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Marine viruses - Wikipedia
Marine viruses
Structure of a typical virus, in this case a phage.[1] The appearance of these viruses has been likened to a miniature lunar lander.[2] They are essential to the regulation of marine ecosystems.[3]
Part of a series of overviews on
Marine habitats
Marine microorganisms
Marine microbiomes
Marine prokaryotes
Marine protists
Marine fungi
Marine vertebrates
Marine primary production
Marine food web
Marine carbon pump
Marine biogeochemical cycles
Human impact on marine life
Marine life portal
Part of a series on
Trophic mode
Phytoplankton
Zooplankton
Mixoplankton
Mycoplankton
Bacterioplankton
Virioplankton
Heterotrophic picoplankton
Microzooplankton
Nanophytoplankton
Photosynthetic picoplankton
Picoeukaryote
Picoplankton
Marine microplankton
coccolithophores
dinoflagellates
foraminiferans
amoebae
ciliates
By habitat
Aeroplankton
Geoplankton
Marine plankton
Freshwater plankton
Gelatinous zooplankton
Holoplankton
Ichthyoplankton
Meroplankton
Pseudoplankton
Tychoplankton
Critical depth
Cyanobacterial bloom
Harmful algal bloom
Great Calcite Belt
Milky seas effect
Algaculture
CLAW hypothesis
Diel vertical migration
Ocean fertilization
Paradox of the plankton
Planktivore
Planktology
Thin layers
NAAMES
Marine viruses are defined by their habitat as viruses that are found in marine environments, that is, in the saltwater of seas or oceans or the brackish water of coastal estuaries. Viruses are small infectious agents that can only replicate inside the living cells of a host organism, because they need the replication machinery of the host to do so.[4] They can infect all types of life forms, from animals and plants to microorganisms, including bacteria and archaea.[5]
When not inside a cell or in the process of infecting a cell, viruses exist in the form of independent particles called virions. A virion contains a genome (long molecules that carry genetic information in the form of either DNA or RNA) surrounded by a capsid (a protein coat protecting the genetic material). The shapes of these virus particles range from simple helical and icosahedral forms for some virus species to more complex structures for others. Most virus species have virions that are too small to be seen with an optical microscope. The average virion is about one one-hundredth the linear size of the average bacterium.
A teaspoon of seawater typically contains about fifty million viruses.[6] Most of these viruses are bacteriophages which infect and destroy marine bacteria and control the growth of phytoplankton at the base of the marine food web. Bacteriophages are harmless to plants and animals but are essential to the regulation of marine ecosystems. They supply key mechanisms for recycling ocean carbon and nutrients. In a process known as the viral shunt, organic molecules released from dead bacterial cells stimulate fresh bacterial and algal growth. In particular, the breaking down of bacteria by viruses (lysis) has been shown to enhance nitrogen cycling and stimulate phytoplankton growth. Viral activity also affects the biological pump, the process which sequesters carbon in the deep ocean. By increasing the amount of respiration in the oceans, viruses are indirectly responsible for reducing the amount of carbon dioxide in the atmosphere by approximately 3 gigatonnes of carbon per year.
Marine microorganisms make up about 70% of the total marine biomass. It is estimated marine viruses kill 20% of this biomass every day. Viruses are the main agents responsible for the rapid destruction of harmful algal blooms which often kill other marine life. The number of viruses in the oceans decreases further offshore and deeper into the water, where there are fewer host organisms. Viruses are an important natural means of transferring genes between different species, which increases genetic diversity and drives evolution. It is thought viruses played a central role in early evolution before the diversification of bacteria, archaea and eukaryotes, at the time of the last universal common ancestor of life on Earth. Viruses are still one of the largest areas of unexplored genetic diversity on Earth.
2 Bacteriophages
3 Archaeal viruses
4 Fungal viruses
5 Eukaryote viruses
5.1 Marine protists
5.2 Marine invertebrates
5.3 Marine vertebrates
6 Giant marine viruses
7 Virophages
8 Role of marine viruses
8.1 Viral shunt
8.2 Limiting algal blooms
8.3 Gene transfer
9 Marine habitats
9.1 Along the coast
9.2 At the ocean surface
9.3 In the water column
9.4 In sediments
9.5 In hydrothermal vents
9.6 Polar regions
9.7 Distribution
Bacteriophages (phages)
Multiple phages attached to a bacterial cell wall at 200,000x magnification
Diagram of a typical tailed phage
Phage injecting its genome into bacteria
Further information: introduction to viruses and viral evolution
Viruses are now recognised as ancient and as having origins that pre-date the divergence of life into the three domains.[7] They are found wherever there is life and have probably existed since living cells first evolved.[8] The origins of viruses in the evolutionary history of life are unclear because they do not form fossils. Molecular techniques are used to compare the DNA or RNA of viruses and are a useful means of investigating how they arose.[9] Some viruses may have evolved from plasmids—pieces of DNA that can move between cells—while others may have evolved from bacteria. In evolution, viruses are an important means of horizontal gene transfer, which increases genetic diversity.[10]
Opinions differ on whether viruses are a form of life or organic structures that interact with living organisms.[11] They are considered by some to be a life form, because they carry genetic material, reproduce by creating multiple copies of themselves through self-assembly, and evolve through natural selection. However they lack key characteristics such as a cellular structure generally considered necessary to count as life. Because they possess some but not all such qualities, viruses have been described as replicators[12] and as "organisms at the edge of life".[13]
The existence of viruses in the ocean was discovered through electron microscopy and epifluorescence microscopy of ecological water samples, and later through metagenomic sampling of uncultured viral samples.[14][15] Marine viruses, although microscopic and essentially unnoticed by scientists until recently, are the most abundant and diverse biological entities in the ocean. Viruses have an estimated abundance of 1030 in the ocean, or between 106 and 1011 viruses per millilitre.[4] Quantification of marine viruses was originally performed using transmission electron microscopy but has been replaced by epifluorescence or flow cytometry.[16]
Bacteriophages[edit]
Cyanophages, viruses that infect cyanobacteria
scale bars: 100 nm
Further information: cyanophage and phage ecology
Bacteriophages, often contracted to phages, are viruses that parasitize bacteria for replication. As aptly named, marine phages parasitize marine bacteria, such as cyanobacteria.[17] They are a diverse group of viruses which are the most abundant biological entity in marine environments, because their hosts, bacteria, are typically the numerically dominant cellular life in the sea. There are up to ten times more phages in the oceans than there are bacteria,[18] reaching levels of 250 million bacteriophages per millilitre of seawater.[19] These viruses infect specific bacteria by binding to surface receptor molecules and then entering the cell. Within a short amount of time, in some cases just minutes, bacterial polymerase starts translating viral mRNA into protein. These proteins go on to become either new virions within the cell, helper proteins, which help assembly of new virions, or proteins involved in cell lysis. Viral enzymes aid in the breakdown of the cell membrane, and there are phages that can replicate three hundred phages twenty minutes after injection.[20]
Bacteria defend themselves from bacteriophages by producing enzymes that destroy foreign DNA. These enzymes, called restriction endonucleases, cut up the viral DNA that bacteriophages inject into bacterial cells.[21] Bacteria also contain a system that uses CRISPR sequences to retain fragments of the genomes of viruses that the bacteria have come into contact with in the past, which allows them to block the virus's replication through a form of RNA interference.[22][23] This genetic system provides bacteria with acquired immunity to infection.[24]
Adsorption of cyanophages onto a marine Prochlorococcus
(a) Slice (~20 nm) through a reconstructed tomogram of P-SSP7 phage incubated with MED4, imaged at ~86 min post-infection. FC and EC show full-DNA capsid phage and empty capsid phage, respectively.
