micro Flashcards
Basis of Baltimore classification
genome, mode of replication
Baltimore classification group
Class 1: ds DNA
Class 2: ss DNA
Class 3: ds RNA
Class 4: ss RNA pos sense
Class 5: ss RNA neg sense
Class 6: ss RNA pos sense w/ ds DNA (retrovirus)
Class 7: ds DNA w/ pos sense, part ss DNA w/ ss RNA (reversiviruses)
Structure vs non-structure protein
SP: Make up viral structure, facilitate enter into cell
NSP: enzymes, codes for viral genome
Typical structure of virus
nucleic acid inside a capsid subunit (naked) or further inside membrane with spikes
replication life cycle of virus
- attachment
- Penetration
- replication of viral genome
- production of late viral proteins
- assembly
- release
Cytopathic effect (CPE)
effect of virus replication oh host cells
used as a diagnostic tool
how does viruses cause disease
- replication within host cell leading to damage to cell directly
- Host defenses lead to cell damage as it tries to clear virus
- Rotavirus code for toxin proteins
Cell lysis
early protein shutdown host macromolecules > Accumulation leads to inhibition of host cell and viral synthesis
Rounding up of cells due to lost of adherence proteins then lysis
types of Cytopathic effect
Cell lysis
Syncytia
Inclusion bodies
Transformation
Viral infection steps
- invade host
- replicate in cell
- overcome/evade local defenses
- spread to other cells and areas
- replicate again
- exit host to infected another host
immune cells responsible for fighting viral infections
Cytotoxic T cells, which targets cells with virus antigenic marker on MHC class 1
how does virus evade immune system
- viruses poorly immunogenic
- don’t display enough antigen on cell surface
- inactivate T and B cells as well as macrophages
- interfere with MHC
- antigen production to bind neutralizing antibodies
- mutation that changes antigenic protein of virus
incubation time for rabies
28-140, Long
what is RO
Reproduction number
ave number of secondary cases generated from the one primary case
Viral symmetry
Icosahedral: all DNA animal viruses except poxvirus
Helical: ssRNA, need envelope
Complex
Syncytia
plasma membrane fuse to form giant multinucleated cells
inclusion bodies
bodies that appear in cells as result of viral infection (aggregation of mature viral particles)
Transformation
cancerous or pre-cancerous like changes, breakdown of cellular regulation due to viral protein
different types of infection
Acute non-persistent: self-limiting, most colds
Persistent: infection not terminated, HIV integrate into host DNA
Latent: some might never cause disease or have episodes, herpes
Virus detection methods
Direct: microscope
virus isolation: cell culture
immunological: serology
molecular methods > PCR, microarray, sequencing
Microscope method
electron: expensive, detect unknown virus
Light: histology section, poor sensitivity and specificity, indirect (changes in cell not the actual virus)
Cell line type
Primary: taken from animal/human and grown, last around 50-70 passages due to shortening of telomere.
Continuous: cancer cell, no limit
Hayflick limit
the number of times (about 50) that normal human embryonic cells can divide before they succumb to senescence
viral serology
Indirect method, detect antibody produced
- can determine immune status, pre/post vaccine
-window period for IgM and IgG
Nucleic acid detection
fast, sensitive, specific typing by sequencing
- need virus to be present (no past infection)
PCR type
multiplex: multiple set of primers
nested: increase sensitivity and specificity but prone to contamination
reverse transcription: initial conversion of RNA to DNA (30mins)
Cycle threshold
cycle when fluorescence becomes detectable
Hight CT = low amount of starting template
Low CT = high amount of starting template
HPV family
Papillomaviridae
HPV infectious cycle
