nodes in the lungs do? Where/what is the hilum?
They remove carbon from the air inhaled
| The hilum is the point at which the pleura reflects from being visceral to parietal
70
What structures pass through the root of each lung? (HINT: there's 3)
bronchus, pulmonary artery, pulmonary vein
71
What is a common pathology that may affect the lungs & pleural cavity?
PNEUMOTHORAX
- air within the pleural cavity causes the lungs to collapse
- a needle is inserted just above the ribs to remove the air
72
What are the major relations of the lungs? (HINT: there's 6)
```
pulmonary artery
pulmonary vein
superior vena cava
bronchi
azygous vein
heart
```
73
What is the mechanism of respiration? (mentioning inhalation, exhalation, )
Inhalation MUST increase the diameters of the thorax to create a negative pressure, which sucks air into the lungs via the trachea & larynx etc
Diaphragmatic contraction causes its descent to increasing vertical diameter
Rib ELEVATION pushes the sternum up & forward & the ribs OUTWARDS, to increase anteroposterior & lateral diameters
Exhalation is by muscle relaxation & elastic recoil
74
Describe the diaphragm (mentioning what it is compmosed of, nervous supply & intercostal muscles)
Muscular at its periphery, but is tendinous centrally
- it has L & R domes
nervous supply = PHRENIC NEVRE (C3, 4, 5)
- during inhalation, the domes descend causing -ve intrathoracic pressure. Between the ribs are layers of intercostal muscles that raise the ribs in inhalation, but some may act in forced exhalation to help lower the ribs
75
What is disease?
| What is the characteristics of disease? (HINT: there's 6)
Disease is a mobile concept, usually defined as a deviation from the normal structure/function of the body & its processes
- aetiology (cause)
- pathogenesis (mechanism)
- manifestations (features)
- complications (consequences)
- prognosis (anticipated course)
- epidemiology (population distribution)
76
Define (i) Pathogenesis (ii) Benign (iii) Malignant (iv) Eponymous disease/lesion (v) Syndrome
(i) the mechanism by which cause produces disease e.g. inflammation, degeneration, carcinogenesis, immune reactions (allergy)
(ii) cells simply expand (iii) cells invade other tissues (iv) named after a person/place associated with it
(v) an umbrella term that describes the symptoms present
77
What is the classification of disease?
FUNCTIONAL - sore head
BIOLOGICAL - haemorrhage, tumour, trauma
SOCIOECONOMIC & HEALTH - hangover
FUNCTIONAL AGAIN - vascular anomaly, migraine
78
What is epidemiology? What is it affected by?
The study of disease in populations (incidence, prevalence, remission, mortality)
It's affected by age, time, geography, socio-economic factors, occupational factors
79
What are the 3 causes of chronic inflammation? Give examples for each.
1. PRIMARY
- resistance of infectious agent to phagocytosis & intracellular killing e.g. tb, leprosy, viral infections
- foreign body reactions to endogenous materials e.g. gout
- foreign body reactions to exogenous materials e.g. asbestos
- some autoimmune diseases e.g. rheumatoid arthritis
- - specific diseases of unknown aetiology e.g. ulcerative colitis
- primary granulomatous diseases e.g. sarcoidosis
2. PROGRESSION FROM ACUTE
- indigestable substances e.g. glass, suture material
- deep seated suppurative inflammation where drainage is delayed/inadequate
3. RECURRENT EPISODES OF ACUTE
e. g. chronic cholecystitis
80
What does chronic inflammation look like? (HINT: there's 5)
- chronic ulcer
- chronic abscess/cavity
- thickening of the wall of a hollow viscus
- granulomatous inflammation e.g. tb
- fibrous
81
What are the cells of chronic inflammation?
Characterised by the dominance of macrophages & some lymphocytes
MACROPHAGES are relatively large cells that can ingest (phagocytose) a wide range of materials, along with producing a range of important cytokines
- they can, however, harbour viable organisms resistant to lysosomal enzymes
- they are activated on migration to an area of inflammation : MAF (macrophage activating factor) MIF (migration inhibition factor)
82
What is a granuloma?
A medical term for a tiny collection of macrophages. They form when the immune system attempts to wall off substances that it perceives as foreign but it is unable to eliminate
- these substances include bacteria, fungi, keratin & suture fragments
83
Define (i) fibrin (ii) fibrous (iii) granulation.
(i) deposited in acute inflammation
(ii) typical scar tissue with collagen
(iii) important healing process with BVs & connective tissue
84
List the 6 characteristics of (i) prokaryotes (ii) eukaryotes.