(b) same image visualised by highlighting the cell wall in orange, the plasma membrane in light yellow, the thylakoid membrane in green, carboxysomes in cyan, the polyphosphate body in blue, adsorbed phages on the sides or top of the cell in red, and cytoplasmic granules (probably mostly ribosomes) in light purple.[25]
scale bar: 200 nm
Process of a phage "landing" on a bacterium
The phage first adheres to the cell surface with its tail parallel to or leaning at an angle to the cell surface in the pre-infection stage. The tail then firmly stands on the cell surface and extends its fibers horizontally, rendering the phage infection-competent, after which viral DNA is released into the cell through an extensible tube.[25]
based on observations of the model cyanophage P-SSP7
interacting with the marine Prochlorococcus MED4 bacterium
The lytic cycle, the reproductive cycle of the bacteriophage, has six stages:
→ attachment: the phage attaches itself to the surface of the host cell
→ penetration: the phage injects its DNA through the cell membrane
→ transcription: the host cell's DNA is degraded and the cell's metabolism
is directed to initiate phage biosynthesis
→ biosynthesis: the phage DNA replicates inside the cell
→ maturation: the replicated material assembles into fully formed viral phages
→ lysis: the newly formed phages are released from the infected cell
(which is itself destroyed in the process) to seek out new host cells [26]
Microbes drive the nutrient transformations that sustain Earth's ecosystems,[27] and the viruses that infect these microbes modulate both microbial population size and diversity.[28][25] The cyanobacterium Prochlorococcus, the most abundant oxygenic phototroph on Earth, contributes a substantial fraction of global primary carbon production, and often reaches densities of over 100,000 cells per milliliter in oligotrophic and temperate oceans.[29] Hence, viral (cyanophage) infection and lysis of Prochlorococcus represent an important component of the global carbon cycle. In addition to their ecological role in inducing host mortality, cyanophages influence the metabolism and evolution of their hosts by co-opting and exchanging genes, including core photosynthesis genes.[25]
Virions of different families of tailed phages: Myoviridae, Podoviridae and Siphoviridae
Tailed V22 phages of Alteromonas bacteria [30]
scale bar : 100 nm
The non-tailed phage Corticovirus
For a long time, tailed phages of the order Caudovirales seemed to dominate marine ecosystems in number and diversity of organisms.[17] However, as a result of more recent research, non-tailed viruses appear to dominate multiple depths and oceanic regions.[31] These non-tailed phages also infect marine bacteria, and include the families Corticoviridae,[32] Inoviridae,[33] Microviridae [34] and Autolykiviridae.[35][36][37][38]
Archaeal viruses[edit]
Evolution of the virus world: origin of the main lineages from the primordial gene pool
Characteristic images of RNA and protein structures are shown for each postulated stage of evolution, and characteristic virion images are shown for the emerging classes of viruses. Thin arrows show the postulated movement of genetic pools between inorganic compartments. Block arrows show the origin of different classes of viruses at different stages of pre-cellular evolution.[5]
Further information: Archaeal viruses
Archaean viruses replicate within archaea: these are double-stranded DNA viruses with unusual and sometimes unique shapes.[39][40] These viruses have been studied in most detail in the thermophilic archaea, particularly the orders Sulfolobales and Thermoproteales.[41] Defences against these viruses involve RNA interference from repetitive DNA sequences within archaean genomes that are related to the genes of the viruses.[42][43] Most archaea have CRISPR–Cas systems as an adaptive defence against viruses. These enable archaea to retain sections of viral DNA, which are then used to target and eliminate subsequent infections by the virus using a process similar to RNA interference.[44]
Fungal viruses[edit]
Further information: mycovirus
Mycoviruses, also known as mycophages, are viruses that infect fungi. The infection of fungal cells is different from that of animal cells. Fungi have a rigid cell wall made of chitin, so most viruses can get inside these cells only after trauma to the cell wall.[45]
See; Nerva, L.; Ciuffo, M.; Vallino, M.; Margaria, P.; Varese, G.C.; Gnavi, G.; Turina, M. (2016). "Multiple approaches for the detection and characterization of viral and plasmid symbionts from a collection of marine fungi". Virus Research. 219: 22–38. doi:10.1016/j.virusres.2015.10.028. hdl:2318/1527617. PMID 26546154.
Eukaryote viruses[edit]
The second melting pot of virus evolution: origin of eukaryotic viruses. Characteristic images of archaeal, bacterial, and eukaryotic viruses are shown.[5]
Marine protists[edit]
By 2015, about 40 viruses affecting marine protists had been isolated and examined, most of them viruses of microalgae.[46] The genomes of these marine protist viruses are highly diverse.[47][48] Marine algae can be infected by viruses in the family Phycodnaviridae. These are large (100–560 kb) double-stranded DNA viruses with icosahedral shaped capsids. By 2014, 33 species divided into six genera had been identified within the family,[49][50] which belongs to a super-group of large viruses known as nucleocytoplasmic large DNA viruses. Evidence was published in 2014 suggesting some strains of Phycodnaviridae might infect humans rather than just algal species, as was previously believed.[51] Most genera under this family enter the host cell by cell receptor endocytosis and replicate in the nucleus.
