Ch. 6 Flashcards
What are viruses?
Microbes that are nonliving. They are small, lack metabolic processes, rely on a host to make more viruses, and can infect any form of life. CANNOT REPRODUCE THEMSELVES
How do viruses work?
Go into host cells and use their machinery to replicate, get nutrients, and survive. They are an obligate intracellular pathogen - live in host cell
Virion
Single infectious viral particle. Goal is to make more of these. Protective protein capsid around the virion
Capsid
Main part of the virus. Has a protein shell that protects and packages the virus’s genome; capsomeres (subunits of the capsid) often involved in antiviral drug development
Viral envelope
Envelopes are gotten from the host membrane while nonenveloped arise from cell lysis (bursts)
Viral spikes (peplomers)
Are on the outside of the capsid and may/may not have envelope around them. *hosts learn to recognize spikes to mount immune response. Spikes change through mutation/evolution
Bacteriophages
Infect strictly bacteria
Viral goal
Get to host, inject its genome, use host machinery to make viral proteins
How is virus DNA transcribed?
DNA viruses use host RNA to transcribe virus DNA
Why do most viruses have fewer than 300 genes?
Because they’re simple, just need genes for their capsid proteins, and no organelles
Why do viruses have a faster rate of genomic change?
bc lots of virions are produced when host cells are infected and have very fast replication since not much genetic material to copy. RNA genomes evolve faster than DNA viruses bc DNA has proofreading mechanisms
Attenuated strain
Stimulate an immune response. Don’t cause disease in a host with normal immune system and used in vaccines (inject host with it so body stimulates immune response and kills it and you don’t get sick)
Beneficial mutations may allow the virus to:
Escape host immune system, broaden host range, become more infectious, expand tropism (type of cell/tissue that the virus can infect)
Antigenic drift
Minor changes; allow virus to evade quick antibody response from host system -> they go unrecognized long enough that they can replicate and make more virions. Eventually the host system might recognize it and perform an immune response and make antibodies
antigenic shift
major genetic reassortment; can lead to new viral strains w/ deleterious features; can be increased infectivity with expanded host range; host doesn’t have any residual immunity to it anymore; lead to pandemics
Covid-19 similar to influenza
enveloped virus, ssRNA virus, encapsidated, has surface proteins (spikes)
Covid-19 differences to influenza
has a genome, type of surface proteins, s-spike proteins, influenza = HA & NA
how SARS-CoV-2 works?
S protein binds to host cell’s ACE2 receptor -> injects RNA into infected host cell -> uses host machinery to replicate genome -> new host cells -> released -> infect other host cells
Pfizer and Moderna
mRNA vaxs; they code for the SPIKE proteins with lipid -> intramuscular injection -> no damage to the RNA bc of lipid coating -> immune systems notices it doesn’t recognize the spike so it will make antibodies so if you come across covid, your immune system recognizes it -> quicker response and recovery
J&J vax
attenuated viral vectored vaccine; has been genetically modified to be replication deficient so it’s incapable of causing human infxn
How are viruses grouped?
type of nucleic acid (DNA or RNA), capsid symmetry (helical, icosahedral, or complex), presence/absence of envelope genome architecture (ssDNA, ssRNA, etc.)
host range
refers to a collection of species that a virus can infect. Ex: measles only infect humans
tropism
refers to the tissues or cell specificity sue to viral surface factors
broad tropism
infect many different tissues/cells
narrow tropism
infect one or a few tissues/cell
bacteriophage replication - lytic replication
1) attach: phage binds to bacterial cell
2) penetration: phage injects genome into the host
3) replication: protein synthesis makes phage parts and genome is replicated
4) assembly: genome packed into capsid and phage structures assembled
5) release: bacterial cell lyses and new phages are released
bacteriophage replication - lysogenic replication
1) attach: phage binds to bacterial cell
2) penetration: phage injects genome into the host
3) replication: *Integration - phage DNA integrates into host genome, forming a prophage *cell division - host and phage genomes r copied b4 cell division. Multiple cells now carry the phage genome *Lytic cycle entered - phage may enter lytic cycle if host is stressed
4) assembly: genome packed into capsid and phage structures assembled
5) release: bacterial cell lyses and new phages are released
animal virus replication - HIV example
1) attachment and penetration: HIV attaches to host cell and enters by fusion
2) uncoating - if it has an envelope
3) reverse transcription: Upon entry, HIV genome is reverse transcribed by viral reverse transcriptase to make DNA
4) viral integration: DNA version of the HIV genome integrates into the host genome to make a provirus
5) replication: provirus is transcribed to make viral genome and translated to make viral proteins
6) assembly
7) release: HIV provirus directs the production of new virions, which bud from the host cell
acute nonpersistent infection
cleared out naturally.
latent persistent infection
have flareups w periods of latency; during flareups, virions are shed and person experiences symptoms. Ex: HIV
chronic persistent infection
builds up
provirus
integration of viral genome into host cell; can remain silent for years; may not be exhibiting symptoms but can still pass it *difference not excised from genome like in lysogenic bacteriophages
acute infections
viruses infect host cell and new virions are made
persistent infections
viruses have replication strategies that allow them to avoid immune system clearance
What can persistent infections lead to?
cancer = oncogenic *cause cancer by stimulating uncontrolled replication of cells or ignore cell death signals
Why would we grow bacteriophages via plaque assay?
to develop vaxs and drugs to combat viruses
Since animal viruses are much harder and more costly to grow, what can we use?
embryonic eggs or live animal hosts like rats
viral titer
quantity of a virus present in a given sample
Diagnostic testing
determine presence of certain viruses
specificity
detect only the virus and does not produce a false negative. won’t say there is _ virus if _ virus is actually not the one being detected
sensitivity
test detects v low levels of the target *no false negatives / will detect _ target bc even just a little small level of _ target will be detected
agglutination tests
clumping
ELISA
detects antigens or abys in a sample *color change indicates binding
Limitations of ELISA and agglutination assays:
cannot detect if antigenic shift occurs, takes time to build up abys to be detected
PCR (polymerase chain reaction)
amplify a region of interest in the genome so that there’s large amounts of it to use for further testing
antiviral drugs
treat infections but don’t typically cure them
What do antiviral drugs target?
any part of viral replication
difficulties in treating viral infections?
can be hard to reach them because they’re in a cell
prions
infectious proteins, nonliving, do not replicate, acellular, no genetic material. only way to ID is by autopsy. Causes transmissible spongiform encephalopathies (TSEs) sponge like holes in brain tissue
what should antivirals be?
selectively toxic.*U don’t wanna kill too many host cells, need balance
what can we do to prevent infections?
vaccinations
