Jump to content
Server time: 2018-02-22, 00:48

RogueSolace

Hall of Famer Dedicated Player

""All the gods, all the heavens, all the hells, are within you.""

  • Content count

    852
  • Joined

  • Last visited

  • Days Won

    1

RogueSolace last won the day on February 13

RogueSolace had the most liked content!

TIME PLAYED

730 h 5.56 Collector

Community Reputation

642 Somewhat Relevant

Account information

  • Whitelisted YES
  • Last played 1 day ago

About RogueSolace

Personal Information

  • Sex
    Female

Recent Profile Visitors

16547 profile views
  1. "Dolores! Listen to me okay, this channel is not safe, okay? A bad person can be listening. They stole the number. You remember the channel that was just you and me, no one else? The one you could contact me, and only me? Please use that channel. Don't say anything more here, it's not safe. I miss you so much. Ella is with me and I am taking care of her as I always have. Call me on my private number and we'll talk OK? "
  2. I'm glad it worked too! I'm also super glad for the rp, was awesome and kicked ass and made me cry in a good way <3
  3. RogueSolace

    1DBA57FA0C17B723939EF2C7B2C4814C4AF3407B

    342A57384DDFE67FA549AEC1176E822D5BECCB5D 

    8426408EC5B0E19D2E1CA3558F489781E367DEF5

     

    1. dimitri

      dimitri

      So they do attack wild life, been wondering that since they got added

    2. Brayces

      Brayces

      Oh cool! Never seen them attack anything besides Infected before! 

      You should start a nature series, "Adventures of Beth in the WILDS."

    3. RogueSolace

      RogueSolace

      Youll have to get @Malet to do it, he found them! 😊

    4. Brayces

      Brayces

      Ah, well. You can be the person who talks to the camera! 

    5. Vandal
  4. RogueSolace

    74287404F86E0BC861A121522F683799DF829DA8 

    • Lyca
    •   
    • RogueSolace

    giphy.gif

    1. Lyca

      Lyca

      <3

    2. Elmo

      Elmo

      giphy.gif.261f834c0bb420b6f1a68f0402df4ce1.gif

    3. FieJaxon

      FieJaxon

      This is an intervention.

    4. RogueSolace

      RogueSolace

      😆

      hey, I do not have a flying umbrella! 

      Also my just waking ups brain response lol

      IMG_3955.GIF.9d93286efef498e168bbb62cd41858fc.GIF

       

    5. Lyca

      Lyca

      Tbh It wouldn't surprise me when you would have one in your backpack. 

      ^_^

    6. RogueSolace

      RogueSolace

      That would be interesting LOL, but totally don't have one of those

    • Ender
    •   
    • RogueSolace

    515?cb=20160212083150

    1. Ender

      Ender

      <3

    2. RogueSolace

      RogueSolace

      😆

  5. ROTFLMAO Flashbacks to Berezino w @TiviylScratch LOL Let me think people who were with us: @Pontito @Lyca @Ender @FieJaxon @SgtSmithy @GreenySmiley @Para @Clumsy sorry if i forgot anyone
  6. Personal Notes of Elizabeth Smith

