Viruses are ubiquitous in aquatic systems and are infectious
agents of many organisms from bacteria up to fish and mammals, yet despite
their huge ecological significance very few studies have been conducted on the
effects of viruses on aquatic metazoans. Copepods are the most dominant members
of such mesozooplankton communities and are responsible for biogeochemical
cycling and fundamental to marine food webs. Whilst previous work has focussed
on the ecology and population dynamics of such organisms, causes of mortality
are still poorly understood.
In the lecture Colin delivered on ‘Diseases of mollusks,
crustaceans and fish’ it was stated Drake and Dobbs (2005) had found no negative
effects of viruses on the fecundity or survival of copepod Acartia tonsa. This,
as mentioned within the lecture, seems rather strange as viruses are central to
controlling algal (phytoplankton) blooms so could be predicted to act in a similar
manner on zooplankton. Consistent with viral disease in phytoplankton,
mortality rates of copepods coincide with population peaks, and with ~35% of
total copepod mortality unexplained by predation, another underlying cause of
mortality must be present.
Using molecular methods the presence of viruses within A.
tonsa and Labidocera aestiva copepods was assessed.
Using metagenomic sequencing on extracted and purified viruses from the sampled copepod species, the presense of circo-like viruses was detected, named LaCopCV and AtCopCV in L. aestiva and A. tonsa respectively. Whilst these viral genomes shared characteristics with known circoviruses; namely a small genome, a stem-loop with a conserved nonanucleotide motif and two nonoverlapping ORF’s coding for replication initiatior (Rep) and capsid proteins, the genomic architecture varied slightly. Unlike the bi-directional orientation of the 2 ORF’s in known circoviruses, the ORF’s in copepod circo-like virus genomes are mono-directional, a characteristic previously observed in environmental viral communities and fecal metagenomes. Additionally, the nonanucleotide motif on the stem-loop in copepod viruses exhibited variations to the normal conserved motif present in circoviruses.
Using metagenomic sequencing on extracted and purified viruses from the sampled copepod species, the presense of circo-like viruses was detected, named LaCopCV and AtCopCV in L. aestiva and A. tonsa respectively. Whilst these viral genomes shared characteristics with known circoviruses; namely a small genome, a stem-loop with a conserved nonanucleotide motif and two nonoverlapping ORF’s coding for replication initiatior (Rep) and capsid proteins, the genomic architecture varied slightly. Unlike the bi-directional orientation of the 2 ORF’s in known circoviruses, the ORF’s in copepod circo-like virus genomes are mono-directional, a characteristic previously observed in environmental viral communities and fecal metagenomes. Additionally, the nonanucleotide motif on the stem-loop in copepod viruses exhibited variations to the normal conserved motif present in circoviruses.
Using a phylogenetic tree based on Rep amino acid sequences,
it was shown that both LaCopCV and AtCopCV are highly divergent from recognised
and identified circoviruses, and are, unsurprisingly, more closely related to
environmental assembled circo-like virus sequences.
Using qPCR of the capsid gene, a high prevalence of LaCopCV
among wild L. aestiva populations was observed in the order of magnitude
similar to that of white spot syndrome virus in postlarval crustaceans, and was
found to be actively replicating, with low levels of transcription detected
using a modified qRT-PCR assay. AtCopCV was also detected, though only in samples
from 7 months of the year principally in spring and autumn during times of
population changes. Despite being suggestive of lower prevalence in comparison
to LaCopCV, the presence of AtCopCV coninciding with population peaks and
previously stated nonpredatory mortality peaks could suggest that AtCopCV has a
greater influence in mortality during zooplankton blooms and LaCopCV accounts
for a steady rate of mortality throughout the year. This is supported by the
frequent identification of LaCopCV in sediments from Tampa Bay, perhaps
signifying a potential reservoir for the virus.
Contrary to the study by Drake and Dobss (2005) the results
of this study provide evidence of not only the presence, but the prevalence and
active replication of previously undocumented viruses within two numerically
dominant species of natural zooplankton populations. Though further study is
required to understand the pathology of the viruses and the larger ecological
implications they may have on marine food webs, the study is an important
breakthrough in understanding potential roles of viruses in the nonpredatory
mortality of zooplankton. Whilst both viruses found were limited to and only
detected in their respective zooplankton species, it’s not to say that other
circo-like viruses don’t propagate in other zooplankton species. With the
demonstrated capacity to test this, it is an area which warrants future study.
Dunlap D., Fei Fan Ng T., Rosario K., Barbosa J., Greco A., Breitbart M. and Hewson I. (2012) Molecular and microscopic evidence of viruses in marine copepods. Proceedings of the National Academy of Sciences, 11(4), 1375-1380
Drake L. and Dobbs F. (2005) Do viruses affect fecundity and survival of the copepod Acartia tonsa Dana? Journal of Plankton Research, 27(2), 167-174
Whilst evidence of the prevalence of viral replication in copepod tissue is blatant, exposing these circo-like viruses as a contributor to zooplankton mortality seems less straightforward. Mesocosms have been used examine phytoplankton mortality, but you could never exclude viruses from a control mesocosm. Another option is controlled laboratory investigations, but they will likely not reflect the true mortality rates in the ocean. Why do so many organisms insist on being too small to see?
ReplyDeleteI agree, their size and ubiquitous nature does make them incredibly hard to study, and does leave a lot of uncertainty. Whilst sampling technique does make it difficult to truly assess whether circo-like viruses to contribute to mortality, i think there is a lot of reason to believe they do. If they are present, and replicating the viruses are obviously active, and most active viruses usually infer some form of structural or biochemical alteration to the host cells, often resulting in damage. Obviously, as previously mentioned, without knowing the pathology of the virus it cannot be said with 100% confidence that these circo-like viruses do cause damage, however i think it is very likely.
ReplyDeleteThis is a really nice gateway study. Does this paper mention any other factors other than predation? It seems to me like they're ruling out a lot of other things which could be associated with population crashes, such as competition and food availability. Also, I'm not sure if this is a moot point, but could the viruses that seem to be associated with these copepods in fact be associated with other micro-organisms found with or on copepods? such as bacteria. It'll be interesting to find out what the actual association is before assuming they interact with one another on a significant level.
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