Chlorovirus

Chlorovirus
Virus classification
(unranked):	Virus
Realm:	Varidnaviria
Kingdom:	Bamfordvirae
Phylum:	Nucleocytoviricota
Class:	Megaviricetes
Order:	Algavirales
Family:	Phycodnaviridae
Genus:	Chlorovirus

Chlorovirus, also known as Chlorella virus, is a genus of giant double-stranded DNA viruses, in the family Phycodnaviridae. This genus is found globally in freshwater environments^[1] where freshwater microscopic algae serve as natural hosts. There are 19 species in this genus.^[2][3]

Chlorovirus was discovered in 1981 by Russel H. Meints, James L. Van Etten, Daniel Kuczmarski, Kit Lee, and Barbara Ang while attempting to culture Chlorella-like algae. During the attempted process viral particles were discovered in the cells 2 to 6 hours after being initially isolated, followed by lysis after 12 to 20 hours. This virus was initially called HVCV (Hydra viridis Chlorella virus) since it was first found to infect Chlorella-like algae.^[4][5]

Though relatively new to virologists and thus not extensively studied, one species,

Chlorovirus is a genus of giant double-stranded DNA (dsDNA) viruses in the family Phycodnaviridae, and Baltimore group 1: dsDNA viruses. The genus contains the following species:^[3]

Ecology

Chloroviruses are widespread in

Chlorovirus titers are variable by season and location, but typically fluctuate between 1 and 100 PFU/mL, although high abundances of up to 100,000 PFU/mL may occur in some environments. Due to the rich genetic diversity and high specialization of individual species with respect to infectious range, variations in their ecology are not unusual, resulting in unique spatio-temporal patterns, which ultimately depend on lifestyle and nature of the host. As such, previous survey data highlighted two prominent seasonal abundance peaks for both Chlorella variabilis NC64A and Chlorella variabilis Syngen viruses — one in late fall, and the other in late spring to mid-summer — which is likely attributed to the fact that they share a host species. Conversely, Chlorella heliozoae SAG viruses peaked at different times of the year and generally exhibited more variability in titers, as compared to the NC64A and Syngen viruses.[1] Additionally, studies revealed that chloroviruses demonstrate some resilience in response to decreased temperatures observed during the winter season, characterized by presence of infectious particles under ice layers in a stormwater management pond in Ontario, Canada.^[11] Further, DeLong et al. (2016) suggest that predation by small crustaceans can play an indirect role in titer fluctuations, as degradation of protist cells passing through the digestive tract results in liberation of large numbers of unicellular algae that become susceptible to viral infection due to disruption of endosymbiosis.^[10] Overall, seasonal abundance of chloroviruses depends not only on the host species, but also on the abundance of other microorganisms, general nutrient status and ecological conditions.^[12]

Collectively, chloroviruses are able to mediate global biogeochemical cycles through phytoplankton turnover. Chlorella, in co-occurrence with other types of microscopic algae like Microcystis aeruginosa, are known to cause toxic algal blooms that typically last from February to June in the Northern hemisphere, resulting in oxygen depletion and deaths of larger organisms in freshwater habitats.^[13][14] Lytic infection of unicellular algae by chloroviruses results in termination of algal blooms and the subsequent release of carbon, nitrogen and phosphorus trapped in the cells, transporting them to lower trophic levels and, ultimately, fueling the food chain.^[12]

Structure

Viruses in the genus Chlorovirus are enveloped, with icosahedral and spherical geometries, and T=169 (

Paramecium bursaria Chlorella virus 1 (PBCV-1) have a 190 nm diameter[9] and a fivefold axis.^[15] One face's juncture has a protruding spike, which is the first part of the virus to contact its host.^[16] The outer capsid covers a single lipid bilayer membrane, which is obtained from the host's endoplasmic reticulum.^[15] Some capsomers on the external shell have fibres extending away from the virus to aid in host attachment.^[17][16]

Hosts

Chloroviruses infect certain unicellular, eukaryotic

Viral replication is nucleo-cytoplasmic. Replication follows the

In three dimensional recreations of PBCV-1, it is seen that the spike first contacts the host’s cell wall[21] and is aided by fibres in order to secure the virus to the host. The attachment of PBCV-1 to its receptor is very specific, and a major source of limitation with regards to viral host range. Virus-associated enzymes allow the host cell wall to degrade, and the viral internal membrane fuses with the host membrane. This fusion allows the transfer of viral DNA and virion-associated proteins into the host cell and also triggers depolarization of the host membrane. This is presumably occurring due to a virus encoded K+ channel. Studies predict this channel is within the virus, acting as an internal membrane releasing K+ from the cell, which may assist in the ejection of viral DNA and proteins from the viral cell to its host. The depolarization of the host’s cell membrane is also thought to prevent secondary infection from another virus or secondary transporters.^[19]