A giant coccolithovirus, Emiliania huxleyi virus 86 (arrowed), infecting an Emiliania huxleyi coccolithophore
Phycodnaviridae play important ecological roles by regulating the growth and productivity of their algal hosts. Algal species such Heterosigma akashiwo and the genus Chrysochromulina can form dense blooms which can be damaging to fisheries, resulting in losses in the aquaculture industry.[52] Heterosigma akashiwo virus (HaV) has been suggested for use as a microbial agent to prevent the recurrence of toxic red tides produced by this algal species.[53] The coccolithovirus Emiliania huxleyi virus 86, a giant double-stranded DNA virus, infects the ubiquitous coccolithophore Emiliania huxleyi.[49][50] This virus has one of the largest known genomes among marine viruses.[54] Phycodnaviridae cause death and lysis of freshwater and marine algal species, liberating organic carbon, nitrogen and phosphorus into the water, providing nutrients for the microbial loop.[55]
The virus-to-prokaryote ratio, VPR, is often used as an indicator of the relationship between viruses and hosts. Studies have used VPR to indirectly infer virus impact on marine microbial productivity, mortality, and biogeochemical cycling.[56] However, in making these approximations, scientists assume a VPR of 10:1, the median observed VPR in the surface ocean.[56][18] The actual VPR varies greatly depending on location, so VPR may not be the accurate proxy for viral activity or abundance as it has been treated.[56][57]
Marine invertebrates[edit]
Virus-host interactions in the marine ecosystem,
including viral infection of bacteria, phytoplankton and fish[58]
Marine invertebrates are susceptible to viral diseases.[59][60][61] Sea star wasting disease is a disease of starfish and several other echinoderms that appears sporadically, causing mass mortality of those affected.[62] There are around 40 different species of sea stars that have been affected by this disease. In 2014 it was suggested that the disease is associated with a single-stranded DNA virus now known as the sea star-associated densovirus (SSaDV); however, sea star wasting disease is not fully understood.[63]
Marine vertebrates[edit]
Fish are particularly prone to infections with rhabdoviruses, which are distinct from, but related to rabies virus. At least nine types of rhabdovirus cause economically important diseases in species including salmon, pike, perch, sea bass, carp and cod. The symptoms include anaemia, bleeding, lethargy and a mortality rate that is affected by the temperature of the water. In hatcheries the diseases are often controlled by increasing the temperature to 15–18 °C.[64]: 442–443 Like all vertebrates, fish suffer from herpes viruses. These ancient viruses have co-evolved with their hosts and are highly species-specific.[64]: 324 In fish, they cause cancerous tumours and non-cancerous growths called hyperplasia.[64]: 325
In 1984, infectious salmon anemia (ISAv) was discovered in Norway in an Atlantic salmon hatchery. Eighty percent of the fish in the outbreak died. ISAv, a viral disease, is now a major threat to the viability of Atlantic salmon farming.[65] As the name implies, it causes severe anemia of infected fish. Unlike mammals, the red blood cells of fish have DNA and can become infected with viruses. Management strategies include developing a vaccine and improving genetic resistance to the disease.[66]
Marine mammals are also susceptible to marine viral infections. In 1988 and 2002, thousands of harbour seals were killed in Europe by phocine distemper virus.[67] Many other viruses, including caliciviruses, herpesviruses, adenoviruses and parvoviruses, circulate in marine mammal populations.[68]
Giant marine viruses[edit]
Most viruses range in length from about 20 to 300 nanometers. This can be contrasted with the length of bacteria, which starts at about 400 nanometers. There are also giant viruses, often called giruses, typically about 1000 nanometers (one micron) in length. All giant viruses belong to the phylum Nucleocytoviricota (NCLDV), together with poxviruses. The largest known of these is Tupanvirus. This genus of giant virus was discovered in 2018 in the deep ocean as well as a soda lake, and can reach up to 2.3 microns in total length.[69]
The largest known virus, Tupanvirus, named after Tupã, the Guarani supreme god of creation
The giant mimivirus
Cryo-electron micrograph of the CroV giant virus [70]
scale bar=0.2 µm
The discovery and subsequent characterization of giant viruses has triggered some debate concerning their evolutionary origins. The two main hypotheses for their origin are that either they evolved from small viruses, picking up DNA from host organisms, or that they evolved from very complicated organisms into the current form which is not self-sufficient for reproduction.[71] What sort of complicated organism giant viruses might have diverged from is also a topic of debate. One proposal is that the origin point actually represents a fourth domain of life,[72][73] but this has been largely discounted.[74][75]
Virophages[edit]
Further information: Virophages
Virophages are small, double-stranded DNA viruses that rely on the co-infection of giant viruses. Virophages rely on the viral replication factory of the co-infecting giant virus for their own replication. One of the characteristics of virophages is that they have a parasitic relationship with the co-infecting virus. Their dependence upon the giant virus for replication often results in the deactivation of the giant viruses. The virophage may improve the recovery and survival of the host organism. Unlike other satellite viruses, virophages have a parasitic effect on their co-infecting virus. Virophages have been observed to render a giant virus inactive and thereby improve the condition of the host organism.
All known virophages are grouped into the family Lavidaviridae (from "large virus dependent or associated" + -viridae).[76] The first virophage was discovered in a cooling tower in Paris, France in 2008. It was discovered with its co-infecting giant virus, Acanthamoeba castellanii mamavirus (ACMV). The virophage was named Sputnik and its replication relied entirely on the co-infection of ACMV and its cytoplasmic replication machinery. Sputnik was also discovered to have an inhibitory effect on ACMV and improved the survival of the host. Other characterised virophages include Sputnik 2, Sputnik 3, Zamilon and Mavirus.[77][78]
Most of these virophages were discovered by analyzing metagenomic data sets. In metagenomic analysis, DNA sequences are run through multiple bioinformatic algorithms which pull out certain important patterns and characteristics. In these data sets are giant viruses and virophages. They are separated by looking for sequences around 17 to 20 kbp long which have similarities to already sequenced virophages. These virophages can have linear or circular double-stranded DNA genomes.[79] Virophages in culture have icosahedral capsid particles that measure around 40 to 80 nanometers long.[80] Virophage particles are so small that electron microscopy must be used to view these particles. Metagenomic sequence-based analyses have been used to predict around 57 complete and partial virophage genomes[81] and in December 2019 to identify 328 high-quality (complete or near-complete) genomes from diverse habitats including the human gut, plant rhizosphere, and terrestrial subsurface, from 27 distinct taxonomic clades.[82]
The giant virus CroV attacks C.roenbergensis
Cafeteria roenbergensis a bacterivorous marine flagellate
A Mavirus virophage (lower left) alongside a giant CroV [83]
A giant marine virus CroV infects and causes the death by lysis of the marine zooflagellate Cafeteria roenbergensis.[84] This impacts coastal ecology because Cafeteria roenbergensis feeds on bacteria found in the water. When there are low numbers of Cafeteria roenbergensis due to extensive CroV infections, the bacterial populations rise exponentially.[85] The impact of CroV on natural populations of C. roenbergensis remains unknown; however, the virus has been found to be very host specific, and does not infect other closely related organisms.[86] Cafeteria roenbergensis is also infected by a second virus, the Mavirus virophage, during co-infection with CroV.[77] This virus interferes with the replication of CroV, which leads to the survival of C. roenbergensis cells. Mavirus is able to integrate into the genome of cells of C. roenbergensis and thereby confer immunity to the population.[78]
Role of marine viruses[edit]
Although marine viruses have only recently been studied extensively, they are already known to hold critical roles in many ecosystem functions and cycles. Marine viruses offer a number of important ecosystem services and are essential to the regulation of marine ecosystems.[3] Marine bacteriophages and other viruses appear to influence biogeochemical cycles globally, provide and regulate microbial biodiversity, cycle carbon through marine food webs, and are essential in preventing bacterial population explosions.[87]
Viral shunt[edit]
The cycling of marine phytoplankton is helped by viral lysis[88]
Main article: Viral shunt
The dominant hosts for viruses in the ocean are marine microorganisms, such as bacteria.[14] Bacteriophages are harmless to plants and animals, and are essential to the regulation of marine and freshwater ecosystems[89] are important mortality agents of phytoplankton, the base of the foodchain in aquatic environments.[90] They infect and destroy bacteria in aquatic microbial communities, and are one of the most important mechanisms of recycling carbon and nutrient cycling in marine environments. The organic molecules released from the dead bacterial cells stimulate fresh bacterial and algal growth, in a process known as the viral shunt.[91]
In this way, marine viruses are thought to play an important role in nutrient cycles by increasing the efficiency of the biological pump. Viruses cause lysis of living cells, that is, they break the cell membranes down. This releases compounds such as amino acids and nucleic acids, which tend to be recycled near the surface.
