Hi there!
I work with the yellow fever vaccine strain 17D and I always inactivate the virus at 56 degrees for 1h as a control group. However, I've also seen UV inactivation and in one of the papers I read Article Yellow fever vaccine YF-17D activates multiple dendritic cel...
the two inactivation methods actually made a difference in the cell response.So my question is: how exactly do these two methods inactivate the virus? In the case of yellow fever virus, the UV light crosslinks the viral RNA right? What does the heat do to the virus then?
Thanks for any suggestions!
Hi Yiqi, generally, virus inactivation methods target either the lipid envelope membrane, the viral capsid, and/or the viral genome. The yellow fever virus is an enveloped RNA virus, therefore, UV inactivate it by damaging the viral genomes as it does not affect the proteins. On the other hand, heat treatment damages both viral proteins and viral genome.
Abdelmalik Ibrahim Khalafalla Thank you so much for your answer! Is it then correct to make such conclusions:
1. Cells don't respond to heat-inactivated virus = the response can be dependent on detection of certain viral protein or viral genome or active replication of the virus
2. Cells don't respond to UV-inactivated virus = the response is specifically dependent on detection of viral genome or replication
I must be careful when tending to such a debatable scientific issue. Theoretically, yes, cells don't respond to UV-inactivated virus because there is no virus multiplication and the response can be dependent on detection of certain viral protein or viral genome or active replication of the virus. However, you need first to prove that the activation of DCs is induced only by a live virus not killed one. Second, you need to rule out the possibility that the activation effect is caused by the YFV not other substances found in the vaccine. As you know live viral vaccines contain not only viral proteins and nucleic acids, but also cellular contaminants derived from the cell lines in which the vaccines were grown. To do so you need to purify your virus first.
Yiqi Huang Hi, hopefully by this time you must have solved your curiosity.
And if not then some points to add to your question.
Heat inactivation of viruses: It affects the receptor binding ability of both type of viruses, ie., enveloped and non-enveloped. Let me assist one by one case. In case of enveloped viruses, it affects the lipid/envelope-glycoproteins, therefore the virus is unable to bind plasma membrane receptors or co-receptors. Probably the same case is with non-enveloped viruses, which use the plasma membrane surface receptors.
UV-inactivation of viruses: You have already mentioned the reason for this. It inactivates the viral genome as it crosslinks them, therefore they cannot multiply or replicate inside the cells. Now, theoretically, they should still be able to enter inside the cells, but since they cannot multiply or replicate, there is no robust or detectable immune response seen.
As you might have read, the RLRs (RIG-I, MDA-5, LGP2) and TLRs (-3, -7, -9) are the primary innate immune sensors for viruses which cause rapid surge in IFN production and immune response. Most of viral proteins are either used for packaging of viruses, entering the cells or evading immune response. Viral proteins cause these effects indirectly, via UPR or ER-stress, as viruses hijack the protein machinery and produce proteins rapidly.
BR,
Cheers.
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