HLTH 101 Lecture Notes - Case Fatality Rate, Entry Inhibitor, Hemolytic Anemia

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Published on 16 Oct 2011
School
Queen's University
Department
Health Studies
Course
HLTH 101
Professor
TOPIC 9. INFECTIOUS DISEASES AND THE FUTURE OF HUMAN
HEALTH
1/ CURRENT/EMERGING PLAGUES
i. AIDS
-approximately 33 million in world HIV positive
2007: 2 million die, 2.7 million infected
-decline in deaths/new cases since 2005 (not in all regions)
- most cases/deaths in sub-Saharan Africa
-greatest increase is in Eastern Europe/Central Asia
-important characteristics:
1) no vectors/animal reservoir (HIV actually no from monkeys)
2) low infectiousness (need to exchange bodily fluids)
3) long latency (10-15 years to see symptoms, opportunity to
transmit)
4) hedonistic transmission (feel good activites (sex, drugs)
making it difficult to eliminate)
5) destroys helper T cells
seeks CD4 receptor, enter, and destroys cell
-increases susceptibility to other infections
-effects in developing world
-implications on treatment: destroy host cells?
Treatment:
1) reverse transcriptase inhibitors (prevent multiplication)
ie. AZT (azidothymidina)
-temporary effectiveness (virus may develop resistance)
-nucleotide (act on DNA) and non-nucleotide inhibitors
(act on enzyme)
2) protease inhibitors
- reduce reassembly, temporary resistance
3) AIDS cocktails
- Highly Active Anti-Retroviral Therapy (HAART)
-combinations of antiviral drugs
-resistance from mutation is less effective as different
drugs can combat
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different mutations
-combination of: -reverse transcriptase inhibitors
-protease inhibitors
-entry inhibitors (disallow CD4 receptor entry)
-integrase inhibitors (blocks activation of
integrase which
injects virus injected DNA
-effective reduction of symptoms, increase life expectancy
-only temporary resistance (eventual development of
resistance)
-can also reduce mother-child transmission
-when to start HAART: 1990’s: at start of AIDS symptoms
Today: early at infection, before
symptoms
- reduces concentration of virus in body
(viral load)
- could reduce transmission as result
(less virus in bodily fluids)
-issues:
-severe side effects
-complicated treatment regime
-expensive (more than $10 000/year) (not effective in
developing countries)
-increased resistance due to new strains; harder to develop
vaccines
-in future, hopefully more prevention emphasis, possibly new resistant
strains
ii. Influenza Viruses
-RNA
-3 types, based on internal antigens
C: mild
B: humans mostly, moderate severity
A: potentially severe, pandemics, animals/humans
-transmitted in aerosol, respiratory droplets
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-first 18-72 hours: cold symptoms, muscle pain, congestion,
fever
-can last 5-10 days
-virus replicates in respiratory epithelial cells resulting in cell
death
-special features: capacity for antigenic change
Viral coat: 2 glycoprotein antigens:
1) Hemglutinin (15 known subtypes: H1-H15)
2) Neuraminidase (9 known subtypes: N1-N9)
-glycoprotein is same but it is the antigens that change
-antigenic shift: genetic recombination from more than 1
strain (different host species)
-ie. pig exposed to human and bird virus
- same cell with both viruses
-new virus with RNA from both viruses
-then transmitted to human, no antibody protection due to
new antigens
-human influenza A pandemics:
1918: H1N1; 1956:H2N2; 1968: H3N2; 1977:H1N1; 2009: H1N1
-H and N not necessarily correlated with
viruklence/infectiousness (ie. 1918, 1977, 2009: H1N1 reduced
virulence each time)
-emergency epidemic/pandemic:
1) H5N1: avian influenza
-asia
-high human case fatality rate (60%)
-not easily transmitted (only from bird to human, so far)
2) H1N1: swine flue
-easily transmittable
-low case fatality rate (less than 10%)
-prevention focus
Vaccines: WHO (world health organization) coordinates response
-identify likely viruses
-prepare trivalent vaccine
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Document Summary

Decline in deaths/new cases since 2005 (not in all regions) Treatment: reverse transcriptase inhibitors (prevent multiplication) ie. azt (azidothymidina) Nucleotide (act on dna) and non-nucleotide inhibitors (act on enzyme) Reduce reassembly, temporary resistance: aids cocktails. Resistance from mutation is less effective as different drugs can combat different mutations. Integrase inhibitors (blocks activation of integrase which injects virus injected dna. When to start haart: 1990"s: at start of aids symptoms. Today: early at infection, before symptoms reduces concentration of virus in body (viral load) Could reduce transmission as result (less virus in bodily fluids) Expensive (more than 000/year) (not effective in developing countries) Increased resistance due to new strains; harder to develop vaccines. In future, hopefully more prevention emphasis, possibly new resistant strains. First 18-72 hours: cold symptoms, muscle pain, congestion, fever. Virus replicates in respiratory epithelial cells resulting in cell death. Viral coat: 2 glycoprotein antigens: hemglutinin (15 known subtypes: h1-h15, neuraminidase (9 known subtypes: n1-n9)