    Lysis-lysogeny paper ‘Communication between viruses guide lysis-lysogeny decisions’ • Nature volume541, pages488–493 (26 January 2017) • doi:10.1038/nature21049 Lysogeny- where temperate viruses can become dormant in their hosts, waiting for cells to decide between two phases The lytic cycle results in the virus spreading via cell division, in the process it destroys the host cells The lysogenic cycle results in the virus spreading via cell division, without damaging the host cells. This type can lay dormant in the cells until a trigger (such as UV light) activates it Phages use a small molecule communication system to coordinate the decision between choosing lyctic or lysogenic. During infection the phage produces a 6 amino-acid long peptide used as a code, it is then released. Other phages measure the peptide and if the concentration is high enough, also lysogenize. “We found that different phages encode different versions of the communication peptide, demonstrating a phage-specific peptide communication code for lysogeny decisions.” “We term this communication system the ‘arbitrium’ system, and further show that it is encoded by three phage genes: aimP, which produces the peptide aimR, the intracellular peptide receptor aimX, a negative regulator of lysogeny The arbitrium system enables a descendant phage to ‘communicate’ with its predecessors, that is, to estimate the amount of recent previous infections and hence decide whether to employ the lytic or lysogenic cycle.” Main While lyctic leads to the death of the host cells Lysogenic, the phage genome integrates into the bacterial genome. Making the lysogenized bacterium become immune to further infection by the same phage. In the current study we report that phages that infect Bacillus species can rely on small-molecule communication to execute lysis–lysogeny decisions. Discussion We have shown that phages belonging to the SPbeta group of phages use communication peptides to decide whether to enter a lytic cycle or lysogenize the infected bacterium In a sense, the communication mechanism we describe allows a descendant phage to ‘communicate’ with its ancestors, that is, to measure the number of predecessor phages that completed successful infections in previous cycles. The biological logic behind this strategy is clear: when a single phage encounters a bacterial colony, there is ample prey for the progeny phages that are produced from the first cycles of infection, and hence a lytic cycle is preferred. In later stages of the infection dynamics, the number of bacterial cells is reduced to a point that progeny phages are at risk of no longer having a new host to infect. Then, it is logical for the phage to switch into lysogeny to preserve chances for viable reproduction. The arbitrium system provides an elegant mechanism for a phage particle to estimate the amount of recent previous infections and hence decide whether to employ the lytic or lysogenic cycle. Lytic Cycle Step one involves the virus particle attaching to the host cell, the Adsorption phase. One key thing to remember is that viruses are extremely fussy about which cell they will infect. No one has ever had a liver cold, nor is there such a thing as a hepatitis respiratory infection. The cold virus affects cells of the upper respiratory tract. Hepatitis virus infects liver cells and no others. The reason these viruses infect specific cells involves this attachment step. Typically, the virus is looking for some sort of specific protein receptor found on its preferred host. That's why HIV infects T-helper cells and not B cells. The capsid proteins or spike proteins of enveloped viruses attach to specific receptors found in certain cells. This specificity is so precise, some viruses that may infect the liver cells in a dog cannot infect liver cells in a human. Other viruses can infect multiple species. Bacteriophage and Lysogeny In medicine they are used to phage type the many sub-strains of any given bacterial species to further identify it for epidemiological purposes. It's possible to infect a particular bacterial sample (an organism responsible for an outbreak of food poisoning for example) and by knowing which phage strain was used, eventually identify the strain of bacteria at hand. Bacteriophage are used in some countries as a method of killing off a bacterial infection in patients rather than using antibiotics. Since these are bacterial viruses they should not harm our cells, only the pathogens causing an infection. This treatment is not used much in Western medicine given the easy access to powerful antibiotics but they are used around the world. There are a couple problems caused by the ability of viruses to enter this Lysogenic or dormant state. First as just noted they carry viral genes that could include genes from other cells that the virus would not otherwise have. In the case of phage, they may pick up disease causing genes from the previous host bacterial cell and carry them into the new host cell. In this way a bacterial cell could acquire genetic traits (often pathogenic traits) that it would not otherwise have. Sometimes otherwise harmless bacteria turn into dangerous pathogens in this way. Second the process of the virus DNA inserting and removing itself from the host cell chromosome may disrupt the genes of the host cell. This actually leads to a variety of cancers in humans for example. The insertion of viral DNA into the cell leads to Transformation of the cell into a cancer cell which is characterized by uncontrolled cell growth. These oncoviruses may contain oncogenes that disrupt host cell cycle regulation leading to runaway cell growth. Sometimes the virus inserts itself into the middle of a host cell gene that controls cell division thereby destroying its function. Again, we get uncontrolled cell growth. There are many ways in which viruses can cause cancer, more than can be easily discussed here. Growing Viruses For bacteriophage this is very easy. Microbiologists have been growing pure cultures of bacteria for well over 100 years. A small amount of phage applied to a petri dish covered in bacteria provides a welcome place for the phage to replicate and multiply. Animal viruses can also be easily grown in miniature, all natural growth vessels: eggs. An egg has a sterile interior full of cells and all the nutrients those cells could need to grow and thrive. If a tiny hole is carefully made in the egg and virus is injected, it will infect and multiply quite nicely inside the egg. While growing host cells in culture is possible, it's expensive, time consuming and the volumes available are limited. With eggs, one can keep adding as many eggs as needed to get the volume of virus production necessary. Eggs are a relatively cheap way to go compared to other methods. Most of the flu vaccine made each year is produced from eggs, though much research is being done to get away from egg based vaccine production. Any one allergic to eggs has problems with this type of vaccine. Biology of Influenza Antigenic Drift - Minor changes in the two proteins allow the virus to evade an Immune system attuned to the "old" proteins. This change is caused by missense mutations which make a new protein shape (antigen) to evade destruction, but does not change the protein function. Antigenic Shift - Only seen in Type A viruses. This is a more dramatic change in the protein structure brought on by rearrangement of entire RNA segments of viruses infecting different species. For example, Avian Flu virus and Human Flu virus can coexist in a pig host. The avian and human viruses "exchange" genes to create entirely new variations. Thus a "new" flu strain can emerge in humans that no one has any immunity against. Recombinant Plasmid / Vector Creation The last step involves looking at a number of bacteria on Petri dishes to find the one with the target gene. This is done by looking for phenotype changes since the plasmid we used had genes that would change the survivability of bacteria in the presence of antibiotics. Remember, the one plasmid shown had two genes for antibiotic resistance but cut sites in the middle of these genes. If we cut the plasmid in the right place and inserted a new gene there, the gene for antibiotic resistance is destroyed. All we need to do then is