Viral activity also enhances the ability of the biological pump to sequester carbon in the deep ocean.[68] Lysis releases more indigestible carbon-rich material like that found in cell walls, which is likely exported to deeper waters. Thus, the material that is exported to deeper waters by the viral shunt is probably more carbon rich than the material from which it was derived.[92][93] By increasing the amount of respiration in the oceans, viruses are indirectly responsible for reducing the amount of carbon dioxide in the atmosphere by about three gigatonnes of carbon per year.[68] Lysis of bacteria by viruses has been shown to also enhance nitrogen cycling and stimulate phytoplankton growth.[94]
The viral shunt pathway is a mechanism that prevents (prokaryotic and eukaryotic) marine microbial particulate organic matter (POM) from migrating up trophic levels by recycling them into dissolved organic matter (DOM), which can be readily taken up by microorganisms. Viral shunting helps maintain diversity within the microbial ecosystem by preventing a single species of marine microbe from dominating the micro-environment.[95] The DOM recycled by the viral shunt pathway is comparable to the amount generated by the other main sources of marine DOM.[96]
The viral shunt pathway facilitates the flow of dissolved organic matter (DOM) and particulate organic matter (POM) through the marine food web
Connections between the different compartments of the living (bacteria/viruses and phytoplankton/zooplankton) and the nonliving (DOM/POM and inorganic matter) environment [97]
Viruses are the most abundant biological entity in marine environments.[5] On average there are about ten million of them in one milliliter of seawater.[98] Most of these viruses are bacteriophages infecting heterotrophic bacteria and cyanophages infecting cyanobacteria. Viruses easily infect microorganisms in the microbial loop due to their relative abundance compared to microbes.[99] Prokaryotic and eukaryotic mortality contribute to carbon nutrient recycling through cell lysis. There is evidence as well of nitrogen (specifically ammonium) regeneration. This nutrient recycling helps stimulates microbial growth.[100] As much as 25% of the primary production from phytoplankton in the global oceans may be recycled within the microbial loop through viral shunting.[101]
Limiting algal blooms[edit]
Microorganisms make up about 70% of the marine biomass.[102] It is estimated viruses kill 20% of this biomass each day and that there are 15 times as many viruses in the oceans as there are bacteria and archaea. Viruses are the main agents responsible for the rapid destruction of harmful algal blooms,[103] which often kill other marine life.[104] Scientists are exploring the potential of marine cyanophages to be used to prevent or reverse eutrophication. The number of viruses in the oceans decreases further offshore and deeper into the water, where there are fewer host organisms.[105]
Gene transfer[edit]
Marine bacteriophages often contain auxiliary metabolic genes, host-derived genes thought to sustain viral replication by supplementing host metabolism during viral infection.[106] These genes can impact multiple biogeochemical cycles, including carbon, phosphorus, sulfur, and nitrogen.[107][108][109][110]
Viruses are an important natural means of transferring genes between different species, which increases genetic diversity and drives evolution.[10] It is thought viruses played a central role in early evolution, before bacteria, archaea and eukaryotes diversified, at the time of the last universal common ancestor of life on Earth.[111] Viruses are still one of the largest reservoirs of unexplored genetic diversity on Earth.[105]
Marine habitats[edit]
Along the coast[edit]
Marine coastal habitats sit at the interface between the land and the ocean. It is likely that RNA viruses play significant roles in these environments.[112]
At the ocean surface[edit]
Viral–bacterial dynamics in the surface microlayer (SML) of the ocean and beyond. DOM = dissolved organic matter, UV = ultraviolet.[113]
See also: Sea surface microlayer
Marine surface habitats sit at the interface between the atmosphere and the ocean. The biofilm-like habitat at the surface of the ocean harbours surface-dwelling microorganisms, commonly referred to as neuston. Viruses in the microlayer, the so-called virioneuston, have recently become of interest to researchers as enigmatic biological entities in the boundary surface layers with potentially important ecological impacts. Given this vast air–water interface sits at the intersection of major air–water exchange processes spanning more than 70% of the global surface area, it is likely to have profound implications for marine biogeochemical cycles, on the microbial loop and gas exchange, as well as the marine food web structure, the global dispersal of airborne viruses originating from the sea surface microlayer, and human health.[113]
In the water column[edit]
Marine viral activity presents a potential explanation of the paradox of the plankton proposed by George Hutchinson in 1961.[114] The paradox of the plankton is that many plankton species have been identified in small regions in the ocean where limited resources should create competitive exclusion, limiting the number of coexisting species.[114] Marine viruses could play a role in this effect, as viral infection increases as potential contact with hosts increases.[4] Viruses could therefore control the populations of plankton species that grow too abundant, allowing a wide diversity of species to coexist.[4]
In sediments[edit]
Marine bacteriophages play an important role in deep sea ecosystems. There are between 5x1012 and 1x1013 phages per square metre in deep sea sediments and their abundance closely correlates with the number of prokaryotes found in the sediments. They are responsible for the death of 80% of the prokaryotes found in the sediments, and almost all of these deaths are caused by cell lysis (bursting). This allows nitrogen, carbon, and phosphorus from the living cells to be converted into dissolved organic matter and detritus, contributing to the high rate of nutrient turnover in deep sea sediments. Because of the importance of deep sea sediments in biogeochemical cycles, marine bacteriophages influence the carbon, nitrogen and phosphorus cycles. More research needs to be done to more precisely elucidate these influences.[115]
In hydrothermal vents[edit]
Further information: hydrothermal vent microbial community
