virology basics Flashcards
viruses: obligate
cells that cannot function on own (cannot reproduce unless are in host cell)
composition of virus
genetic material enclosed in protein coat (some have envelope as well), DNA OR RNA (not both, single or double stranded), capsid that keeps genetic info safe, have surface glycoprotein that protrude to bind to host cell
viral replication steps
- attachment
- entry
- gene expression (mRNA synthesis and protein translation)
- genome replication
- assembly
- egress
- release
do viruses use only one receptor on host cell all the time?
no, complex viruses may need to bind to more than 1 (ex: HIV binds first to CD4 on T cells and then to chemokine receptors)
viral receptor interacting proteins
- spikes and knobs
- envelope glycoproteins
- receptor binding proteins
- lipid interactions (pore formation, membrane disruption and fusion)
cellular receptors
- integral membrane proteins
- cellular surface/plasma proteins
- apical v basolateral location v cell junctions
- endosome
- protein v non protein interacting molecules
- *entry initiated by receptor interactions
viral load
how much DNA or RNA of virus in blood (can also seems quantity of receptor on host cell)
Where do most viruses replicate?
most in host cell cyto (some in nucleus = influenza and retroviruses, DNA viruses replicate in nucleus except for poxvirus)
-/+ single strand RNA
- strand needs to be converted to + strand (needs to go through translation and needs to make more - strand rna…both)
+ strand RNA
ready to go and replicate, but during process makes more - strand RNA
DNA polymerase
copies viral genome to make more DNA
RNA polymerase
assists in transcription (to eventually make protein)
assembly of virion
package DNA or RNA and capsized proteins into nucleocapsids (assembly of capsid is coupled to replication of viral genome and this may occur on CM or ER that may become viral envelope, unless doesn’t have envelope)
viral pathogenesis
process by which viral infection leads to disease (not all cells infected end up in disease)
disease from virus
- virus at target organ
- produces signs and symptoms associated with disease (not all symptomatic though) -> these are a fxn of virus (virulence factors and sites of replication) and the host (genetics, immunocomp)
DNA and RNA?
No! Can have both in cell, but only one type is packaged
acute infection
- get infection
- have period of virema (symptoms)
- then virus goes away (short lived, finite period of infection then virus is gone)
persistant infection, latent
- acute primary infection (can be subclinical)
- viral replication (cleared by IS)
- virus will remain with you, dormant (absence of viral replication)
- followed by reoccurrence (viral rep active)
- PERIODS OF LATENCY
persistant infection, slow
- initial primary infection
- persistent low level viral replication (not a true latent phase where have no viral replication), until host dies
most common route of viral infection is..?
respiratory tract (have large surface area)
fecal oral infection
- infection through gut
- virions must be resistant to extreme conditions
- usually associated with childhood infection (except for noro)
- short incubation periods before disease onset
skin infection
-virus enters through breaks in skin, animal bite or injected by anthropod vector
cellular changes: cytopathic effect
degenerative changes in cells that are associated with multiplication of certain viruses
- cell transformation -> malignancy (some immortalize cells, make them go on to replicate and cause cancer)
- cell death
serology
detects IgG and IgM antibodies
culture
detects LIVE virus (replaced by molecular diagnostic techniques), highest specificity
DFA (direct fluor antibody)
detects viral protein
PCR
detects viral nucleic acid (RNA and DNA), sensitive, specific, fast (cannot detect live virus, so cannot tell if someone has active infection -> can have nuc acid hanging around long after virus dead)
-clinically relevant: if someone is responding well to therapy or not
IgM
marker of recent, acute infections (right meow)
IgG
more remote infection (remain high forever in host), will be IgG - in first few weeks of disease
EIA
enzyme immunoassay: based on flow technology, not sensitive, but fast (used in urgent care settings)
histopathology
gold standard for diagnosis of tissue invasive disease (immunostaining for viral protein)
if virus in latent state, is antiviral effective?
No! (it will suppress virus for reactivating, does not cure infection)
-when virus latent, DNA polymerase isn’t active (which is what drug works on) so drug won’t do anything
antigenic drift
small changes in the genes of influenza viruses that happen continually over time as the virus replicates
antigenic shift
abrupt change in the virus