find a cell resistant to one antibiotic but not the other. By using Petri plates containing combinations of antibiotics one can figure out which cells contain the gene of interest. Human Engineering: Gene Therapy The trick is to get the proper gene into the proper cell. A vector is needed. In bacteria, a plasmid could be constructed and inserted into a cell. Eucaryotic cells will not function with a plasmid so another approach is needed. Viruses function by attaching to host cells and inserting their genetic material. They then take over the host cell and use it to manufacture more viruses. If the viral DNA is removed and the proper human gene is inserted, the virus will then infect a target cell and deliver the functional gene. Anti-serum Once collected, the venom is highly diluted and injected into an animal like a horse or rabbit. The animal will then begin to produce antibodies against the venom. More injections follow, each with an increasing dose of the venom. This effectively increases the titer of anti-venom antibodies in the animal. Blood is then drawn and the antibodies are purified to make the antivenom injections. Characteristics of Antibiotics The fundamental principle of chemotherapy is selective toxicity. Any compound used to treat an infectious disease must be harmful to the parasites but not to host cells. This is in essence the principle of Paul Ehrlich's "magic bullet". Selective toxicity distinguishes an antibiotic which only attacks bacteria, from disinfectants and antiseptics which harm both bacteria and host cells. Fortunately antimicrobial agents are readily available in the world of the microbes. These organisms are essentially engaged in a form of chemical warfare with each other. Soil organisms in particular produce a variety of bacteria killing compounds. Many spore forming bacteria including members of the Bacillus and Streptymyces groups produce antibiotics as do spore forming fungi like Penicillium. Antibiotics have two different effects on the growth and viability of bacteria. Some antibiotics exhibit Bacteriostatic effects in that they slow the growth of bacteria or prevent their multiplication. This type is not an outright cure, that relies on an active immune response to actually destroy the invading microbes. Because of this some infections become difficult to treat on patients that have weakened immune system like AIDS patients or anyone who is immunocompromised. The other effect of some antibiotics is Bacteriocidal. These types of drugs are able to kill the microbes directly and do not rely on followup immune system responses. One major drawback of this type is they only work on metabolically active organisms. Some slow growing microbes like Mycobacteria (Tuberculosis and Leprosy) are not effectively treated with this category Antibiotic Mechanisms The basis for selective toxicity of an antibiotic rests on the ability of the drug to attack or interfere with a structure found in bacterial cells that our cells do not have. There are 5 mechanisms by which an antibiotic can attack a bacterial cell: Inhibition of cell wall synthesis Inhibition of cell membrane function Inhibition of protein synthesis Inhibition of nucleic acid synthesis Inhibition of bacterial enzymes / metabolic pathways Antibiotics Active at the Cell Wall Penicillin and its derivatives (ampicillin, amoxicillin) interfere with the ability of bacteria to build peptidoglycan. This weakens the cell wall, making gram positive cells susceptible to lysis in hypotonic environments. It tends to work best on growing cells that are building new cell wall components. Since our cells do not contain peptidoglycan, penicillin is relatively non toxic to our cells. Allergic reactions are always a possibility but not everyone experiences such complications. Cephalosporins are considered the next generation of penicillin derivatives. This group has good activity against gram positive and gram negative bacteria. The newest ones are used against MRSA (methicillin resistant Staph aureus) infections, a particularly nasty illness. This is a good option for anyone allergic to penicillin. Whole Cell Vaccines Killed (or Inactivated) Vaccines Organisms treated with a solution of formalin will lose all capacity to cause an illness when injected as part of a vaccine. Therefore these are very safe vaccines. They are also not terribly effective. A formalized organism will have the protein structures distorted. Since the immune system needs a good look at the 3D shapes, these vaccines often may require follow up booster shots over a person's lifetime. Not all diseases are caused by the direct action of a living organism. Many organisms merely secrete dangerous toxins into the environment that may disastrously affect human physiology. The Botulinum toxin is highly damaging to motor neurons, the nerves that control breathing. Also tetanus toxin causes muscle spasms that prevent breathing. A subtype of killed vaccines is the toxoid vaccine. A toxiod is an inactivated bacterial toxin that is used to develop immunity. The diptheria and tetanus vaccines are examples of toxoid vaccines. They have all of the same problems as noted above. Attenuated Vaccines Another way to make a vaccine involves using a strain that has become weakened or attenuated. In this case the organism is alive but sort of old and worn out due to they way it is grown or even manipulated genetically. Therefore when injected the organism will grow and multiply but (hopefully) not cause the full blown disease. In the end a high level of immunity develops that often lasts a lifetime. However, there is a chance that the weakened antigen will mutate back to it's full strength version and end up causing the disease we're trying to prevent. This is not a good option for immunocompromised patients. An example of this type of vaccine is the MMR vaccine for measles, mumps and rubella. Now there is the MMRV vaccine which contains the varicella or chickenpox antigen. Other Vaccine Types Component or Subunit Vaccines The most recent and arguably the best vaccine option involves the injection of an intact part of the infectious agent. A component vaccine uses only a part of the agent not the whole intact, reproducing agent. For example the capsid protein coat of a virus would serve as an antigen but since no nucleic acid is present it cannot possibly reproduce and cause an illness. Yet the immune system gets a good look at an intact antigen. Many times these antigen parts are proteins that are made through genetic engineering. Thus, component vaccines are often called Recombinant Vaccines, since they are made using recombinant DNA technology. These vaccines are very safe and quite effective. They have the bonuses of the earlier vaccines without the dangers involved. The problem is that producing them via genetic engineering is a slow process. Current examples include the Hepatitis B vaccine. DNA Vaccines Remember in gene therapy the idea is to insert a desirable gene into a vector (virus or plasmid) and inject that vector into a host animal. The hope is that cells will take up the gene and begin producing the gene protein throughout the body. Here the gene is not growth hormone or insulin but rather a component of a disease causing organism you want to protect against. Rather than giving a component vaccine which may require boosters, here genes are inserted so the cells produce a continuous supply of antigen which should strongly provoke an immune response. Recently the FDA halted an experimental HIV vaccine because is proved to be ineffective but this is the sort of thing they're working towards. Phage Therapy The bacterial host range of phage is generally narrower than that found in the antibiotics that have been selected for clinical applications. Most phage are specific for one species of bacteria and many are only able to lyse specific strains within a species. This limited host range can be advantageous, in principle, as phage therapy results in less harm to the normal body flora and ecology than commonly used antibiotics, which often disrupt the normal gastrointestinal flora and result in opportunistic secondary infections by organisms such as Clostridium difficile. The potential clinical disadvantages associated with the narrow host range of most phage strains