banfield review Flashcards
describe epigenetic regulation of herpesvirus
With normal tegument proteins:
- herpes inserts its DNA into the nucleus, but it is damaged and not histone bound.
- PML nuclear bodies (composed of histones and Daxx protein) can form around this, recognizing that its damage and not histone bound
- Daxx recruits histone deacetylase (HDAC) which deactylate the histones, which compacts the viral genome so that its not accessible to host RNA polymerases (therefore no transcription)
- the tegument proteins act to counteract the PML nuclear body formation, meaning chromatin remains in open state (and transcription of viral genome can occur)
if there is a mutation in these tegument proteins, they cannot counteract this and thus transcription will NOT occur of viral genome
what are OAS and RNAse L?
they are both interferon stimulated gene products
its important these molecules are not active right away. seeing double stranded RNA in the cytoplasm, they become activated.
when OAS1 recognizes the double stranded RNA, it changes from a monomer to a tetramer (Active form), and produces oligo A nucleic acid.
RNAse L recognizes this oligo A nucleic acid and RNAse L converts into an active dimer form.
RNAse L degrades cellular and viral mRNAs in the cell, which shuts down protein synthesis in the cell and ultimately induces apoptosis
what is a concatemer in poxvirus DNA replication?
once the DNA has been replicated, the concatemer is the structure that has the little hairpin loops of inverted repeats.
these hairpin loops serve as a signal for a nuclease to come along and cleave these inverted repeated into individual genomes (and get resealed)
what does pleconaril do?
- effective against rhinoviruses
- stabilizes the virus particle and prevents uncoating
explanation:
polioviruses, same with rhinoviruses, normally don’t have to penetrate into the cell to uncoat, they usually get endocytosed, and react with a receptor in the endosome that allows them to rearrange the capsid proteins and form a hole in the host membrane through which the viral genome can be inserted.
what pleconaril does is it blocks the receptor from binding to the capsid which prevents the reorganization meaning there is no infection since the genome cant get out
what are late genes transcribed from in HSV lytic cycle?
they’re NOT transcribed by the incoming genome
only transcribed from the genome thats been copied into concatemers
how does acyclovir (drug) work? what type of cells is it specific for?
by preventing viral DNA synthesis
very specific for herpes infected cells
basically acyclovir is a modified guanine with no free 3’OH.
viral thymidine kinase activates acyclovir by adding the first phosphate onto it. the next two phosphates are added by cellular kinases.
Now, when the next guanine is incorporated, it will terminate the chain since there is no free 3’OH on this modified guanine to add to
describe corona replication briefly
- has to get into endosome
- pH must drop
- releases + stranded RNA genome
- two polyproteins form off this
- RNA dependent RNA polymerase is also made to copy the genome
describe b18R
Poxvirus encodes type 1 IFN decoys receptors which are secreted from virally infected cells. These receptors (B18R) are like a sponge in a sense that they bind type 1 IFN preventing them from interacting with the receptors of neighboring cells
- essentially it removes the ligand from the JAK STAT signaling pathway