Viruses are part of the hydrothermal vent microbial community and their influence on the microbial ecology in these ecosystems is a burgeoning field of research.[116] Viruses are the most abundant life in the ocean, harboring the greatest reservoir of genetic diversity.[103] As their infections are often fatal, they constitute a significant source of mortality and thus have widespread influence on biological oceanographic processes, evolution and biogeochemical cycling within the ocean.[105] Evidence has been found however to indicate that viruses found in vent habitats have adopted a more mutualistic than parasitic evolutionary strategy in order to survive the extreme and volatile environment they exist in.[117] Deep-sea hydrothermal vents were found to have high numbers of viruses indicating high viral production.[118] Like in other marine environments, deep-sea hydrothermal viruses affect abundance and diversity of prokaryotes and therefore impact microbial biogeochemical cycling by lysing their hosts to replicate.[119] However, in contrast to their role as a source of mortality and population control, viruses have also been postulated to enhance survival of prokaryotes in extreme environments, acting as reservoirs of genetic information. The interactions of the virosphere with microorganisms under environmental stresses is therefore thought to aide microorganism survival through dispersal of host genes through horizontal gene transfer.[120]
Polar regions[edit]
Further information: Marine food web § Polar microorganisms
In addition to varied topographies and in spite of an extremely cold climate, the polar aquatic regions are teeming with microbial life. Even in sub-glacial regions, cellular life has adapted to these extreme environments where perhaps there are traces of early microbes on Earth. As grazing by macrofauna is limited in most of these polar regions, viruses are being recognised for their role as important agents of mortality, thereby influencing the biogeochemical cycling of nutrients that, in turn, impact community dynamics at seasonal and spatial scales.[121] The polar regions are characterised by truncated food webs, and the role of viruses in ecosystem function is likely to be even greater than elsewhere in the marine food web, yet their diversity is still relatively under-explored, and the way in which they affect polar communities is not well understood,[122] particularly in nutrient cycling.[123][124][125][121]
Distribution[edit]
Viruses are highly host specific.[126] A marine virus is more likely to infect cooccurring organisms, those that live in the same region the virus lives in.[127] Therefore, biogeography is an important factor in a virion's ability to infect.
Knowledge of this variation in viral populations across spatiotemporal and other environmental gradients is supported by viral morphology, as determined by transmission electron microscopy (TEM). Non-tailed viruses appear to be dominant in multiple depths and oceanic regions, followed by the Caudovirales myoviruses, podoviruses, and siphoviruses.[31] However, viruses belonging to families Corticoviridae,[128] Inoviridae[129] and Microviridae[130] are also known to infect diverse marine bacteria. Metagenomic evidence suggests that microviruses (icosahedral ssDNA phages) are particularly prevalent in marine habitats.[130]
Metagenomic approaches to assess viral diversity are often limited by a lack of reference sequences, leaving many sequences unannotated.[131] However, viral contigs are generated through direct sequencing of a viral fraction, typically generated after 0.02-um filtration of a marine water sample, or through bioinformatics approaches to identify viral contigs or viral genomes from a microbial metagenome. Novel tools to identify putative viral contigs, such as VirSorter[132] and VirFinder,[133] allow for the assessment of patterns of viral abundance, host range, and functional content of marine bacteriophage.[134][135]
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text:
Turkey Pulse
Turkey steps up efforts to shun dollar
READ IN: Türkçe
Mehmet Cetingulec August 8, 2018
As the Turkish lira plunges to a record low, some voices in Ankara are warning that the United States is furious over Turkey's efforts to reduce its dependency on the dollar.
OZAN KOSE/AFP/Getty Images
A display of foreign exchange rates against the Turkish lira seen on Istiklal Avenue, Istanbul, Turkey, Aug. 2, 2018.
The United States slapped unprecedented sanctions on two Turkish ministers Aug. 1 over Ankara's refusal to release a detained American pastor, but some in Turkish government quarters have a different view of what lies behind the crisis. The United States, the argument goes, is furious over Turkey's efforts to replace the dollar with national currencies in its trade with Iran and the BRICS countries — Brazil, Russia, India, China and South Africa.
As the row over pastor Andrew Brunson escalated July 26 with President Donald Trump's threat of sanctions, Burhan Kuzu, an administrative board member of the Justice and Development Party (AKP) and former adviser to President Recep Tayyip Erdogan, tweeted, "The issue is not Brunson, don't you get it yet? Trump has become a hostage to the Jewish lobby. This reaction stems from Turkey's warm relations with Russia, Iran and China. The United States has gone mad over developments related to trade in national currencies and casting off the dollar."
Erdogan seemed to send a similar message in his meeting with Russian President Vladimir Putin on the sidelines of the BRICS summit in South Africa the same day. "The solidarity between us is making some jealous," he said, and Putin reportedly reacted with a smile.
The more than 1,600 likes for Kuzu's tweet suggest that his narrative resonated well with AKP supporters. Yet many others rejected his argument and responded with critical comments and sarcasm. One user wrote, "I think we should immediately set up a makeshift court outside Brunson's home [where he is under house arrest] and send him back to the United States tonight. Or things will go bad." Another user posed a stinging question referring to a recent credit deal: "Why didn't we cast off the dollar when getting the $3.6 billion loan from China?"
Turkey's efforts to use national currencies in foreign trade have already made progress vis-a-vis Iran and Russia. Ankara seeks to reduce its dependency on the dollar and strengthen the Turkish lira, whose dramatic depreciation this year has only worsened amid the tensions with Washington. According to Erdogan, "One of the best means to curb the pressure of foreign exchange rates is to trade in national currencies on the international platform."
Turkey's drive also has to do with its widening current account deficit, which stood at a staggering $57.6 billion in May. But can it resolve a chronic problem solely by using national currencies in trade with certain partners?
