Viruses help maintain marine biodiversity by keeping populations in check: in particular, bacteria and algae, which make up the vast majority of living matter in the ocean. According to suttle (2007) Viruses are probably responsible for killing about 25-30 % of the living material in the oceans every day. Furthermore, during the infection process, a virus can alter the host cell’s metabolism for example, increasing the rate of photosynthesis, thereby changing the rate of carbon fixation. And when a virus causes host lysis, both new viral particles and the carbon and other organic nutrients that were trapped inside the cell are released. These materials then become available for utilization by nearby microbes, a potentially beneficial process known as viral priming. “Viral priming,” has been documented in experimental model systems using microbes that predominantly occur near the ocean surface. in one example from a study by Weitz (2013) , viral lysis of a bacterium infected in the lab released organic-iron complexes that were quickly taken up by other marine bacteria, as well as by diatoms (unicellular eukaryotic algae). This assimilation increased growth rates of the nontargeted organisms. in a second example, the removal from an experimental system of viruses that infect and lyse heterotrophs slowed synechococcus cell growth and proliferation, presumably due to a decrease in virus-mediated nutrient release (Weinbauer et al,2011). Therefore, what is bad for one microbial cell may be good for others. in the deep ocean, however, it is still unknown what happens to virus-released organic matter. Free carbon in the deep ocean is “ancient” (4,000–6,000 years old) and largely recalcitrant to assimilation by microbes, suggesting there may be another supply of this material. Viral lysing of deep-ocean microbes may be a potential source.
Viruses also perform a key service called the “viral shunt.” When they infect and kill organisms, nutrients such as carbon and phosphorous are released into the ocean. This keeps microbes and phytoplankton thriving. “if you take the viruses out of seawater, photosynthesis stops,” according to shuttle (2007). And photosynthesis by marine algae and phytoplankton is responsible for over half the oxygen on the planet
This process of viral infection, lysis, and nutrient release occurs over and over again. Bacteria are, in essence, cannibalising each other with the help of their associated viruses. The elements that support the food web are quickly put back into circulation with the help of viruses, as shown in the figure below(Jiao et al,2010) .
This interaction ensures inorganic nutrients are readily available to algae and plants on which ecosystems depend. it’s the combination of high bacterial growth and viral infection that keeps ecosystems functioning. This explains why we don’t see bacteria in food webs. Viruses short circuit bacterial production passing higher up the food chain so it doesn’t become fish food in freshwater ecosystems(Jiao et al,2010).
The death of a host cell and the release of viral progeny are but one part of the ways of how viruses affect the ocean ecosystem. so although viruses may be minute, the scale of the services they perform is global.
Just as viruses can be pathogenic to plants they can also be beneficial e.g. provide a trait to crop plants that increases their value or growth potential, or decreases the need for the use of chemical fertilizers or pesticide. scientists have found that certain viruses can render some plants drought tolerant, and at least one example of virally-conferred cold tolerance has been discovered– discoveries like this can become useful for expanding the ranges of crops (Roossinck,2015).
Plants are often infected with “persistent viruses” that are passed down from generation to generation, perhaps over thousands of years, with viruses that are transmitted to nearly 100 percent of their plant progeny, but that have never been shown to be transmitted from one plant to another. An example as mentioned by Johnson (2012) , is the White Clover Cryptic virus, “which suppresses formation of nitrogen-fixing nodules when adequate nitrogen is present in the soil, saving the plant from producing a costly organ when it is not needed”
During an experiment conducted by Rohwer et al (2014) at san Diego state University in California they noted that few plants grow in the hot soils surrounding the geysers in Yellowstone National Park. One such plant, which is a type of tropical panic grass, is a symbiosis that includes a fungus that colonizes the plant, and a virus that infects that fungus. All three members of this symbiosis are necessary for survival in soils simmering at more than 50ºC. in the laboratory, Rohwer created symbioses between the same virus-infected fungus and other plants. This has enabled every plant her group has tested to survive at these elevated soil temperatures, including tomato, noting that she has pushed the soil temperature to 60 ºC without killing the plant.
Many plant viruses can also confer drought tolerance or cold tolerance to plants. The mechanism behind this is still unknown but, for example, elevated sugar is very common in virus-infected plants. More sugar would allow the plant cells to retain more water, protecting them from drought. Things that are really sweet freeze slowly, so extra sugar would make plants cold-resistant. Other examples of beneficial plant viruses include several acute viruses (Brome mosaic virus, family Bromoviridae, Cucumber mosaic virus, family Bromoviridae, Tobacco rattle virus, family Virgaviridae, and Tobacco mosaic virus, family Virgaviridae), which confer tolerance to drought and freezing temperatures in several different crops
Viruses hold the potential for safe, inexpensive and non-destructive improvements to cropping practices.