is addressed through the development of a large collection of well-characterized phage for a broad range of pathogens, and methods to rapidly determine which of the phage strains in the collection will be effective for any given infection. Phage therapy can be very effective in certain conditions and has some unique advantages over antibiotics. Bacteria also develop resistance to phages, but it is incomparably easier to develop new phage than new antibiotic. A few weeks versus years are needed to obtain new phage for new strain of resistant bacteria. As bacteria evolve resistance, the relevant phages naturally evolve alongside. When super bacterium appears, the super phage already attacks it. We just need to derive it from the same environment. Phages have special advantage for localized use, because they penetrate deeper as long as the infection is present, rather than decrease rapidly in concentration below the surface like antibiotics. The phages stop reproducing once as the specific bacteria they target are destroyed. Phages do not develop secondary resistance, which is quite often in antibiotics. With the increasing incidence of antibiotic resistant bacteria and a deficit in the development of new classes of antibiotics to counteract them, there is a need to apply phages in a range of infections. ytic phages are similar to antibiotics in that they have remarkable antibacterial activity. However, therapeutic phages have some advantages over antibiotics, and phages have been reported to be more effective than antibiotics in treating certain infections in humans and experimentally infected animals. F For example, in one study, Staphylococcus aureus phages were used to treat patients having purulent disease of the lungs and pleura. The patients were divided into two groups; the patients in group A (223 individuals) received phages, and the patients in group B (117 individuals) received antibiotics. Also, this clinical trial is one of the few studies using i.v. phage administration (48 patients in group A received phages by i.v. injection). The results were evaluated based on the following criteria: general condition of the patients, X-ray examination, reduction of purulence, and microbiological analysis of blood and sputum. No side effects were observed in any of the patients, including those who received phages intravenously. Overall, complete recovery was observed in 82% of the patients in the phage-treated group as opposed to 64% of the patients in the antibiotic-treated group. Interestingly, the percent recovery in the group receiving phages intravenously was even higher (95%) than the 82% recovery rate observed with all 223 phage-treated patients. “When it became clear that every antibiotic had failed, that Tom could die, we sought an emergency investigational new drug application from the FDA to try bacteriophages,” “To our knowledge, he is the first patient in the United States with an overwhelming, systemic infection to be treated with this approach using intravenous bacteriophages. From being in a coma near death, he’s recovered well enough to go back to work. Of course, this is just one patient, one case. We don’t yet fully understand the potential — and limitations — of clinical bacteriophage therapy, but it’s an unprecedented and remarkable story, and given the global health threat of multidrug-resistant organisms, one that we should pursue.” Patterson had become infected with a multidrug-resistant strain of Acinetobacter baumannii, an opportunistic and often deadly pathogen. The bacterium has proved particularly problematic in hospital settings and in the Middle East, with many injured veterans and soldiers returning to the U.S. with persistent infections. nitially, the only antibiotics with any effect proved to be a combination of meropenem, tigecycline and colistin, a drug of last resort because it often causes kidney damage, among other side effects. Patterson’s condition stabilized sufficiently for him to be airlifted Dec. 12, 2015, from Germany to the Intensive Care Unit (ICU) at Thornton Hospital at UC San Diego Health. Upon arrival, it was discovered that his bacterial isolate had become resistant to all of these antibiotics. At Thornton Hospital, now part of Jacobs Medical Center, Patterson began to recover, moving from the ICU to a regular ward. But the day before scheduled discharge to a long-term acute care facility, an internal drain designed to localize his infection and keep it at bay slipped, spilling bacteria into his abdomen and bloodstream. Patterson immediately experienced septic shock. His heart began racing. He could not breathe. He became feverish and would subsequently fall into a coma that would last for most of the next two months. He was, in effect, dying. Strathdee began doing research. A colleague mentioned a friend had traveled to Tblisi, Georgia to undergo “phage therapy” for a difficult condition and had been “miraculously cured.” Strathdee had learned of bacteriophages while she was a student, but they were not part of mainstream medical doctrine Bacteriophages are ubiquitous viruses, found wherever bacteria exist. It’s estimated there are more than 1031 bacteriophages on the planet. That’s ten million trillion trillion, more than every other organism on Earth, including bacteria, combined. Each is evolved to infect a specific bacterial host in order to replicate — without affecting other cells in an organism. The idea of using them therapeutically is not new. Described a century ago, phage therapy was popular in the 1920s and 1930s to treat multiple types of infections and conditions, but results were inconsistent and lacked scientific validation. The emergence of antibiotics in the 1940s pushed phage therapy aside, except in parts of Eastern Europe and the former Soviet Union, where it remained a topic of active research. With emergency approval from the Food and Drug Administration, each source provided phage strains to UC San Diego doctors to treat Patterson, with no guarantee that any of the strains would actually work. “ Phage therapy is typically administered topically or orally. In Patterson’s case, the phages were introduced through catheters into his abdominal cavity and intravenously to address a broader, systemic infection, which had not been done in the antibiotic era in the U.S. “That makes them more effective,” said Schooley. “The action is at the interface of the patient and the organism.” With tweaking and adjustments — his physicians were learning on the fly — Patterson began to improve. He emerged from his coma within three days of the start of IV phage therapy. His abdomen had swelled, distended by the pseudocyst teeming with multi-drug resistant A. baumaunnii. His white blood cell count had soared — a sign of rampant infection. He developed respiratory failure and hypotension that required ventilation and recurrent emergency treatment. He became increasingly delirious. When he lapsed into a coma in mid-January, he was essentially being kept alive on life support. Bacteriophage therapy began March 15, 2016, with a cocktail of four phages provided by Texas A&M and the San Diego-based biotech company AmpliPhi, pumped through catheters into the pseudocyst. If the treatment didn’t kill him, Patterson’s medical team planned to inject the Navy’s phages intravenously, flooding his bloodstream to reach the infection raging throughout his body. As far as Patterson’s doctors knew, such treatment had never been tried before. On March 17, the Navy phages were injected intravenously. There were fears about endotoxins naturally produced by the phages. No one knew what to expect, but Patterson tolerated the treatment well — indeed there were no adverse side effects — and on March 19, he suddenly awoke and recognized his daughter. One of NMRC's goals with respect to bacteriophage science has been providing military members infected with multidrug-resistant organisms additional antimicrobial options so we were experienced and well-positioned to provide an effective phage cocktail for Dr. Patterson,” Subsequent treatment, however, would not be easy. The learning curve was steep and unmarked. There were bouts of sepsis — a life-threatening complication caused by massive infection. Despite improvement, Patterson’s condition remained