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Something i dont understand, it says in UW that it only works on cells with DS Rna inside the cells, when do rna viruses become double stranded? besides hiv, reo etc.
Interferon UW
- Thread starter aspiringmd1015
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side note: why is there no effect of ERV in emphysema patients? they have an obstruction to getting air out, so it should be decreased?
Perhaps this paper may shed some light. It doesn't seem to be completely clear as to when these dsRNA intermediates occur. However, eukaryotic host RNA is very unlikely to become double stranded in the cytoplasm since our RNA does not go on to make more RNA nor does it become DNA. In addition, eukaryotics generally do not transcribe the negative sense DNA- meaning we don't get negative sense RNA in the cytoplasm, and so we don't have negative sense RNAs combining in the cytoplasm to make dsRNA. However in the process of replicating, a negative sense RNA will make positive sense RNA, which has the capacity to bind with itself, and a positive sense RNA will also need to make negative sense RNA in order to make more positive sense RNA for itself. The end result is that many viruses will end up having both positive and negative stranded RNA in the cytoplasm, and either by happenstance or as a desirable component of viral replication leads to the formation of dsRNA which is picked up on by intracellular sensors such as RIG-1 which will go on to make anti-viral gene products. Hope this helps!
http://jvi.asm.org/content/80/10/5059.long
"Clearly, both host and viral pathogens apply a range of measures to deal with dsRNA, indicating that this molecule represents a danger signal of central importance for the innate immune response. It is widely assumed that dsRNA is generated by viral RNA polymerases either as an intermediate in genome replication (RNA viruses) or as an erroneous product due to converging bidirectional transcription (DNA viruses) (25, 32). However, to our knowledge, this has been directly shown for only a few viruses (33, 57, 69), whereas in most cases, only indirect evidence, such as activation of the dsRNA-dependent enzymes PKR, 2-5-OAS, and RNA-specific adenosine deaminase (28, 50, 70), activation of TLR3 (60), and investigation of the dsRNA content of cellular lysates (25, 32, 40), is available."
http://jvi.asm.org/content/80/10/5059.long
"Clearly, both host and viral pathogens apply a range of measures to deal with dsRNA, indicating that this molecule represents a danger signal of central importance for the innate immune response. It is widely assumed that dsRNA is generated by viral RNA polymerases either as an intermediate in genome replication (RNA viruses) or as an erroneous product due to converging bidirectional transcription (DNA viruses) (25, 32). However, to our knowledge, this has been directly shown for only a few viruses (33, 57, 69), whereas in most cases, only indirect evidence, such as activation of the dsRNA-dependent enzymes PKR, 2-5-OAS, and RNA-specific adenosine deaminase (28, 50, 70), activation of TLR3 (60), and investigation of the dsRNA content of cellular lysates (25, 32, 40), is available."
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It's a simple explanation:
When viral RNA is replicating, it is making a new strand so for a moment it will be double-stranded. Double-stranded RNA just doesn't happen in eukaryotic cells so if a cell detects this via its interferon products it shuts down.
When viral RNA is replicating, it is making a new strand so for a moment it will be double-stranded. Double-stranded RNA just doesn't happen in eukaryotic cells so if a cell detects this via its interferon products it shuts down.