Turkey's exports lag well behind its imports, which is a major factor fueling the problem. In 2017, exports rose 10.2% to $157 billion, while imports grew 18% to reach $234 billion. Accordingly, the country's foreign trade deficit expanded 37% to $76.7 billion. Shunning the dollar offers no magic solution as long as this imbalance persists.
According to figures compiled by the financial daily Dunya, 54% of Turkey's exports and 36% of its imports last year were paid in euros, while the dollar was used in 39% of exports and 58% of imports. Only 3% of exports and 2% of imports were paid in Turkish liras.
Turkey's trade volume with the BRICS countries was worth $60.7 billion last year, including $53.4 billion in imports and only $7.3 billion in exports. In Turkey's $391 billion overall foreign trade, the BRICS countries account for 15.5%, while European countries and the United States represent the bulk of the remaining trade volume. The dollar and the euro are the dominant currencies in commercial exchanges with the BRICS countries.
These figures alone illustrate the uphill task that Turkey faces in creating the desired alternatives in trade.
The drive to curb the use of the dollar also reflects the drift away from the West that Turkey has experienced under the AKP. Though a member of NATO and still a candidate for European Union membership, Ankara is seeking to build new alliances in "a new world" beyond Europe and the United States. Its desire to join the BRICS group is yet another manifestation of its mistrust of the West.
Turkey is seeking to boost cooperation with China, keen to benefit from its economic potential. Apart from talks on using national currencies in bilateral trade, the two sides have discussed the prospect of China building two nuclear power plants and taking part in major infrastructure projects in Turkey, including the artificial waterway Canal Istanbul, Erdogan told reporters after the BRICS summit.
In another notable move, he said Aug. 3 that Turkey would issue yuan-denominated bonds for the first time to counter the "biased reports" of Western credit rating agencies and diversify funding sources.
Another option that Ankara is promoting against hard-currency pressures is the use of gold. The Central Bank itself has been actively replacing foreign exchange reserves with gold. According to the World Gold Council, Turkey's gold reserves reached 546.8 tons in February, up from 116 tons in September 2011. The huge increase put Turkey in 10th place among the countries with the largest gold reserves. The expansion of Islamic banking has been another way of promoting the use of gold in financial activities.
The chill between Ankara and Washington is unlikely to end soon even if the row over Brunson is resolved. US officials said last week that they were reviewing Turkey's duty-free access to the American market after Ankara levied tariffs on US goods in retaliation for Trump's steel tariffs. Yet neither the pastor's detention nor Turkey's efforts to shun the dollar are the essential reason for the bilateral crisis, which appears bound to continue. Turkish-US ties are fraught with many serious problems, including Turkey's plans to acquire Russian S-400 missiles, the involvement of its state-owned Halkbank in Iranian schemes to evade US sanctions, differences in Syria and its growing political, economic and military ties with Russia, Iran and China. Still, the Brunson case is of symbolic significance, illustrating how far the bonds between the two countries — NATO allies for 66 years — have eroded.
Found in: Economy and trade
Mehmet Cetingulec is a Turkish journalist with 34 years professional experience, including 23 years with the Sabah media group during which he held posts as a correspondent covering the prime minister's and presidential offices, economy news chief and parliamentary bureau chief. For nine years, he headed the Ankara bureau of the daily Takvim, where he also wrote a regular column. He has published two books.
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text:
Comparison of attitude of smokeless tobacco users taking dental treatment versus not seeking dental treatment toward cessation of smokeless tobacco use
P Linda1, Sandhya Gupta2, Sonali Jhanjee3, Vijay Prakash Mathur4
1 Nursing Officer, AIIMS, New Delhi, India
2 Faculty, Department of Mental Health Nursing, AIIMS, New Delhi, India
3 Professor, Department of Psychiatry and NDDTC, AIIMS, New Delhi, India
4 Professor, Centre for Dental Education and Research, AIIMS, New Delhi, India
Dr. Sandhya Gupta
Department of Mental Health Nursing, AIIMS, New Delhi
Background: Tobacco exposure is the single greatest preventable cause of morbidity, disability, and mortality for chronic and debilitating diseases. In public health education, an important aspect is the treatment of tobacco use dependence. This experimental study is intended to deter the use of smokeless tobacco (ST) for the users who seek treatment and who do not seek treatment as well. Materials and Methods: The study was conducted using a pretest–posttest design on ST users (dental group = 40 and nondental group = 40) in a tertiary care setting. Educational video: A video film of 14 min was developed by a researcher that included contents related to the chemical properties of tobacco, its harmful health effects, the diseases caused by tobacco use, and the facilities available for treatment. Tools: The tools used were subject datasheet and attitude questionnaire. Results: The mean age of the participants in dental group was 39 years and in nondental group was 34 years. Most of the participants in dental group and nondental group were using gutka. Attitude scores of participants significantly increase from pretest (55.32 ± 7.0) to posttest (62.74 ± 4.2). There was a statistically significant difference between attitude scores of participants in dental group (60.3 ± 13.23) and nondental group (62.6 ± 4.19) at 1-month follow-up (P ≤ 0.05). Conclusion: The educational video film regarding the ill effects of tobacco use and its treatment was effective in enhancing positive attitude of both the equally useful.
Keywords: Tobacco, attitude regarding smokeless tobacco use, smokeless tobacco user
Linda P, Gupta S, Jhanjee S, Mathur VP. Comparison of attitude of smokeless tobacco users taking dental treatment versus not seeking dental treatment toward cessation of smokeless tobacco use. Indian J Psy Nsg 2019;16:31-4
Linda P, Gupta S, Jhanjee S, Mathur VP. Comparison of attitude of smokeless tobacco users taking dental treatment versus not seeking dental treatment toward cessation of smokeless tobacco use. Indian J Psy Nsg [serial online] 2019 [cited 2021 Jan 19];16:31-4. Available from: https://www.ijpn.in/text.asp?2019/16/1/31/269156
Tobacco is a highly addictive substance. Tobacco use is among the most preventable causes of disease and premature death worldwide.[1] The Global Adult Tobacco Survey India 2009–2010 revealed that more than one-third (35%) of adults in India use tobacco in some form, 21% use smokeless tobacco (ST), 9% smoke, and 5% are mixed users.[2] The World Health Organization predicts that tobacco deaths in India may exceed 1.5 million annually by 2020.[3] ST use is a significant part of the overall world tobacco problem. The prevalence of use is relatively high in many countries, especially in South Asia, there is strong evidence that ST use leads to oral mucosal lesions, including oral precancerous lesions and gingival recession.[4] Substantial evidence indicates that tobacco cessation not only reduces the prevalence of a range of diseases but also limits their progression and improves treatment outcomes.[5] Patients who visit dental clinic routinely have little interaction with health-care professionals about tobacco use and related hazardous effects and so do the persons who accompany the patient to the dental clinic. To minimize the gap, improvement of education and counseling in tobacco cessation should be considered. As a first step, data have been collected from patients who seek dental treatment and who do not seek dental treatment about attitude of tobacco use and cessation.