precarious. Doctors discovered that the bacterium eventually developed resistance to the phages, what Schooley would characterize as “the recurring Darwinian dance,” but the team compensated by continually tweaking treatment with new phage strains — some that the NMRC had derived from sewage — and antibiotics. In early May, Patterson was taken off of antibiotics. After June 6, there was no evidence of A. baumannii in his body. He was discharged home August 12, 2016. Recovery has not been entirely smooth and steady. There have been setbacks unrelated to the phages. Derived from the Greek words meaning “bacteria eater,” bacteriophages are ancient and abundant — found on land, in water, within any form of life harboring their target. According to Rowher at San Diego State University and colleagues in their book Life in Our Phage World, phages cause a trillion trillion successful infections per second and destroy up to 40 percent of all bacterial cells in the ocean every day. Thousands of varieties of phage exist, each evolved to infect only one type or a few types of bacteria. Like other viruses, they cannot replicate by themselves, but must commandeer the reproductive machinery of bacteria. To do so, they attach to a bacterium and insert their genetic material. Lytic phages then destroy the cell, splitting it open to release new viral particles to continue the process. As such, phages could be considered the only “drug”’ capable of multiplying; when their job is done, they are excreted by the body. Several companies have engineered such viruses, called bacteriophages, to use the CRISPR gene-editing system to kill specific bacteria, according to a presentation at the CRISPR 2017 conference in Big Sky, Montana, last week. These companies could begin clinical trials of therapies as soon as next year. Initial tests have saved mice from antibiotic-resistant infections that would otherwise have killed them, said Rodolphe Barrangou, chief scientific officer of Locus Biosciences in Research Triangle Park, North Carolina, at the conference. Bacteriophages isolated and purified from the wild have long been used to treat infections in people, particularly in Eastern Europe. These viruses infect only specific species or strains of bacteria, so they have less of an impact on the human body’s natural microbial community, or microbiome, than antibiotics do. They are also generally thought to be very safe for use in people But the development of phage therapy has been slow, in part because these viruses are naturally occurring and so cannot be patented. Bacteria can also quickly evolve resistance to natural phages, meaning researchers would have to constantly isolate new ones capable of defeating the same bacterial strain or species. And it would be difficult for regulatory agencies to continually approve each new treatment. To avoid these issues, Locus and several other companies are developing phages that turn the bacterial immune system known as CRISPR against itself. In Locus' phages, which target bacteria resistant to antibiotics, the CRISPR system includes DNA with instructions for modified guide RNAs that home in on part of an antibiotic-resistance gene. Once the phage infects a bacterium, the guide RNA latches on to the resistance gene. That prompts an enzyme called Cas3, which the bacterium normally produces to kill phages, to destroy that genetic sequence instead. Cas3 eventually destroys all the DNA, killing the bacterium. “I see some irony now in using phages to kill bacteria,” says Barrangou. Another company, Eligo Bioscience in Paris, uses a similar approach. It has removed all the genetic instructions that allow phages to replicate, and inserted DNA that encodes guide RNAs and the bacterial enzyme Cas9. Cas9 cuts the bacterium’s DNA at a designated spot, and the break triggers the bacterium to self-destruct. The system will target human gut pathogens, says Eligo chief executive Xavier Duportet, although he declined to specify which ones. Other companies are working to get phages to perform different tasks. ‘Supercharged’ phages, created by a group at Synthetic Genomics in La Jolla, California, could contain dozens of special features, including enzymes that break down biofilms or proteins that help to hide the phages from the human immune system. But engineered phages still have to overcome some hurdles. Treating an infection might require a large volume of phages, says Elizabeth Kutter, a microbiologist at Evergreen State College in Olympia, Washington, and it’s unclear whether this would trigger immune reactions, some of which could interfere with the treatment. Phages could also potentially transfer antibiotic-resistance genes to non-resistant bacteria, she notes. Lu adds that bacteria may still develop resistance even to the engineered phages. So researchers might have to frequently modify their phages to keep up with bacterial mutations. But as the problem of antibiotic resistance increases, more countries are revisiting phage therapy. Last year, for instance, the European Union (EU) funded a project called Phagoburn to explore the use of phage therapy to treat burn wounds infected with bacteria. Phagoburn involves institutions and hospitals in Belgium, France and Switzerland. Countries that aim to introduce phage therapy will need to prepare their own guidelines for approving it, including methods for phage selection, preparation and administration. But recent advances in phage therapy suggest that such regulatory efforts would bring big rewards in treating bacterial infections. Phages are a natural part of the microbial ecosystem. Environments such as sea water, fresh water and soil all contain millions of phage species. Different phage species are specific to particular bacterial species, and they can infect bacteria without harming animal or plant cells. When faced with a bacterial infection, scientists first isolate candidate phages from the environment. The bacteria can be treated with a sample of water that naturally contains phages. If the bacteria die, the sample can be centrifuged, leaving the phages at the top to be collected and tested to see which ones killed the bacteria. Either the phage or its products, such as bacteriolytic enzymes called endolysins, can then be used as antibacterial agents in pills and ointments, often requiring just a single dose. However, despite early success, phage therapy was largely abandoned when antibiotics came along, and is used today in only a few countries, including Russia, Georgia and Poland. Phage therapy declined in part because it focuses on treating specific infections, rather than on treating a range of bacteria. Some studies concluded that it failed because highly specific phages were simply tested against the wrong bacteria. Opponents of phage therapy often raise two potential problems: the appearance of phage-resistant mutant bacterial strains, and adverse reactions caused by the host's immune system against the phage. Modern techniques make it possible to address both of these concerns, however. First, using a cocktail of several different phages, or the advance preparation of mutant phages, overcomes any issue of bacterial resistance. Second, to stop phage therapy activating someone's immune system, a medical treatment can use phages with innate characteristics that are unlikely to elicit an immune response, use mutant phages that are not recognized by the immune system, or use some combination of the two. If a phage does somehow turn on the immune system, it can be treated with polyethylene glycol, for example, which will reduce the immune response. Some phages can also produce toxins, but there is a way of resolving that problem too. Modern high-throughput techniques have moved phage therapy beyond screening water samples for potential treatments. Next-generation sequencing, for example, allows genomic DNA sequences from multiple phages to be analysed simultaneously. This makes it easier to detect suitable candidates for phage therapy that lack harmful genes, such as those that produce toxins or drug resistance. We have used silkworm larvae to test phage therapy against Staphylococcus aureus infections. Using two new phages to infect the bacterium, we found no adverse effects on the silkworm, but the phages did destroy the bacteria