Humans can become infected with numerous herpesviruses throughout their childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease (Rickson and Kief, 2007). studies show that latent herpesvirus also confers a surprising benefit to the host. in contrast to the gastrointestinal disease it causes in humans, the Murine (mouse infecting) norovirus plays a role in the development of the mouse immune system and intestine(Virgin et al,1997), mice carrying this latent virus shows to be resistant to infection with the bacterial pathogens Listeria monocytogenes and Yersinia pestis (plague) . According to Roossinck (2016) this virus can also replace the beneficial effects of certain gut bacteria when they have been destroyed by antibiotics. Healthy gut bacteria help prevent gastrointestinal infection however antibiotics taken excessively can destroy these helpful bacteria and make one susceptible to gastrointestinal illness. However the norovirus infection of mice has shown to restore the normal function of the immune system’s lymphocytes and the normal morphology of the immune system. Latent herpesviruses also arm natural killer cells- an important component of the immune system – which kill cells that are infected with pathogenic viruses and mammalian tumour cells. Recent research by Liu et al (2010) shows that bacteriophage stick to the mucus membranes of many animals. These membranes are the point of entry for many bacterial pathogens which suggest that they provide the first line of defence against invading bacteria by host by infection and lysis. .
Thus, whereas the immune evasion capabilities and lifelong persistence of certain viruses are commonly viewed as solely pathogenic, data from Rickson (1997), Liu et al (2010) and Roossinck (2016) suggest that latency is a symbiotic relationship with immune benefits for the host.
A virus known as GB-C can help people who suffer from HiV by slowing down the progression if viral spread in the body. Much has been published over the past 10 years regarding the influence of GB virus C (GBV-C) on HiV infection (Heringlake, 1998). GB virus C (GBV-C) is a member of the Flaviviridae family and the most closely related human virus to HCV. However, GBV-C does not replicate in hepatocytes, but rather in lymphocytes. GBV-C has a worldwide distribution and is transmitted sexually, parenterally and through mother-to-child transmission. Thus, co-infection with HCV and HiV is common (schwarze-Zander et al,2012). Until now, no human disease has been associated with GBV-C infection. However, there are several reports of a beneficial effect of GBV-C on HiV disease progression in vivo. several studies have reported that coinfection with HiV and GBV-C leads to a more favourable outcome in patients, with a delay in the development of AiDs, compared with the outcome in patients infected with HiV alone (Yeo,1998) . This has led some scientists to look for the supposed mechanism of this beneficial effect, and alterations in the cellular immune response have been studied (schwarze-Zander et al,2012).
Different mechanisms to explain these observations have been proposed, including modification of antiviral cytokine production, HiV co-receptor expression, direct inhibition of HiV-1 entry, T-cell activation and Fas-mediated apoptosis. Further understanding of these mechanisms may open new strategies for the treatment of HiV/AiDs. (Berzsenyi, 2006).
some viruses even become an integral part of their host, with their genes incorporated into the host’s DNA. The term “symbiogenesis” usually refers to organelles such as the mitochondria and the chloroplast which were of bacterial origin and then incorporated in the evolution of eukaryotic life. Now, the more genomes that are being sequenced the more viruses are being found – not just retroviruses, which are known to intergrate into host genomes- but all kinds of RNA viruses and small DNA viruses.
There are a lot of things that a virus could do in a host genome for example, they are able to turn genes on or off. An example of symbiogenesis is the breakdown of starches by saliva. An enzyme called amylase, in our saliva, breaks the starch down into sugars. A more obvious place for amylase is in the gut, to break down food. The reason it’s made in the salivary glands too is because viral genetic material integrated in front of the amylase gene, turns it on in salivary glands (Roossinck, 2011)
Another example of symbiogenesis is in the evolution of the mammalian placenta. A protein called syncytin fuses cells together to make a placenta, and it evolved from a virus protein. so the gene for this protein, normally part of the membrane that surrounds a virus, integrated into the mammalian genome during the evolution of the placenta (Feschotte,2012).
in addition to providing benefits to the macro-hosts of many microbes, viruses also directly benefit their microbial hosts. The killer viruses of yeasts and bacteria allow their hosts to invade new territories by killing off competitors while providing immunity to the virus-containing hosts (Roossinck,2011). Phage also encode essential functions for bacteria, such as the production of toxins that allow them to invade their macro-hosts, the horizontal gene transfer of essential elements, and in some cases, the ability to form biofilms (Mai-Prochnow et al,2015). Viruses of other eukaryotic microbes have positive effects on the growth, fecundity, or persistence of their host (Márquez and Roossinck,2012)
Viruses are being redefined as more than just pathogens. They are also critical symbiotic partners in the health of their hosts. in some cases, viruses have fused with their hosts in symbiogenetic relationships. Mutualistic interactions are found in plant, insect, and mammalian viruses, as well as with eukaryotic and prokaryotic microbes, and some interactions involve multiple players of the halobiont. With increased virus discovery, more mutualistic interactions are being described and more will undoubtedly be discovered
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