Archaeal Viruses


Our understanding of archaeal viruses lags significantly behind that of bacterial viruses and animal viruses.

However, as more archaeal viruses are isolated and studied, virologists are beginning to develop a clearer picture of the nature of these interesting biological entities.

Nearly all known archaeal viruses have dsDNA genomes; the few exceptions have ssDNA genomes. However, metagenomic evidence suggests that RNA archaeal viruses exist; they have not yet been isolated. Archaeal virus genomes can be either linear or circular.

Some archaeal viruses exhibit morphologies similar to that of other viruses. However, many others have unusual morphologies, such as bottle-shaped, droplet-shaped, and spindle-shaped (see also Microbial Diversity & Ecology 6.1 box figure.) These unusually shaped viruses have defined several new virus families.

Unlike most bacteriophages, many archaeal viruses are enveloped. With a few exceptions, relatively little is known about archaeal virus life cycles. However, they do exhibit some interesting differences from those of bacteriophages. Thus far, most archaeal viruses studied establish chronic infections, whereby viruses are continuously produced and extruded from the host cell.

This type of infection is similar to that of fd bacteriophage and other related ssDNA phages in the family Inoviridae (section). Some archaeal viruses have been shown to establish lysogeny by integrating their genomes into the host cell’s chromosome. Although relatively few archaeal viruses always cause lytic infections, one such virulent archaeal virus is of particular interest.

Sulfolobus turreted icosahedral virus 1 Bicaudavirus
Virion Morphology of Some Archaeal Viruses. 
(a) Sulfolobus turreted icosahedral virus (STIV) has a virion morphology similar to some bacterial and animal viruses. Scale bar 5 500 nm. Transmission electron microscopy (TEM).
(b) TEM image of Sulfolobus shibatae virus 2 (SSV-2-Ss) virions. These droplet-shaped virions have a short tail at one end. Virus particles often attach to membranes or each other by their tails. (c) TEM image of an Acidianus two-tailed virus virion 

The Sulfolobus turreted icosahedral virus (STIV) is released from its host Sulfolobus spp. in an unusual way. After the genome enters the host cell (by an unknown mechanism), transcription of the viral genome begins.

Some of the viral gene products regulate host cell genes, thus enabling the virus to control the replication process using the host’s DNA replication, transcription, and translation machinery. Eventually the assembly phase begins.

STIV virions have an icosahedral capsid that surrounds an internal lipid bilayer; the lipid bilayer encloses the virus’s genome. Electron cryotomography studies suggest that during assembly, the capsid and internal membrane are assembled together, leading to the formation of an empty virion (procapsid) devoid of the viral genome

 Once the procapsids (capsid plus membrane) are complete, the DNA is packaged by an unknown mechanism. Virion release results from the formation of pyramid-like structures on the surface of the host cell (figure ).

These virus-associated pyramids, as they are called, open up, much like the petals of a flower bud open. This allows the escape of the progeny virions, leaving the empty cell ghosts behind.

Virus Associated pyramids
Virus-Associated Pyramids.
 STIV virions are released from the cell by way of pyramid-like structures that form on the surface of the infected cell. The pyramids are seven-sided, and each face of the pyramid “peels back,” providing an opening through which the virions escape. 

The CRISPR/Cas System: Bacteria and Archaea Fight Back

In our discussion of T4 bacteriophage, we introduce a defense mechanism—restriction—used by bacteria to protect themselves against attack from viruses. Many bacteria and archaea have another defense mechanism: the CRISPR/Cas system.

This intriguing defense system has been likened to the adaptive immunity used by animals to protect themselves from microbial attack. The similarity is based on the observation that the CRISPR/Cas system uses parts of the invading virus’s genome to “remember” an attack and prepare for a possible future attack, just as the adaptive immune system uses parts of an invading microbe to remember and prepare for the next invasion.

CRISPR/Cas was discovered when analyses of numerous bacterial and archaeal genomes identified sets of repeated nucleotide sequences separated by short spacers. These sets form a CRISPR system, CRISPR being short for clustered, regularly interspaced short palindromic repeats.

The sequence of base pairs in the repeats are identical (or nearly so) within each CRISPR system. The spacers, however, differ considerably in sequence. Surprisingly, when the spacer sequences were used to probe nucleic acid databases, it was discovered that the spacers exhibit significant similarity to a variety of bacterial and archaeal virus genomes.

CRISPR regions were later shown to be associated with a set of genes encoding proteins called Cas proteins (short for CRISPR-associated sequences). Thus the new designation: a CRISPR/Cas system (figure 27.14).

A Typical CRISPR Cas System
A Typical CRISPR/Cas System

The surprising similarity between viral genes and CRISPR/ Cas spacers led scientists to question how the spacers came to exist and what their role was in the host cell. The function of CRISPR/Cas systems is currently divided into three stages: acquisition, CRISPR RNA biogenesis, and interference.

The acquisition stage occurs when a cell is infected by a virus. If the cell survives (e.g., because the virus is defective and can’t successfully complete its life cycle), it adds portions of the viral genome to its CRISPR region.

The addition is made at the end of the region closest to the CAS genes, and each new addition consists of a new repeat and a spacer consisting of DNA from the infecting virus. Thus the CRISPR sequences are akin to the growth rings on trees. Just as the history of the yearly growth of a tree can be ascertained by examining its growth rings, so too can the history of viral infections be determined.

In any given bacterial or archaeal strain, a CRISPR sequence inserted during the oldest infection is located farthest from the Cas genes and the most recent is closest to the CAS genes. During the CRISPR RNA (crRNA) biogenesis stage the CRISPR region is transcribed to yield a large RNA containing all repeats and spacers.

Cas proteins associate with this full-length RNA and process it into mature crRNAs. Each of these consists of one repeat and one spacer. Cas proteins remain associated with the crRNAs, and during a subsequent infection, the Cas-crRNAs associate with either viral DNA or mRNA, leading to destruction of the molecule (interference).

This prevents virus multiplication, and infection is thwarted. The interference stage bears significant similarity to silencing RNAs (siRNAs), as we describe in our content.

Our focus has been on the use of CRISP/Cas systems by bacteria and archaea to defend against viral attacks. However, there is considerably more to these systems. It is now clear that bacteria and archaea use CRISPR/Cas for the more general process of protecting their genomes from foreign nucleic acids that might enter via conjugation or natural transformation.

Furthermore, evidence suggests that crRNAs may regulate gene expression of host genes. Finally, viruses have been shown to evolve to evade their hosts’ CRISPR/Cas defense, often by having a mutation in the target sequence. The host cell, in turn, responds by obtaining new spacers specific for that virus.

It has been suggested that this back-andforth interaction between virus and host plays an important role in the evolution of both  Bacterial conjugation requires cellcell contact |Bacterial transformation is the uptake of free DNA from the environment.