cells3. Our results using silkworm larvae were similar to those using these phages against S. aureus infections in mice. Phages are simple, yet incredibly diverse, non-living biological entities consisting of DNA or RNA enclosed within a protein capsid. As naturally-occurring bacterial parasites, phages are incapable of reproducing independently (i.e., non-living) and are ultimately dependent on a bacterial host for survival. Phages typically bind to specific receptors on the bacterial cell surface, inject their genetic material into the host cell, and then either integrate this material into the bacterial genome (so-called “temperate” phages) and reproduce vertically from mother to daughter cell, or hijack the bacterial replication machinery to produce the next generation of phage progeny and lyse the cell (so-called “lytic” phages). Upon reaching a critical mass of phage progeny, which can be anywhere from a few to over 1000 viral particles, depending on environmental factors, the lytic proteins become active and hydrolyze the peptidoglycan cell wall, releasing novel phage to reinitiate the lytic cycle Most phages are infectious only to the bacteria that carry their complementary receptor, which effectively determines lytic phage host range[20]. Host specificity varies among phages, some of which are strain-specific, whereas others have demonstrated the capability of infection across a range of bacterial strains and even general One 1931 trial of phage therapy as a treatment for cholera in the Punjab region of India involved a cohort of 118 control subjects and 73 experimental subjects who received phage treatment; d’Herelle observed a 90% reduction in mortality with 74 lethal outcomes in the control group and only 5 in the experimental group[1]. When challenged with gut-derived sepsis due to P. aeruginosa, oral administration of phage saved 66.7% of mice from mortality compared to 0% in the control group[38]. In a hamster model of Clostridium difficile (C. difficile)-induced ileocecitis, a single dose of phage concurrent with C. difficileadministration was sufficient prophylaxis against infection; phage treatments post-infection saved 11 of 12 mice whereas control animals receiving C. difficile and clindamycin died within 96 h hage combinations also significantly reduced C. difficile growth in vitro and limited proliferation in vivo using a hamster model[40]. Intraperitoneal administration of a single phage strain was sufficient to rescue 100% of mice in bacteremia models using vancomycin-resistant E. faecium[41], extended spectrum β-lactamase producing E. coli[42], and imipenem-resistant P. aeruginosa Phage cocktails have also been used to treat antibiotic-resistant P. aeruginosa infections of the skin, lungs, and gastrointestinal tract in animal models[38,44]. Additional animal studies show similarly promising results for multidrug-resistant E. coliO25:H4-ST131[45], Vibrio parahaemolyticus[46], S. aureus[44,47], and A. baumanii[38]. There is even an indication that phage are capable of restoring antibiotic sensitivity in antibiotic-resistant bacteria, as in the case of multidrug-resistant P. aeruginosa[48]. In a 1938 clinical trial, 219 patients with bacterial dysentery (138 children and 81 adults) were treated solely with a phage cocktail consisting of a variety of phage targeting Shigella flexneri, Shigella shiga, E. coli, Proteus spp., P. aeruginosa, Salmonella typhi, Salmonella paratyphi A and B, Staphylococcus spp., Streptococcus spp. and Enterococcus spp.; cocktails were administered both orally and rectally. Within 24 h, 28% of patients with blood in their stools were relieved of this symptom, with a further 27% showing improvement within 2-3 d. Overall, 74% of the 219 patients showed improvement or were completely relieved of symptoms Additionally, during a 1974 typhoid epidemic, a cohort of 18577 children was enrolled in a prophylactic intervention trial using typhoid phages. Phage administration resulted in a 5-fold decrease in typhoid incidence compared to placebo[49]. The potential for phage therapy has yet to be fully realized since phages tend to be more effective against the target pathogen when used in combination with antibiotics[52], a treatment option that has not yet been investigated in humans. Virophage http://scienceblogs.com/notrocketscience/2008/08/07/the-virophage-a-virus-that-infects-other-viruses/ Viruses may cause disease but some can fall ill themselves. For the first time, a group of scientists have discovered a virus that targets other viruses. It is so unique that they have classified it in an entirely new family – the “virophages” – in honour of the similarities it shares with the bacteriophage viruses that use bacteria as hosts. The story of Sputnik started in 1992 with some dirty English water. A group of scientists were studying an amoeba taken from a cooling tower in Bradford, England, when they discovered a microscopic giant – a virus so large that it was originally mistaken for bacterium. It was only in 2003 that La Scola and colleagues conclusively showed that the new find was indeed a virus. But what a virus – APMV, or ‘mimivirus’, measures a whopping 400 nanometres across. The search for giant viruses continued. La Scola’s team identified another strain of APMV by inoculating the same species of amoeba with water taken from another cooling tower, this time from Paris. The new specimen seemed to eclipse even the original giant in size, and the researchers decided to call it ‘mamavirus’. When this record-breaker infects amoebae, it forms gigantic viral factories that pump out new copies of itself. When the team looked at these under an electron microscope, they found the equivalent of microscopic Russian dolls – tiny viral particles, just 50 nanometes in size and distinct from mamavirus itself. It’s all very meta, and to the researchers, the fact that mamaviruses can “get sick” themselves is further evidence that viruses are indeed living things. La Scola and Desnues found that Sputnik couldn’t multiply within the amoeba by itself; it could only spread within cells that had also been infected with mamavirus. But Sputnik is no partner – by hijacking the mamavirus’s replication machinery, it spreads at the expense of its larger host and substantially hinders its reproduction. In the presence of the tiny intruder, mamavirus particles assemble abnormally and surround themselves with unusually thick outer coats. As a result, their ability to infect the amoeba fell by 70%. The virophage name is perhaps a bit misleading. Bacteriophages reproduce within the cells of bacteria, whereas Sputnik is a satellite virus, in more than name only. Like hepatitis D, it depends on another virus coinfecting a host in order to spread. But it’s the fact that it does so at the expense of the mamavirus that makes it a true parasite. In comparison to its sizeable host, Sputnik is tiny and sports a genome that is almost a hundred times smaller. Its 18,000 base-pairs of DNA contains just 21 genes and when La Scola and Desnues analysed these, they found that Sputnik is a genetic chimera – a mish-mash of different genes from different sources. Thirteen of these have no equivalent in any other known virus, while the remainder have similarities to genes from other viruses, bacteria and even more complex cells. