Abstract

San Miguel Sea Lion virus (SMSV) is well established as a cause of disease in marine mammals. Small RNA viruses have the fastest mutating genomes found in nature, and tracking evolution of these viruses is highly clinically significant. This high rate of mutation often results in these viruses behaving as a cluster of related sequences, known as a quasispecies, rather than a single species. A quasispecies does not evolve toward a single fittest sequence.¹ It is therefore essential to understand population structure and mutation spectra of viruses behaving as quasispecies. An understanding of quasispecies provides information useful for clinical case management.² We have used pyrosequencing, a novel sequencing methodology which can result in thousands of sequences from a single reaction, to examine SMSV population structures. When dealing with a small genome such as that found in caliciviruses, this enables a snapshot of an entire population, enabling the study of quasispecies. Virus populations in a clinical sample are compared to cultured virus from the same sample, and virus populations in clinical samples from two outbreaks of differing virulence are compared. This data demonstrates that SMSV behaves as a quasispecies, which has significant clinical implications for fluctuations in serotyping and clinical disease, use of cultured virus, and expected virus behavior.

References

1.  de la Torre JC, Holland JJ. RNA virus quasispecies populations can suppress vastly superior mutant progeny. J Virol. 1990 Dec;64(12):6278-81.

2.  Domingo E, Gomez J. Quasispecies and its impact on viral hepatitis. Virus Res. 2007 Aug;127(2):131-50.