(i) 1. nucleoid that is free
2. circular DNA
3. DNA 'naked' with plasmids of DNA present
4. No membrane bound organelles independent of plasma membrane
5. Mesomes are used in aerobic respiration
6. Transcription & translation occur SIMULTANEOUSLY
(ii) 1. "true" nucleus bound by a double membrane
2. linear DNA
3. DNA organised into chromosomes & complexed with proteins
4. Large complex ribosomes with many types of rRNA & proteins
5. Mitochondria with cristae are "energy centres"
6. Transcription requires formation of mRNA & movement of mRNA from nucleus - cytoplasm for translation
85
What are the 6 components of bacteria? Describe them. (NOTE: this is excluding the cell wall)
1. CAPSULE
- loose polysaccharide structure that protects the bacteria from phagocytosis & desiccation. The most OUTER layer
2. PILI (meaning 'hair')
- appendages used for bacterial conjugation, when 2 bacteria attach via this method it provides a means of transportation of bacterial plasmid DNA
3. FIMBRAE (meaning 'thread')
- facilitate bacterial attachment to host surfaces. They may contain lectin which recognise oligosaccharide units on host cells NOT present in all bacteria
4. FLAGELLAE (meaning 'whip')
- organs of locomotion. Bacteria can have one, or many, flagellae. Each of which is a 20nm thick hollow tube composed of flagellin protein. Are driven by a rotatory engine at anchor points on the inner cell membrane
5. SPORES = metabolically inert forms of bacteria triggered by adverse environmental conditions & are adapted for LONG term survival, allowing regrowth under suitable conditions. Have hard, multi-layered coats making them difficult to kill
6. SLIME = polysaccharide material secreted by some bacteria growing in biofilm. Function is to protect against immune attack & eradication by antibodies
86
What are the 2 groups that bacterial cell walls divide into? Describe them both.
GRAM POSITIVE: has 2 layers; a thick peptidoglycan layer & a cell membrane. LTA (lipoteichoic acid) provides rigidity & is recognised by host immune cells
GRAM NEGATIVE: has 3 layers; an outer membrane, a thinner peptidoglycan layer & an inner membrane. LPS (lipopolysaccharide) is essential for function of outer membrane, elicits potent immune & inflammatory host responses
87
What are the 4 components of a virus? Describe them.
1. NUCLEIC ACID - can be DNA or RNA & can be single or double stranded. Knowing which of these a bacteria is, can help treatments.
2. CAPSID - protein coat/shell composed of protein subunits (capsomeres). Capsomeres consist of aggregated protomeres
3. ENVELOPE - an amorphous structure surrounding some viruses that is composed of lipid, protein & carbohydrate. E.g. herpes
4. SPIKES - glycoprotein projections arising from the envelope that are highly antigenic & may have enzymatic adsorption OR haemoglobin activity. E.g. adenovirus
88
Describe (i) protozoa (ii) fungi (iii) helminths.
(i) single eukaryotic cells. Classified as:
- sporozoa: intracellular parasites
- flagellates: possess tail-like structures for motility
- amoeba: use temporary cell-body projections
- ciliates: move by beating multiple hair-like structures (cilia)
(ii) multinucleate/multicellular eukaryotic organisms that have thick carbohydrate wall containing chitin & glucans. Usually grow as thread like filaments & reproduce by budding (& occasionally binary fission)
(iii) is the term used for parasitic 'worms'. There are 3 main groups in humans:
cestoda - tapeworms
trematoda - flukes
nematoda - roundworms
- infections from these are most common in tropical/sub-tropical climates & usually intestinal species.
89
Bacterial replication is done by binary fission, describe briefly what this means.
Asexual
- gives rise to 2 daughter cells from 1 cell
- the genetic info found in the circular DNA is self-replicating (begins at "origin") & is distributed equally between each daughter cell
90
Bacterial growth has 4 phases, describe these.
1. LAG PHASE: represents period of active growth (in size, not number) as bacteria prepare for reproduction
2. LOG/EXPONENTIAL PHASE: where cells divide at the maximum rate where replication is uniform
3. STATIONARY PHASE: where cessation of growth due to an exhaustion of nutrients & an accumulation of metabolic/oxygen availability. Cell death=cell replication so the population stabilises
4. DEATH/DECLINE PHASE: no. of dying cells exceeds the no. of newly born cells so the no. viable cells declines
91
What are the 6 steps to viral replication? Describe them.
1. ADSOPRTION - virus binds to the host cell
2. PENETRATION - virus infects its genome into the host cell by fusion, binding & ingestion
3. REPLICATION - when the capsid is digested by proteolytic enzymes & the viral genome replicates using host's cellular machinery
4. ASSEMBLY - viral components & enzymes are produced & begin to assemble
5. MATURATION - when the virus fully develops
6. RELEASE - occurs at the site of nucleic acid replication. Viral enzymes breakdown bacterial cell wall; RNA viruses released as they are produced. Dna viruses are expelled to the host cell
92
What do viruses do once they are replicated?
They migrate to either plasma membrane OR nuclear membrane, envelopes form around nucelocapsids by "budding" of cell membrane. There's then a slow continuous release of mature viral particles with NO inclusion bodies