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4072922/ The recently discovered, Sputnik virophage is a satellite virus that inhibits replication of its target phage and thus acts as a parasite of that virus in aquatic environments (Jassim and Limoges 2013). These virophages may also coexist as the natural predator of the phages that target foodborne pathogens, perhaps transmitted from their aquatic environments by fish and seafood. Virophages in aquatic environments hijack virus DNA in order to replicate and often deform phage/virus particles, making them less infective (Jassim and Limoges 2013). We have found no published report of their existence or survival outside of aquatic environments, but if confirmed, it may help to explain why, according to the US Center for Science in the Public Interest (CSPI 2008), fish and shellfish are more likely to cause foodborne-illness than any other category of food product. Even if these virophages exist only in aquatic environments, much of their work to hamper the effectiveness of phages is already accomplished prior to the food harvest. These foods are also considered a potential entry source of foodborne pathogens into the home (Scott 2003). It is worthwhile to investigate this postulation and potential association of virophages with aquatic foodborne pathogens in order to aid the understanding of phage ecology and bacterial evolution in greater clarity, assisting in the application of phages in therapy and biocontrol of bacterial infections. The ecology of both phages and bacteria were also not understood, resistance, failure to neutralize gastric pH prior to oral administration, inactivation of phages by host immune responses and environmental contamination issues are other obstacles (Kutter 2005). It was also suggested that changes of the bacterial hosts used for maintenance of phages must be avoided as these can drastically modify the parameters of the phage preparations, including host range and lytic activity (Sillankorva et al. 2010; Sulakvelidze 2011). The generally poor efficacy of commercial phage preparations led to widespread criticism and disagreement about the effectiveness of phages in treating disease (Atterbury 2009). It was found that the most successful route of administration for the treatment of systemic infections was via the parenteral route. Oral delivery is mainly used to treat gastrointestinal infections. However, in some cases phages can also reach the systemic circulation. Local delivery (skin, ears, and teeth) has proved extremely successful in the treatment of topical infections, as has the inhalation of phages for the treatment of lung infections Using viruses to fight viruses: New approach eliminates 'dormant' HIV-infected cells https://www.sciencedaily.com/releases/2017/12/171218090616.htm · Researchers have discovered that the Maraba virus, or MG1, can target and destroy the kind of HIV-infected cells that standard antiretroviral therapies can't reach. If this technique works in humans, it might possibly contribute to a cure for HIV. · This virus attacks cancer cells that have defects in their interferon pathway, which makes the cells more vulnerable to viruses. Dr. Angel and his team previously found that latently HIV-infected cells also have defects in this pathway. · "We thought that because latently HIV-infected cells had similar characteristics to cancer cells, that the virus would enter and destroy them," said Dr. Angel, senior scientist and infectious disease physician at The Ottawa Hospital, and professor at the University of Ottawa. "It turns out we were right." · When the researchers added MG1 to relevant blood cells taken from HIV-positive individuals, the levels of HIV DNA in the sample dropped. This indicated that the HIV-infected cells had been eliminated. · "We know that the Maraba virus is targeting and killing the latently HIV-infected cells, but we don't know exactly how it's doing this," said Dr. Angel, who is also Head of the Division of Infectious Disease. "We think the virus is able to target the cells because of an impaired interferon pathway, but we need to do more research to know for sure." Virotherapy https://en.wikipedia.org/wiki/Virotherapy · Virotherapy is a treatment using biotechnology to convert viruses into therapeutic agents by reprogramming viruses to treat diseases. · There are three main branches of virotherapy: o anti-cancer oncolytic viruses, o viral vectors for gene therapy and o viral immunotherapy. · In a slightly different context, virotherapy can also refer more broadly to the use of viruses to treat certain medical conditions by killing pathogens. Oncolytic virotherapy · Oncolytic virotherapy is not a new idea – as early as the mid 1950s doctors were noticing that cancer patients who suffered a non-related viral infection, or who had been vaccinated recently, showed signs of improvement;[1] this has been largely attributed to the production of interferon and tumor necrosis factors in response to viral infection, but oncolytic viruses are being designed that selectively target and lyse only cancerous cells. In the 1940s and 1950s, studies were conducted in animal models to evaluate the use of viruses in the treatment of tumors.[2] In the 1940s–1950s some of the earliest human clinical trials with oncolytic viruses were started.[3][4] However, for several years research in this field was delayed due to the inadequate technology available. Research has now started to proceed more quickly in finding ways to use viruses therapeutically. As well as the direct anti-cancer effect, oncolytic viruses are also capable of inducing an anti-tumor immune response. o The oncolytic virus Rigvir developed at the Institute of Microbiology in Latvia was registered in 2004 in Latvia (national registration).[5] Since 2004 Rigvir is approved and since 2008 Rigvir is available in pharmacies of Latvia. Virotherapy with Rigvir is successfully used in Latvia and by patients from more than 25 countries around the world. Recent retrospective study published in Melanoma Research revealed that IB-IIC melanoma patients treated with oncolytic virus Rigvir were 4.39–6.57-fold lower mortality than those, who according to melanoma treatment guidelines did not receive virotherapy and were only observed.[6] Also in 2015 Rigvir was included into the Latvian National guidelines for treatment of skin cancer and melanoma.[7] Since 2015 Rigvir is approved in Georgia, but in 2016 it was approved in Armenia. Since then Rigvir registration in Latvia has become under questioning, because of complete lack of appropriately documented efficiacy, and unethical (and occasionally unlawful) practices of its sellers. Viral gene therapy · Viral gene therapy most frequently uses non-replicating viruses to deliver therapeutic genes to cells with genetic malfunctions. Early efforts while technically successful, faced considerable delays due to safety issues as the uncontrolled delivery of a gene into a host genome has the potential to disrupt tumor suppressing genes and induce cancer, and did so in two cases. Immune responses to viral therapies also pose a barrier to successful treatment, for this reason eye therapy for genetic blindness is attractive as the eye is an immune privileged site, preventing an immune response. An alternative form of viral gene therapy is to deliver a gene which may be helpful in preventing disease that would not normally be expressed in the natural disease condition. For example, the growth of new blood vessels in cancer, known as angiogenesis, enables tumors to grow larger. However, a virus introducing anti-angiogenic factors to the tumor may be able to slow or halt growth. o ProSavin is one of a number of therapies in the Lentivector platform under development by Oxford BioMedica. It delivers to the brain the genes for three enzymes important in the production of dopamine, a deficiency of which causes Parkinson's disease. o TNFerade (a non replicating TNF gene therapy virus) failed a phase III trial for pancreatic cancer.[16] Viral immunotherapy · Viral immunotherapy uses viruses to introduce specific antigens to the patient's immune system. Unlike traditional vaccines, in which attenuated or killed virus/bacteria is used to generate an immune response, viral immunotherapy uses genetically engineered viruses to present a specific antigen to the immune system. That antigen could be from any species of virus/bacteria or even human disease antigens, for example cancer antigens. o Trovax is an immunotherapy that uses a pox-virus bearing the tumour antigen 5T4, to induce an immune response against a variety of cancer types. The therapy was developed by Oxford BioMedica and failed to improve overall survival in a phase 3 trial in renal cell carcinoma.