Sulfolobus islandicus rod-shaped virus 2

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By Andrew Van Horn


Introduction

Sulfolobus islandicus rod-shaped virus 2 (SIRV2) is a lytic double-stranded DNA archaeal virus that infects Sulfolobus archaea [1] [2]. SIRV2 falls into the greater taxonomy of the Rudiviridae family. Microbiologists have taken interest in SIRV2 due to its thermophilic and acidophilic properties needed to infect Sulfolobus. SIRV2 displays unique properties from many other viruses [1]. These include a unique viral release mechanism of which there are very few similar structures found in the natural world. Furthermore, SIRV2 is a lytic virus that acts by severely degrading host chromosomes. Additionally, SIRV2 is commonly at the forefront of the generally limited field of archaeal viral research [3][4].

Sulfolobus islandicus Archaeon

Sulfolobus islandicus is an archaeon commonly found in Icelandic sulfur hot springs [5]. S. islandicus is a member of the Sulfolobaceae family and the Sulfolobales order. Once more, S. islandicus is a member of the Crenaracheota kingdom of the phylum Archaea. S. islandicus thrives in extreme environments of acidic pH 3 and high temperatures around 80°C. Notably, the intracellular pH of S. islandicus is only slightly acidic, approximately pH 6. Additionally, S. islandicus metabolizes sulfur, though the methods can vary between strains and species [6]. Sulfur metabolism can be done through sulfur oxygenase/reductase and sulfur reductase, among others. However, the extensive methods of sulfur metabolism in S. islandicus are poorly understood.

Pathogenicity

While believed until very recently to be a host-carrier virus that transmitted vertically without lysing host cells[2], this has been revealed to not be the case[1]. In 2009, Bize et al. used flow cytometry to document large-scale chromosomal degradations and DNA damage that led to them recharacterizing SIRV2 as a cytocidal lytic virus. In S. islandicus cells infected with SIRV2, reduction in genome size were documented as early as half an hour after infection. After 12 hours, the majority of their cells populations did not contain any flow cytometry-detectable DNA. Interestingly, a slight increase in intracellular DNA of 1.3 Mb was detected around 3 hours after infection. Following the spike, decreases in intracellular DNA occurred. This spike was attributed to viral DNA replication that occurs quickly after infection.

The latent period of SIRV2 was determined by Bize et al. to be 8-10 hours[1]. After 8-10 hours, almost no host DNA was detectable. Additionally, virions are then released through Virus-Associated Pyramids. Estimates of burst size for SIRV2 in S. islandicus is generally estimated around 30-50 virions[1][2][7]. Bize et al. also showed that no virions were released before the 8-10 hours after infections. Furthermore, cell death was associated with virion release at 8-10 hours by using a membrane potential sensitive probe.

Additionally, it was demonstrated that SIRV2 is able to superinfect S. islandicus. This means that a cell infected by SIRV2 is unable to be infected by other viruses while presently infected by SIRV2.

Genome Structure

Viral Life Cycle

Infection

SIRV2 binds to filaments protruding from the surface of S. islandicus to reach the cell for infection [8]. SIRV2 virions use their tail fibers to bind the tips of long filaments on the cell surface. Virions then migrate down the length of the filament until reaching the cell surface. Upon contact with the cell surface, the virions begin to dissemble and release their genome into the new host cell. Approximately three virions can be bound to an individual filament at a given time. Virions show an initial binding preference for the tips of the filaments for initial attachment. While only two virions can be bound at a given time to the tip of the filament, other virions can simultaneously be migrating down the length of the filament towards the cell surface. Fortunately, filaments are highly abundant on the S. islandicus cell surface. Once virions are bond to the filaments or cell surface, they are irreversibly bound.

Moreover, the rate of infection by SIRV2 of S. islandicus is extremely high[8]. In Quemin et al. 2013, they demonstrated that approximately 80% of virions injected to a culture of s. islandicus were absorbed within thirty seconds, and almost all virions were absorbed after approximately 25 minutes. This rapid absorption is likely facilitated at least in part by the great abundance of filaments for virions to bind to. Furthermore, the ability of multiple virions to bind to each filament allows for a rapid infection process. This rapid infection process combined with lengthy latent period of 8-10 hours has led scientists to suggest that this cycle timing is highly evolved for the extreme conditions in which S. islandicus, and thus SIRV2, live[1][8]. If living in an unfavorable environment of Icelandic hot springs in which the temperatures are greater than 80°C and as acidic as pH 3, it is favorable for SIRV2 to reduce exposure to the extreme environment by minimizing infection time and increasing the time spent within the safety of S. islandicus.

Genome Replication

Virion Release

Anti-CRISPR Defense Mechanisms

CRISPR-editing of the SIRV2 Genome

Nanotechnology

Conclusion

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Bize A, Karlsson EA, Ekefjä Rd B K, Quax TEF, Pina M, Prevost M-C, Forterre P, Tenaillon O, Bernander R, Prangishvili D. 2009. A unique virus release mechanism in the Archaea.
  2. ↑ 2.0 2.1 2.2 Prangishvili D, Arnold HP, Götz D, Ziese U, Holz I, Kristjansson JK, Zillig W. 1999. A Novel Virus Family, the Rudiviridae: Structure, Virus-Host Interactions and Genome Variability of the Sulfolobus Viruses SIRV1 and SIRV2.
  3. ↑ Peng X, Mayo-Muñoz D, Bhoobalan-Chitty Y, Martínez-Álvarez L. 2020. Anti-CRISPR Proteins in Archaea.
  4. ↑ Mayo-Muñoz D, He F, Jørgensen JB, Madsen PK, Bhoobalan-Chitty Y, Peng X. 2018. Anti-crispr-based and crispr-based genome editing of sulfolobus islandicus rod-shaped virus 2. Viruses 10.
  5. ↑ Lewis AM, Recalde A, Bräsen C, Bräsen B, Counts JA, Nussbaum P, Bost J, Schocke L, Shen L, Willard DJ, Quax TEF, Peeters E, Siebers B, Albers S-V, Kelly RM. 2021. The biology of thermoacidophilic archaea from the order Sulfolobales. FEMS Microbiology Reviews 063:1–60.
  6. ↑ Dai X, Wang H, Zhang Z, Li K, Zhang X, Mora-López M, Jiang C, Liu C, Wang L, Zhu Y, Hernández-Ascencio W, Dong Z, Huang L. 2016. Genome sequencing of sulfolobus sp. A20 from costa rica and comparative analyses of the putative pathways of carbon, nitrogen, and sulfur metabolism in various sulfolobus strains. Frontiers in Microbiology 7.
  7. ↑ Prangishvili D, Quax TEF. 2011. Exceptional virion release mechanism: One more surprise from archaeal viruses. Current Opinion in Microbiology.
  8. ↑ 8.0 8.1 8.2 Quemin ERJ, Lucas S, Daum B, Quax TEF, Kühlbrandt W, Forterre P, Albers S-V, Prangishvili D, Krupovic M. 2013. First Insights into the Entry Process of Hyperthermophilic Archaeal Viruses. Journal of Virology 87:13379–13385.



Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2022, Kenyon College

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