Because PBCV-1 does not have an RNA polymerase gene, its DNA and viral-associated proteins move to the nucleus where transcription begins 5–10 minutes post infection. This rapid transcription is attributed to some component facilitating this transfer or viral DNA to the nucleus. This component is assumed to be a product of the PBCV-a443r gene, which obtains structures resembling proteins involved in nuclear trafficking in mammalian cells.

Host transcription rates decrease in this early phase of infection, and host transcription facilitators are reprogrammed to transcribe the new viral DNA. Minutes after infection, host chromosomal DNA degradation begins. This is presumed to occur through PBCV-1 encoded and packaged DNA

Viral DNA replication initiates after 60 to 90 minutes, which is then followed by the transcription of late genes within the host cell. Roughly 2–3 hours post infection, the assembly of virus capsids begins. This occurs within localized regions of the cytoplasm, with the virus capsids becoming prominent 3–4 hours after initial infection. 5–6 hours after PBCV-1 infection, the cytoplasm of the host cell fills with infectious progeny virus particles. Shortly after that (6–8 hours post infection), localized lysis of the host cell releases progeny. ~1000 particles are released from each infected cell, ~30% of which form plaques.^[19]

Effects of infection

In algae infected with Cloroviruses the result is lysis, and thus death. As such, Chloroviruses are an important mechanism to the termination of algal blooms and play a vital role in the supply of nutrients to the water column^[17] (See Ecology section for more information). Chloroviruses are also able to change the wall structure of infected cells. Some chloroviruses contain chitin synthase (CHS) genes while some others contain hyaluronan synthase (HAS) genes, respectively triggering the formation of chitin sensitive fibres or hyaluronan sensitive fibres. Though the function of producing a fibrous mat is not definitively known, it is believed that the fibres could: deter the uptake of the infected cell by symbiotic protozoans, which cause the digestion of the lysed cell; infect another host that takes up the fibre covered algae; or join with other infected and fibre covered cells. The ability to encode enzymes that trigger the synthesis of hyaluronan (hyaluronic acid) is found in no other viruses.^[23]

Recently, chlorovirus ATCV-1 DNA has been found in human oropharyngeal samples. Prior to this is it was not known chlorovirus could infect humans, so there is limited knowledge about infections in people. People who were found to be infected had delayed memory and decreased attention. Humans found to be infected with ATCV-1 showed a decreased visual processing ability and reduced visual motor speed. This led to an overall decline in the ability to perform tasks based on vision and spatial reasoning.^[6]

Studies infecting mice with ACTV-1 have been performed following the discovery chlorovirus can infect humans. The studies conducted on infected mice show changes in the

Chloroviruses, as well as the remaining members of the family Phycodnaviridae, are considered part of the broader group of microbes called nucleocytoplasmic large DNA viruses (NCLDVs). Although phycodnaviruses are diverse genetically and infect different hosts, they display high levels of similarity on the structural level to each other and other NCLDVs. Phylogenetic analysis of the major capsid protein within the group indicates great likelihood of close relatedness, as well as prior divergence from a single common ancestor, which is believed to be a small DNA virus.^[24][25] Additionally, studies suggest that genome gigantism, characteristic of all chloroviruses, is a property which evolved early on in the history of NCLDVs, and subsequent adaptations towards respective hosts and particular habitats resulted in mutations and gene loss events, which ultimately shaped all currently existing chlorovirus species.^[25]

Infection cycle studies in PBCV-1 revealed that the virus relies on a unique capsid glycosylation process independent of the host's ER or Golgi machinery. This feature has not yet been observed in any other virus currently known to science and potentially represents an ancient and conserved pathway, which could have evolved before eukaryogenesis, which was estimated to occur around 2.0-2.7 billion years ago.^[26]

Recent discovery regarding presence of DNA sequences homologous to ATCV-1 in the human oropharyngeal virome, as well as the subsequent studies demonstrating successful infection of mammalian animal model by ATCV-1, also point to the likelihood of ancient evolutionary history of chloroviruses, which possess structural features and utilize molecular mechanisms that potentially allow for replication within diverse animal hosts.^[6][27][28]

References