The objective of the study
The main objective is to compare the attitude of ST users taking dental treatment versus not seeking dental treatment.
H1- ST users who are seeking dental treatment, who receive educational video will show enhanced attitude scores toward cessation as measured by the attitude scale significant at P < 0.05 as against those who are not seeking dental treatment.
This includes a quantitative, experimental approach, preexperimental design, one group pretest–posttest, time-series design [Table 1].
Table 1: Diagrammatic representation of research design
Treatment includes educational video regarding the ill effects of tobacco use and its treatment.
Outcome was tested on the attitude of ST users toward quitting.
Persons currently using ST were chosen from a tertiary care hospital of New Delhi. Participants using smoking tobacco along with ST were excluded from the study. A total of 80 patients were enrolled for the study, 40 in each group. Seventeen participants did not come for the follow-up on posttest 1. A total of 62 participants, 32 in Subgroup 1 (seeking dental treatment) and 30 in Subgroup 2 (not seeking dental treatment) completed the study, by convenient sampling method.
Subject datasheet
Demographic data form: It has 13 items eliciting the demographic details. Demographic data include age, sex, marital status, educational status, occupation, monthly family income, and area of residence. Tobacco-related characteristics include type of tobacco, use per day, age of initiation, age started chewing regularly, and interest in quitting.
Tool 1: Fagerstrom test for nicotine dependence-smokeless tobacco
A standardized tool developed by Ebbert Jo, Patten CA, and Schoeder DR to assess the severity of nicotine dependence. It consists of six items. Total score ranges from 0 to 10, in which 0–2 = very low dependence, 3–4 = low dependence, 5 = medium dependence, 6–7 = high dependence, and 8–10 = very high dependence. Internal consistency reliability coefficient was 0.47.
Tool 2: Attitude questionnaire
Attitude questionnaire was developed for assessing the attitude of ST users regarding tobacco use. Content validity of attitude questionnaire was obtained by three experts in the field. Reliability was established by test–retest method. Attitude questionnaire was found to be reliable (Cronbach's alpha: 0.82). It was a five-point Likert scale consisting of 15 items. The positive worded items were scored from 5 to 1 and negative worded items were worded from 1 to 5. Minimum score was 15 and maximum score was 75.
Intervention (educational video film) regarding ill effects of tobacco use and its treatment
It was a 14 min long educational video regarding the ill effects of tobacco use and its treatment was validated by four experts in the field. The educational video includes, description of tobacco and tobacco products, effects and complications of tobacco use, complications of tobacco use on oral cavity, strategies available for cessation of tobacco use, and resources available for cessation of tobacco use.
Ethical clearance was obtained from the ethics committee of the institute, informed written consent was obtained from the study participants and their confidentiality and anonymity was maintained.
Description of the subjects
The mean age of the participants in dental group was 39 years (standard deviation [SD] ±11.2) and in nondental group was 34 years (SD ± 6.23). Most of the participants were male, 95.5% in dental group and 95% in nondental group. Most of the participants were married, 72.5% in dental group and 95% in nondental group. Educational status of 35% of participants in dental group was of primary level and 52.5% of nondental group was of secondary level. More than half of the participants were employed, 60% in the dental group and 62.5% in the nondental group. Most of the participants had monthly income of Rs. 5001–10,000, 45% in dental group and 50% in nondental group. Most of the participants were from urban area, 57.5% in dental group and 62.5% in nondental group.
Seventy-three percent of participants in dental group and 42.55% in nondental group were using gutka. The mean number of ST pouch used per day was five (SD ± 1.08) in participants of dental group and three (SD ± 1.9) in nondental group. The mean number of ST pouches chewed per day was two (SD ± 1.6) in participants of dental group and three (SD ± 2.0) in nondental group. The mean age of initiation of tobacco was at 23 years (SD ± 6.13) in participants of dental group and at 22 years (SD ± 5.77) in nondental group. The age of the participants for initiating chewing regularly was 24 years (SD ± 7.08) in participants of dental group and at 22 years (SD ± 5.61) in nondental group. Most of the participants (>50%) were "very interested in quitting of tobacco use" in dental group as compared to nondental group before the intervention.
As shown in [Table 2], attitude mean scores increased from pretest (55.32 ± 7.0) to posttest (62.74 ± 4.2) and was statistically significant at P < 0.05.
Table 2: Comparison of pre- and post-test attitude scores of smokeless tobacco users
There was a significant increase in the positive attitude of ST users after 1-month follow-up of the intervention.
As shown in [Table 3], mean attitude scores for dental group and nondental group in pretest, were 54.3 ± 5.8 and 54.3 ± 10.9, respectively. Both groups were comparable in the pretest. Whereas mean attitude scores of participants increased from pretest (55.32 ± 7.0) to posttest (62.74 ± 4.2) which was statistically significant, P < 0.05 (mean difference = 6.42) in attitude scores in nondental group as compared to dental group after one month of educational package intervention.
Table 3: Comparison of pre- and post-test attitude scores between Subgroup 1 and Subgroup 2
This study is the first one to document the attitude regarding tobacco use cessation simultaneously among ST users who seek dental treatment and who were not seeking dental treatment.
In the present study, mean attitude scores of participants increased from pretest (55.32 ± 7.0) to posttest (62.74 ± 4.2) which was statistically significant, P < 0.05 (mean difference = 6.42). Hence, there was significantly increased attitude scores of ST users for leaving ST use after 1-month follow-up of the intervention.
In the present study, the baseline attitude mean score was 55.32 ± 7.0 which is in contradictory to the findings of Horn et al.[6] (West Virginia), where it was reported that the baseline attitude score was 25.86 ± 5.38.
The authors found that, there was a statistically significant difference between the attitude scores of subjects in the dental group (60.3 ± 13.23) and nondental group (62.6 ± 4.19) at 1 month follow up, P < 0.05. Therefore, Research hypothesis: H1 Smokeless Tobacco users who are seeking dental treatment, who receive educational video will show enhanced attitude scores toward cessation as measured by attitude scale significant at P < 0.05 as against those who are not seeking dental treatment is rejected.
Hence, it implies that participants in nondental group have more positive attitude as compared to the dental group after 1 month follow up of the intervention [Table 3]. This surprising finding could be attributed to higher educational qualifications of nondental group as compared to the dental group.
