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Lecture Notes for BIOL123: Infection and Immunity
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  • Course
  • BIOL123: Infection and Immunity (BIOL123)
  • Institution
  • Lancaster University (LU)

Lecture 1: Global Impact of Infectious Diseases Lecture 2: Innate Immune System Lecture 3: Adaptive Immunity Lecture 4: Immune Processes Lecture 5: Influenza Lecture 6: Human Immunodeficiency Virus Lecture 7: The Plague Lecture 8: Malaria Lecture 9: Nematodes Lecture 10: Schistosomes Lect...

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Document information

  • September 17, 2021
  • 45
  • 2020/2021
  • Class notes
  • -
  • All classes

Subjects

  • infectious diseases
  • global impact
  • innate immune system
  • adaptive immunity
  • b cells
  • t cells
  • cell mediated immunity
  • humoral immunity
  • immune processes
  • influenza
  • hiv
  • the plague
  • malaria
  • nematodes
  • schistosome

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  • Lancaster University (LU)
  • Lancaster University
  • BIOL123: Infection and Immunity (BIOL123)
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Lecture 1: Global Impact of Infectious Diseases

Diversity of Infectious Agents
- viruses, bacteria & fungi usually cause acute infections
- parasites cause chronic infections
 protozoa (protists) and worms (helminths)

Parasitism
- type of symbiosis
- symbiosis: interaction between two different organisms living in close physical association
- parasitism: relationship between two species where one species is benefited and other is harmed
- organisms can be mutualistic, commensal or parasitic under different conditions in different hosts
etc




Stages of Infectious Disease
- incubation period: time between infection and first occurrence of symptoms
- prodromal period: short time of generalised, mild symptoms
 not all infectious diseases have this stage
- illness: most severe stage when symptoms most evident and host immune system has responded
- convalescence: body gradually returns to normal
 time depends on pathogen and damage
 sometimes may not occur if infection is chronic

Biological Response Gradient
- uncommon for pathogens to have same severity in all infected individuals
- severity of infected individual depends on infecting dose, age, gender, genetics, nutritional status &
co-infection with other pathogens

Disease Progression: Invasion:
- entry into host and transmission from one host to another
- inhalation, direct skin contact, oral transmission, intra-uterine, sexual transmission
- direct inoculation, insect bite
- route of transmission influences disease control measures

Disease Progression: Multiplication
- some pathogens multiply in body but others can’t
- protists can cause diseases following inoculation of only a few infectious stages as they can multiply
quickly
 disease severity may depend on how quickly they multiply
- most helminths can’t multiply in body
 disease severity depends on no. of infectious stages acquired by host over time

,Disease Progression: Spread
- ability of organism to move from initial infection site to other areas of body
- includes movement between body systems
- some infectious agents can undergo developmental changes at same time which can affect host
immune response

Disease Progression: Pathogenesis
- causation & development of clinical disease influenced by:
1) no. of pathogenic organisms present
2) virulence of organism
 direct killing of host cells, blockages in host organs, toxins, inappropriate activity of immune
system
3) reaction of host e.g. degree of resistance

Global Burden of Disease
- incidence: no. of new infection cases occurring in population in defined period of time
- prevalence: total no of infected individuals in population at given point in time
 includes old & new cases
- mortality: total no. of deaths in population in defined period of time




Mortality
- some countries have had shifts in burden of infectious diseases
- in other countries, infectious diseases

Economics
- high income countries have 70% of deaths for people aged 70+ and 1% of deaths are <15
 deaths are predominantly due to long term chronic diseases
- low income countries have 20% of deaths for people aged 70+ and 40% of deaths are <15
 deaths are predominantly due to infectious diseases
- higher income countries also spend more money on health per person

Disability
- mortality doesn’t give full picture of diseases burden by individuals of different population
- morbidity: amount of disease in a population
- disability adjusted life year (DALY) is measure used to give indication of overall burden of disease

DALY
- measure life years lost due to premature mortality & equivalent years lost due to morbidity
- calculates by adding ‘years of life lost (YLL) to premature mortality’ and ‘years lost to lived with

,disability (YLD)
- DALY = YLL + YLD
- allows comparison to be made across range of health issues
- provides quantitative basis for deciding health policies & evaluating cost effectiveness of control
programmes
- only measures direct health loss and doesn’t consider economic impacts resulting from disease e.g.
lost agriculture, lost school attendance etc
- doesn’t account for direct costs of treatment, surveillance & prevention measures
- doesn’t consider social stigma associated with disease e.g. loss of tourism, health system overload

Increasing Importance of Infectious Diseases
- drug resistant pathogens & vectors
- refugee movement
- rapid & widespread air travel
- increased immuno-deficient people
- lifestyle e.g. urbanisation, drug use
- natural / social disasters
- environmental changes
- pandemics

, Lecture 2: Innate Immune System

Immune System
- lymphatic system in blood
- bone marrow, thymus, lymph nodes & spleen in organs
- innate & adaptive properties in cells
- antibodies, cytokine, complements etc in molecules

Mechanical Barriers: Skin
- dead cells & bacteria
- sebaceous gland has fatty acids, lactic acid & low pH
- skin is dry preventing bacterial growth

Mechanical Barriers: Tight Junctions
- stop ingested antigens passing into body

Mechanical Barriers: Mucosal Surfaces
- lining of many organs coated with slippery mucus that traps microorganisms
- cilia brushes out mucus
Physiological Barriers: pH & Environment
- low pH in stomach kills pathogens
- normal commensal microbiota out-compete pathogenic strains for nutrients

Physiological Barriers: Chemical Mediators
- anti-microbial peptides – defensins damage pathogens
- anti-microbial proteins: lysozyme in tears & saliva
- cytokines – interferons induce anti-viral cell state
- complements –MAC lyses bacteria
 enzyme cascade that joins together forming core structure (membrane attached complex) that is
inserted in bacterial membrane

Effective Parasites as Pathogens
- evade innate immune response
- use vectors, can hook to avoid being flushed or burrow straight through skin
- too big to be phagocytosed

Innate Immune Cells: Phagocytes
- macrophages survey body, sample environment and display them to show other cells what’s going
on in body
- neutrophils kill pathogens by rapidly ingesting them or by releasing granule content
 send messages to other cells and sacrifice themselves by releasing their DNA & coating it in
histones to kill bacteria by extracellular trapping
- dendritic cells are professional antigen presenting cells that activate T cells

Innate Immune Cells: Granulocytes
- neutrophils
- natural killer cells that target & kill cancerous or infected cells
- eosinophils release granular content to kill pathogens
 important in allergies as they use cell signalling to activate mast cell
- mast cells contain histamines that increase vasodilation & enhance inflammation

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