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Chlorovirus, also known as Chlorella virus, is a genus of giant double-stranded , in the family Phycodnaviridae. This genus is found globally in freshwater environments where freshwater microscopic algae serve as natural hosts. There are six species in this genus.
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.
Though relatively new to virologists and thus not extensively studied, one species, Chlorovirus ATCV-1, commonly found in lakes, has been recently found to infect humans. New studies focusing on effects of infection in mouse model are currently emerging as well.
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. 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. 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. 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.
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 that typically last from February to June in the Northern hemisphere, resulting in oxygen depletion and deaths of larger organisms in freshwater habitats. 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 and, ultimately, fueling the food chain.
Paramecium bursaria Chlorella virus 1 (PBCV-1) have a 190 nm diameter and a fivefold axis. One face's juncture has a protruding spike, which is the first part of the virus to contact its host. The outer capsid covers a single lipid bilayer membrane, which is obtained from the host's endoplasmic reticulum. Some Capsomere on the external shell have fibres extending away from the virus to aid in host attachment.
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 restriction endonucleases. Degradation of the host chromosomal DNA inhibits host transcription. This results in 33-55% of the polyadenylated mRNAs in the infected cell being of viral origin by 20 minutes after initial infection.
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 Viral plaque.
Recently, chlorovirus ATCV-1 DNA has been found in human Pharynx 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.
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 Cdk5 pathway, which aids with learning and memory formation, as well as alterations in gene expression in the dopamine pathway. Further, infected mice were found to be less social, interacting less with newly introduced companion mice than the control group. Infected mice also spent longer in a light-exposed portion of a test chamber, where the control mice tended to prefer the dark side and avoided the light. This indicates a decrease in anxiety with ACTV-1 infection. The test mice were also less able to recognize an object that had been moved from its previous location, showing a decrease in spatial reference memory. As in humans, there is a decrease in vision spatial task ability. Within the hippocampus (area of brain responsible for memory and learning), changes in gene expression occur, and infection presents a change in the pathways of immune cell functioning and antigen processing. It has been suggested that this possibly indicates an immune system response to the ACTV-1 virus causing inflammation which may be the cause for the cognitive impairments. The symptoms presented may also suggest hippocampus and medial prefrontal cortex interference from ACTV-1 infection.
Genome sequencing and functional screening of proteins from PBCV-1 and ATCV-1 revealed large number of horizontally transferred genes, which indicates a long history of co-evolution with the unicellular host and lateral gene transfer with other seemingly unrelated organisms. Further, both viruses were found to encode several so-called "progenitor enzymes", which are smaller, but less specialized than their modern-day analogues. For example, one of the sugar-manipulating enzymes in PBCV-1 (GDP-d-mannose 4,6 dehydratase or GMD) was shown to mediate catalysis of not only the dehydration of GDP-D-mannose, but also reduction of the sugar molecule produced in the initially predicted process. Such dual functionality is uncommon among the currently existing sugar-manipulating enzymes, and possibly suggests the ancient nature of the PBCV-1 GMD.
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 apparatus 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 Eukaryote, which was estimated to occur around 2.0-2.7 billion years ago.
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.
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