The educational video film regarding the ill effects of tobacco use, and its treatment was effective in enhancing the positive attitude toward cessation of ST use. Hence, video film regarding the ill effects of tobacco use and its treatment is found equally useful for both potential and current ST users, those having dental/oral cavity complications as well as those who are not yet seeking for dental/oral cavity treatment.
General public: The educational video regarding the ill effects of tobacco use and its treatment should be shown in schools/colleges to motivate the students to deter them from tobacco use, should be included in schools curriculum and be made available in public libraries to motivate the public to quit tobacco use
Nursing practice: Nursing educators should conduct training programs for in service nurses and preservice nurses for learning the ill effects of tobacco use and its treatment, early identification of tobacco users, brief intervention, and motivational counseling to leave tobacco use. Useful video film, should be made available in OPD, wards, various specialty clinic so that not only the patients but the general public also can be delivered educational information and motivational messages in ways that are engaging and deterring the use of tobacco.
Strength and limitations
Time series design was used and postintervention discussion was benefitted by ST users. The attrition rate was 20%.
Similar study can be done on a larger sample size, community-based study can be done and can be replicated to different regional languages.
USDHHS. Healthy People 2010, ed. US Department of Health & Human Services, National Centre for Chronic Diseases Prevention & Health Promotion. Office of Smoking and Health. Atlanta, GA. https://www.cdc.gov/nchs/data/hpdata2010/hp2010_final_review.pdf.
Dhumal GG, Pednekar MS, Gupta PC, Sansone GC, Quah AC, Bansal-Travers M, et al. Quit history, intentions to quit, and reasons for considering quitting among tobacco users in India: Findings from the tobacco control policy evaluation India wave 1 survey. Indian J Cancer 2014;51 Suppl 1:S39-45.
Murray CJ, Lopez AD. The Global Burden of Disease: A Comprehensive Assessment of Mortality and Disability from Diseases, Injuries and Risk Factors in 1990 and Projected to 2020. Cambridge, Massachusetts: Harvard School of Public Health; 1996.
Recommendation on Smokeless Tobacco Products - Scientific Advisory Committee on Tobacco Products Regulation. https://www.who.int/tobacco/sactob/recommendations/en/smokeless_en.pdf
Preshaw PM, Heasman L, Stacey F, Steen N, McCracken GI, Heasman PA, et al. The effect of quitting smoking on chronic periodontitis. J Clin Periodontol 2005;32:869-79.
Horn KA, Gao X, Dino GA, Kamal-Bahl S. Determinants of youth tobacco use in West Virginia: A comparison of smoking and smokeless tobacco use. Am J Drug Alcohol Abuse 2000;26:125-38.
Linda P
Jhanjee S
Mathur VP
attitude regarding smokeless tobacco use
smokeless tobacco user


Protecting the privacy of personal information is an important principle at the Vision Travel Solutions. We are committed to collecting, using and disclosing personal information responsibly and only to the extent necessary for the travel products and services we provide. We strive for openness and transparency when handling personal information. This document describes our privacy policies.
Personal information is information about an identifiable individual. Personal information includes information that relates to an individual's personal characteristics (e.g., gender, age, income, home address or phone number, ethnic background, family status), health (e.g., health history, health conditions, health services received by them) or activities and views (e.g., religion, politics, opinions expressed by an individual, an opinion or evaluation of an individual). Personal information is to be contrasted with business information (e.g., an individual's business address and telephone number), which is not protected by privacy legislation. In addition, due the nature of the travel agency business, we also include in our policies and staunchly protect therein an individual's financial information, including chequing account information and credit card information.
Our travel agency, Vision Travel Solutions, is a full-service travel agency business, and we arrange travel products and services for our clients with a wide spectrum of industry suppliers. Accordingly, we deal with a number of consultants and third parties that may, in the course of their duties, have limited access to personal information we hold. These include airlines, railroads, cruise lines, tour operators, computer reservations system providers, and other travel-related vendors. We restrict their access to any personal information that we hold as much as is reasonably possible. We also have their assurance that they follow appropriate privacy principles in accordance with their own policies under the Personal Information Protection and Electronic Documents Act (PIPEDA).
Like all travel agencies, we collect, use and disclose personal information in order to serve our clients. For our clients, the primary purposes for collecting personal information are as follows: to make and secure reservations, to issue transportation documents and vouchers, and to provide travel suppliers with information to complete the necessary purchasing arrangements for a wide array of travel and tourism products. Examples of the type of personal information we collect for those purposes include the following: name, address, telephone, age, credit card information, passport or visa information, Social Insurance Number, website cookies, and similar personal information necessary to properly identify our clients and their entitlement to the services we arrange. We also collect personal information from our employees and contractors to assure our proper compliance with employment laws, remuneration, tax payments, and other employee/contractor functions.
Electronic hardware is either under supervision or secured in a locked or restricted area at all times. In addition, passwords are used on all computers.
External consultants and agencies with access to personal information must enter into privacy agreements with us or acknowledge that the abide by PIPEDA.
We need to retain personal information for a period to ensure that we can answer any questions you might have about the services provided and for our own accountability to external regulatory bodies. However, in order to protect your privacy, we do not like to keep personal information indefinitely. We hold client files for about 3 years. Our client and contact directories are much more difficult to systematically destroy, so we remove such information when we can if it does not appear that we will be contacting you again. However, if you ask, we will remove such contact information right away. We keep any personal information relating to our general correspondence with people who are not our clients, newsletters, seminars and marketing activities for about 6 months after the newsletter, seminar or marketing activity is over. We destroy paper files containing personal information by shredding. We destroy electronic information by deleting it and, when the hardware is discarded, we ensure that the hard drive is physically destroyed. Alternatively, we may send some or all of the client files to our clients.
With only a few exceptions, you have the right to see what personal information we hold about you. Often, all you have to do is ask. We can help you identify what records we might have about you. We will also try to help you with any information you do not understand (e.g., various industry forms, technical language, etc.). We will need to confirm your identity, if we do not know you, before providing you with this access. We reserve the right to charge a nominal fee for such requests. If there is a problem, we may ask you to put your request in writing. If we cannot give you access, we will tell you within 30 days if at all possible and tell you the reason, as best we can, as to why we cannot give you access.
If you believe there is a mistake in the information, you have the right to ask for a correction. This applies to factual information and not to any professional opinions we may have formed. We may ask you to provide documentation that our files are wrong. Where we agree that we made a mistake, we will make the correction and notify anyone to whom we sent this information. If we do not agree that we have made a mistake, we will still agree to include in our file a brief statement from you on the point and we will forward that statement to anyone else who received the earlier information.