Bloom forming algae are important in global carbon and
sulphur cycles due to the production of dimethylated sulphur species (DSS) such
as dimethylsulphoniopropionate (DMSP) and dimethylsulphide (DMS). These
compounds eventually form cloud condensation nuclei which, as the name
suggests, provide the basis for cloud formation, and can significantly alter
the earth’s radiation budget. Emiliania
huxleyi forms large, dense blooms annually and these blooms produce a huge
amount of DSS. Generally, the blooms end as a result of host-specific viral
infection, in this case by E. huxleyi Virus
(EhV).
The Intergovernmental Panel on
Climate Change predicts that by 2100 sea surface temperature will have
increased by 1.5-3oC, yet the effect of this increase in
temperature on host-virus interactions had been unexplored until Kendrick et al remedied this in 2014. In the
study they inoculated bottles of growth media with axenic cultures of E. huxleyi CCMP 374, and kept half at 18oC
and half at 21oC, to represent the predicted increased in sea
surface temperature. Cultures were infected with EhV86 when they had attained a
cell density comparable to that of a typical bloom, and were thereafter sampled
daily to measure various parameters including culture density, viral abundance,
burst size, and total DMSP (DMSPt). A series of experiments was also
carried out using six different E.
huxleyi strains to see if the temperature effect was shared.
Kendrick et al ensured that the increase in temperature was affecting the
host’s susceptibility to infection, rather than directly affecting the
infectivity of the virus by incubating EhV86 isolates at 18oC and 21oC
and then using these to infect E. huxleyi
374 growing at 18oC. Burst size (number of viral progeny per
lysed host cell) was significantly higher in both treatments than in the
controls, indicating that exposing EhVs to increased temperature alone does not
affect infectivity.
In the 18oC treatment,
successful viral adsorption is seen – where over 24 hours virus density initially
decreases as the virions contact and cross the host plasma membrane, then
increases at around 4 hours post-infection as viral progeny are released. In
the 21oC treatment this pattern in virus density is not seen, and
this is explained due to changes in the cell membrane which prevent the virions
from binding or crossing the membrane. The authors hypothesise that temperature
induced changes in cell membrane lipids may be responsible for the viral resistance.
Temperature induced resistance did not affect DSS production, but if the
resistance lengthens the bloom duration this could possibly affect the total
amount of DSS produced which could in turn impact global sulphur cycles.
This is a fascinating study which
makes it clear that temperature plays an important role in host-virus
interactions and shows how they may change as our global climate changes. As in
any lab based experiment, the results may not accurately reflect real life as
it lacks microbial ecosystem complexity. Further research into the changes in
lipids at different temperatures, and the difference in lipid content or
concentration between strains of E.
huxleyi, may confirm the mechanism of the viral resistance.
Kendrick B.J., DiTullio
G.R., Cyronak T.J., Fulton J.M., Van Mooy B.A.S., Bidle K.D.(2014) Temperature-Induced
Viral Resistance in Emiliania huxleyi (Prymnesiophyceae). PLoS ONE 9(11) e112134
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0112134
Hi Tabby Figgins,
ReplyDeleteThank you for your post. It’s fascinating that changes to the lipidome could confer viral resistance as well as thermoadaptation! As homeoviscous adaptations to regional differences in temperature alters the membrane lipid composition, do you think that certain Ehux populations from cooler regions would be more susceptible to viral infection than warmer-adapted strains? Or do you think a Red Queen Effect could compensate against regional Ehv strains? The reason I ask is that a recent PNAS paper (Sharoni et al, 2015) has provided evidence that aerosolized Ehv particles can remain infectious and be widely dispersed over tens of kilometres across the ocean surface. Could it be that the regional temperature differences of the Ehux cells would affect the infectivity of dispersed Ehv particles – particularly the introduction of Ehv’s into cooler waters? It’d be great to know what you think. This phenomenon may well play a big role in the connectivity of marine pathogens and global carbon flow.
Sharoni, S., Trainic, M., Schatz, D., Lehahn, Y., Flores, M. J., Bidle, K. D., ... & Vardi, A. (2015). Infection of phytoplankton by aerosolized marine viruses. Proceedings of the National Academy of Sciences, 112(21), 6643-6647. http://www.pnas.org/content/112/21/6643.short
Thanks a lot,
Davis
Hi Davis,
DeleteI'm not sure whether E. huxleyi populations in cooler regions are more susceptible or whether they have adapted differently to cope with the higher infection rate. It would be interesting to see whether the length of Ehux blooms in warmer regions is higher than in cooler regions to shed some light on this.
This study showed that the temperature doesn't affect the infectivity of Ehv's
so I don't think aerosolized viral particles would be any more infectious if they were transported to a cooler region. Unless the Red queen hypothesis is in effect, then maybe Ehv's from cooler regions that were spread to warmer regions would be better able to infect the 'less evolved' Ehux populations.
I hope this answers your questions,
Thanks
Tabby