How about some healthy scientific debate!!!
What do all of you think about the theory (Tom Schwan May PNAS)
that after a tick infected with B.burgdorferi begins to ingest a blood meal, the
spirochetes use a signal to induce a phenotypic switch between ospA and ospC.
It certainly would explain alot of research findings. I was thinking that there must
therefore at some time be a switch from ospC -> ospA in order for the spirochete to
survive better in the tick. So if OspC were first turned OFF in the mammalian host,
it could survive in an infected individual in the face of antibodies against OspA and
OspC which are the predominant antibodies found in polyclonal Ab preparations.
-->Chronic infection?
I asked my labmates these questions and no-one seemed to be sure of the answers.
1. We routinely grow borrelia in BSK containing gelatin. I have,
however, read Methods sections which specifically state use of media
lacking gelatin. I assumed that the use of gelatin in BSK made the
media more closely approximate in vivo conditions. Anybody have any
thoughts?
2. Has anybody who has tried electroporating B.burgdorferi tried freezing
"competant" cells down at -70, after preparation such as per Samuels
et.al. 1994
3. It seems to me that you need a minimal number of Borrelia in order to get
growth in vitro. Has anyone tried a serial dilution to see how few
you need? Just wondering - may try it out
