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Emails received from Dr Anthony Wilson of the Arbovirus Modelling and Entomology Epidemiology Division, Institute for Animal Health Pirbright

Dec 12, 2008 copied to
Dear Sabine
My apologies - I think I misread your original post. If you get what is called 'sterile immunity', this means that the vaccine stops any virus from circulating. There are then degrees of vaccine efficacy; at one end, a vaccine may reduce virus circulation so that the virus will never reach high enough levels to be transmitted onwards by midges; a vaccine at the other end may reduce clinical disease but onwards transmission may still be possible. Your Intervet IBR example sounds like it could be the latter, although I'm not familiar with the details of this one.
I thought that you were suggesting that midge bites could stimulate the recrudescence of live virus in vaccinated animals. Some work conducted a few years ago here at Pirbright showed that BTV could infect certain sheep immune cells persistently (in the lab). The same cells are involved in the inflammation response triggered by midge bites. The resulting paper therefore suggested that BTV might be capable of remaining in the immune cells of an infected sheep for some time following recovery, and that when the animal was bitten by more midges (say, the following spring) these infected immune cells would flock to the skin areas being bitten and the next generation of midges could be infected even though the animal had recovered. This "recrudescence" was therefore suggested as a possible explanation for overwintering, and might yet turn out to be an important route for other strains; overwintering has been seen in many bluetongue outbreaks, while transplacental transmission has only been seen in BTV-8 and certain tissue-adapted lab strains (despite being looked for).
However, inactive vaccine should not contain any live virus, so recrudescence could not occur in vaccinated animals, only in those which were naturally infected and had since recovered.
The more you look at bluetongue epidemiology, the more complicated it gets!
PS the recrudescence paper was Takamatsu et al. (2003) "A possible overwintering mechanism for bluetongue virus in the absence of the insect vector", Journal of General Virology 84: 227-235. I can send a PDF if it is of interest, although as this will be under copyright it could not be published on the site.
Previous emails

Dear Mary

.... just seen the comment from Sabine on your site. I would agree with nearly all of the points made - the only point I would disagree with is the statement that vaccinated animals are capable of developing a viraemia when bitten by a midge. With an efficacious inactivated vaccine no viraemia should be seen at any stage - there should never be any live virus in the animal to multiply up.

A positive PCR result indicates that viral RNA is present in an animal; it does not on its own indicate that active ("live") virus is present. Naturally infected animals which have recovered and cleared all active virus may still have traces of viral RNA in their bloodstream, and therefore demonstrate a PCR-positive test result, for up to six months.
The same is true for midges - a PCR-positive result indicates that fragments of viral RNA are present, but not necessarily active virus. A midge which ingests a viraemic blood-meal but is not "competent" will never become infected - virus will never spread beyond the gut walls - but traces of viral RNA remaining in the gut may cause it to show up as PCR-positive. This has been a major cause of the current confusion over which Culicoides species are acting as vectors in northern Europe; several papers have recently been published claiming that a species has been "confirmed" as a vector on the basis of a PCR-positive result (when in fact this shows only that the individual has fed on an infected animal - nothing about the potential for onwards transmission). On a related note, the suggestion a few years ago that BTV might be able to spread vertically from adult midges to their offspring was based on a PCR-positive result rather than virus isolation. I discussed this in slightly more detail in my recent overwintering review article (
You and Sabine are also correct that during the "vector-free" period the risk of onwards transmission is minimised, but given the various findings during 2008 about secondary transmission routes and the possibility of vectors sheltering in animal housing I suspect that most policy-makers would be nervous about saying that the risk is actually zero during this period.
I hope this helps. 
(See previous email from Dr Wilson Nov 2008 )