HSCI 338 Final: hsci 338 post midterm notes

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Simon Fraser University
Health Sciences
HSCI 338
Nienke Van Houten

Notes for post-midterm Chapters 13, 14, 15, 16, 18, 19, 20, 21, 24. 25, 26 Interactions between animal viruses and cells - ch 15 Virus Host Interactions - Ch 16 Immune System innate and adaptive defences - Ch 13 & 14 Modes of transmission - Ch 18 Human viral disease - Ch 19 HSV & latency - found in Ch 17 (not phage section) HIV-1 & AIDs - Ch 21 Influenza - Ch 20 Ebola - Ch 24 + Supplemental articles Vaccines - Ch 26 Emerging Infections - Ch 24 + supplemental articles Tumour Viruses - Ch 25 There will also be 1 or 2 cumulative exam questions. ---- •Pick one of the following pairs of viruses: IFV and HIV, HepB (hepadenovirus) and polio virus (picornavirus), HSV (herpes virus) and Measles. • •Be able to describe how they compare and differ with respect to all the things we discussed this term: Entry, genome replication, assembly, regulation of gene expression, disease it causes, types of treatments or vaccines available, Severity of disease, immune evasion or pathology and and other impacting factors. --- 1.Connect course long features of IFV 2.Relate animal reservoirs, HA & NA variation, and mechanisms of mutation to pandemics and requirement for regular flu vaccines and current circulating strain. 3.Predict how antigenic drift occurs in a lab 4.Explain how immunity within a population changes over time RESOURCES: 1.​http://www.phac-aspc.gc.ca/naci-ccni/assets/pdf/flu-2016-2017-grippe-eng.pdf 2.http://healthycanadians.gc.ca/diseases-conditions-maladies-affections/disease-maladie/flu-gri ppe/surveillance/index-eng.php ● --- --- Vaccine: •Differentiate between whole live, whole killed, & subunit vaccines. •Broadly list pros and cons of whole live (attenuated), whole killed, & subunit vaccines with respect to safety and elicitation of correlates of protection for the cognate infection. •Use Poliovirus as an example of pros and cons for live -attenuated vs. killed •Define features that make a virus suitable for eradication and predict whether a virus is suitable candidate for eradication. --- Ebola: •List the major events that lead to the largest ever Ebola outbreak in west Africa in 2013 (info graphic) •Connect to the human impact and horror that is experienced by people living in that time (brief video) •In broad terms, explain the pathology of Ebola infection •Describe a Canadian Ebola vaccine candidate, how it was implemented in field and preliminary results from trial ---- Tumor: 1.Explain why viruses are named tumour associated viruses, not “tumour virus” 2.Define and distinguish between immortalisation, transformation and tumourigenesis 3.Define oncogene, proto-oncogene, and tumour suppressor 4. Describe 3 ways that viral genes promote tumourigenesis 5.Explain why transmission of viral genes to daughter cells is important and list three ways that viral genes can be spread to daughter cells 6.Design an experiment that would test the hypothesis that certain viral genes are associated with tumour formation and interpret data with respect to viral gene involvement in tumourigenesis * 7.Diagram interplay between 3 viral protein domains and cellular growth regulators that could lead to tumourigenesis.* ----- Emerging infections •Define emerging infection •Explain, with examples, how climate change, travel and animal interactions can contribute to emerging infections. •Diagram molecular basis of cross-species transmission (Howard & Fletcher)* •List 3-4 human infections that are emerging and identify common themes between emerging infections * ----- 6 ways for virus-host interactions - Acute cytopathogenic - Persistent - Latent - Transforming - Abortive infection - Null Acute cytopathogenic infection (= lytic) - Infection results in cell death - Cells die necrotic or apoptotic - Easily studied (CPE) - Unknown mechanism 1. Apoptosis - Programmed process - Cell contents stay within cell plasma membrane - Cells disintegrate in necrosis - Causes inflamatory reaction, needs clean up - Dna fragmentation, etc - Engulfed by phagocyte and hydrolysed - Usually cell’s response, not included by virus infection - Reduces progeny virus production 2. Persistent infection - No evolutionary advantage for viruses in killing the host - Latent infection - Productive persistent infection established: i. Virus-cell interaction alone ii. Virus-cell interaction with antibody or IFN effect iii. Virus-cell interaction with DI particles - Persistent infection caused by virus-cell interaction - Virus replication without damaging cells; - I.e cells and virus both keep replicating - Certain combination of virus and cell Persistent infection caused partly by immune response - Limited infection - Decreased interferon production - More infected cells - Interferon induction from infected cells - Limited infection, etc - When cell growth is faster than increase of infected cells - Persistent infection caused by DI particles - DI genome compete for replication with the infectious genomes 1. If DI genome is smaller than infectious genome, DI overwhelm the production of infectious virus 2. DI decreases when infectious virus decreases 3. Infectious virus decreases a. Back to #1 3. Latent infection - Little or no virus protein production - Not recognized by immune system - No cell killing - Mechanisms to maintain virus genome in latently infected cells - Mechanisms to reactivate infectious virus production - 4. Transforming infections - Some DNA viruses and retroviruses infectious - Cell transformation = rapid multiplication with altered properties - Evolutionary advantages - Some may, i.e. retrovirus and herpes - Only when reactivation mechanism exists 5. Abortive infection - Cells wiht spcific receptors but not other essential factors - E.g. cell type-specific transcription factors - Enzymes that requires for virus maturation - Cell killing by viruses - Mechanism not known - Dying cells are hard to synchronize and analyze --- Virus - host interactions (ch 16) - Biological success of viruses depend on success of host - Counter productive to kill host - host- virus interaction is complex interplay - Different outcomes - Immune response is critical in determining outcome Koch’s postulates 1. Agent must be present in every case of disease a. Same microorganism may exist in healthy individuals 2. agent must be isolated from host and grown in vitro a. May not be possible 3. Disease must be reproduced when a pure culture of the agent is inoculated into healthy susceptible host a. Impossible in many cases 4. Same agent must be recovered once again from experimentally infected host a. Production of antigen specific antibody Infection / infecious disease - Infection =/= infectious disease (subclinical infectious) - Cell death =/= disease condition (cell replacement) HIV-1 can be categorized in many ways 1. Acute​ ​infection​: short , flu-like disease at the beginning 2. Persistent​ / ​chronic​ ​infection​: asymptomatic for years (persistent) that becomes symptomatic from time to time 3. Latent​ ​infection​: suppression of virus by latently infected cells, chronic reservoir 4. Slow​ ​progression​: slow, progress of disease, long duration Immune-mediated infections - Difference between acute and subclinical - Presence of disease - Difference between chronic and persistent - Presence of disease Disease​: a pathological condition of a part, organ, or system of an organism resulting from infection Caused by: 1. Virus destroying cells (poliovirus in neurons) 2. Immunopathologies a. Measles rash = antigen/antibody complexes under skin b. Vaccinia pock = t-cell mediated response c. Interferon produce flu-like symptoms Acute infections - Similar to cytopathogenic infections in vitro - Most viruses attack particular organs or tissue (target) - due to receptors on the surface and host gene expression - Infectious organisms are determined by: - Clinicial signs (objective) and symptoms (subjective) - Lab tests: virus isolation, detection of antigen in blood, PCR, EM Key points: Infection (small amount) Target organ/tissue Incubation period ---------------------- virus sheds Clinical signs/symptoms Recovery/death - Immune response - Antibody (e,g. Picorna virus, othomyoxvirus) - Activated T cells (herpes, poxvirus) classic example: commom cold Subclincal infections: Aka: inapparent or silent infections Infection Target organ/tissue Incubation period ---------------------- virus sheds No clincal signs/symptoms Recovery - Viruses that infect host subclinically are evolutionarily selected - In new host, severe diseases can develop different from natural host species Persistent and chronic infections - infections not terminated by immune response - Persistent​: infect few cells, low level of virus - Chronic​: more active - These viruses inhibt the immune response - E.g. decrease MHC, IFN - Chronic response can cause long term damage Incomplete immune response associated with persistent and chronic infections - Virus poorly immunogenic, fail to display antigen on cell surface - Virus produces excess soluable antigen that binds neutralizing antibody - Virus stimulate non-neutralizing antibody that binds to virions and blocks neutralizing antibody (HIV) - Insufficient interferon production - HBV causes 4 types of infection - Transmitted by blood/saliva - HepB potentially life-threatening - 100% acute - 10% persistent (subclinical) - 1% chronic - 0.1% heptocellular carinoma Latent infection - No infectious virus produced - Usually subclincal - Characteristic to certain virus - Herpesvirus, retrovirus - All latent infectious start and end as acute infectious ------ Immune system and virus neutralization Where is the immune system? - Primary: red bone marrow, thymus gland - Secondary: lymph nodes, spleen, appendix Immune system - Innate - Phagocytosis E.g NK cells, macrophages, neutrophilis, complement - Antigen presenting cells bring antigen to lymph nodes E.g. dendritic cells, macrophages - Adaptive - T cell mediated (cellular) ----- ​CD8+ - Actively kills infected cells (effector cells) - Some become memory cells - TH1 dependent - B cell mediated (humoral) - Produce antibody (plasma cells) - Some become memory cells - TH2 dependent Viral infection - Viral particles - Infected cells Phagocytes: - First line of defense (intrinsic vs. induced) - Constitutively phagocytosing virus particles - Destry engufled particles in lysosomes - Enzymes in lysosomes - Prevent viruses from infecting their target cells - Infection aborted without trace - Establish infection in phagocytes - *As target cell: HIV - *With non-neutralizaing Ab: Dengue v
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