[17] New phase II trials have since begun at Cardiff University (UK) with colorectal cancer and at the Velindre Cancer Centre (Cardiff, UK) with malignant pleural mesothelioma. About Virotherapy https://www.virotherapy.eu/about-therapy.php · Oncolytic virotherapy is an effective cancer treatment using a special virus, which is capable of finding and destroying malignant tumour cells in the body. There are only three live virus-containing medication in the world and Rigvir is the first registrated and still the one and only genetically unmodified virus available worldwide. · The goal of virotherapy, not unlike that of radiation therapy and chemotherapy, is to destroy cancer cells, but virotherapy has several distinct advantages: o Virotherapy destroys tumour cells selectively without affecting the healthy cells of the body. o Virotherapy stimulates the body’s natural defence mechanisms by activating the immune system, which is often supressed by other treatment methods. o Virotherapy can be used against tumours that don’t respond well to radiation or chemotherapy, such as melanomas. o Virotherapy can be used at various stages throughout the treatment process: before or after surgery and also between radiation or chemotherapy treatments. o Virotherapy is recognised as a safe and efficient cancer treatment method. Can viruses form symbiotic relationships with humans? https://www.quora.com/Can-viruses-form-symbiotic-relationships-with-humans These guys are often thought of nothing but evil. In fact, in the Matrix Agent Smith says that humans are like a virus, since neither benefit their host. This metaphor is brought up in the Kingsmen as well. But they do form symbiotic relationships with humans. Now, we can easily imagine engineering a virus which imparts some gene to humans, but that’s humans influencing viruses for our own ends. What about just in nature? Polydnavirus is a fairly unique virus which has a mutually beneficial relationship with wasps. How does it work? Well, the wasp inserts lavae into a host. The host is ALSO infected by the virus. The virus will help attack the host’s immune system while altering the cells to be more beneficial to the larvae which have also infected the host. But what about humans? In all mammals, including humans, there are things called “endogenous retroviruses”. These are viruses that are ALREADY in your genome. They make up 5–8% of your genes. Now, most of these viruses are defective and don’t work, making up garbage DNA for the most part. However, some of these viruses are actually active while the placenta is being formed during pregnancy. That’s right, your genes have viruses in them, and those viruses are necessary for reproduction by helping form the placenta. External viruses can also lead to beneficial relationships. Hepatitis G, a nonpathogentic virus, is believed to actually suppress HIV progression in humans. So yes, viruses do form mutually beneficial relationships with animals, even humans. This relationship is more complex in plants as well, where some viruses will actually aid in drought and frost protection. Viral symbioses https://www.ukessays.com/essays/biology/viral-symbioses.php · In ecology, symbiosis is described as a relationship between two different species in which one organism lives off on another and the other organism lives inside the other. · Symbiotic relationships are characterized based on the kind of relationship they share with another organism. · Although symbiosis usually occurs between virus-virus and virus-host, virus-host relationships are among the most studied and familiar relationships.(Kimball) Viruses are known to be good at the process of symbiosis as there are retroviruses, including HIV1 and Influenza that epitomizes the symbiotic relationship between the virus and the host. Symbiotic relationship between two organisms sometimes harms one species and benefits the other and in other cases neither of the species is benefited from the relationship. (Abott) · The three well known symbiotic relationships that occur are known as mutualism, commensalism and parasitism. Mutualism interaction occurs between two organisms when each organism is being benefits, whereas commensalism is a relationship between two organisms where only one of them benefits but the other is unaffected. Viruses that are living inside a host have a symbiotic relationship known as parasitism. Parasites live in the body of the host from whom they feed off and also harm in some ways. (Abott) · Viruses have the ability to live and replicate within a host cell by reverse transcriptase and integrase. HIV-1 and HIV-2 are retroviruses that cause AIDS. The genome of retroviruses consists of RNA which is reverse transcribed into DNA (Kaiser). For a virus to achieve a symbiotic relationship with its host, it first has to attach itself to CD4 cells which enable the virus to invade its host. Once the retrovirus infects a cell, the reverse transcribed DNA enters the nucleus where it is inserted into the host's DNA. (Kimball) · Bacteriophages are viruses that infect the bacteria causing a symbiotic relationship. Lysogeny is the steady relationship that occurs between a bacteriophage and its host. During the lygoenic cycle, the bacteriophage is called a prophage. When the prophage DNA is inserted into the chromosome of it host cell, the virions releases contain some host genes and some of their own. Once the virions infect another host, they genetically transfer these bacterial genes via transduction. (Gregory) · Prophage can express many of its genes while it is present in its host genome. The genes that encodes for diphtheria toxin and cholera toxin are actually a phage gene, therefore phages are known to have genes that make the bacteria more stable. · Viral symbioses are known to be more parasitic to their hosts than bacterial symbiotic relationships. How Wasps Use Viruses to Genetically Engineer Caterpillars And caterpillars might be using the same viral genes to defend themselves against other viruses https://www.theatlantic.com/science/archive/2015/09/parasitic-wasps-genetically-engineer-caterpillars-domesticated-viruses/405874/ · The wasps in question are called braconids. There are more than 17,000 known species, and they're all parasites. The females lay their eggs in the bodies of still-living caterpillars, which their grubs then devour alive. · As early as 1967, scientists realised that the wasps were also injecting the caterpillars with some kind of small particle, alongside their eggs. It took almost a decade to realise that those particles were viruses, which have since become known as bracoviruses · Each species of braconid wasp has its own specific bracovirus, but they all do the same thing: They suppress the caterpillar’s immune system and tweak its metabolism to favour the growing wasp. · Unlike most other kinds of virus, these bracoviruses cannot make copies of themselves. They are only manufactured in the ovaries of the wasps, and once they get into the caterpillars, their life cycle ends. Some might say they’re not true viruses are all. They're almost like secretions of the wasp’s body. · The bracoviruses can't independently reproduce because they lack genes for making the protein coats that give them form and structure. Those coat genes didn't vanish. In 2009, Anne Bezier and Jean-Michel Drezen from Francois Rabelais University showed that they exist within the wasp genomes. The bracoviruses aren’t just allies for the wasps: They are part of the wasps. · that the wasp genomes contain two separate clusters of viral genes. The first is a replication set, which the wasps use to turn their ovaries into virus-making factories. The second is a virulence set, which attacks the caterpillars. But when the wasps build the viruses, they fill them only with the virulence genes, not the replication ones. That’s why the resulting particles can attack caterpillars, but can’t reproduce or spread to new hosts. They are fully domesticated. · Either way, caterpillars occasionally survive their encounters with braconids, but still end up with swarms of bracoviruses in their bodies. What happens then? Since those viruses were originally part of one insect genome (the wasp’s), could they find their way into another (the caterpillar’s)? · The answer is yes. The duo described the wasps as “accidental genetic engineers,” implanting the genomes of their caterpillar victims with their own (viral) DNA. In other words, one insect was genetically modifying another with viral genes, via a sting. · found similar genes in a wider range of butterfly and moth species, including important pests like the beet armyworm and fall armyworm. And they’ve found that these sequences may not just be passive hitchhikers. · It looked as if these viral genes, which had hopped from wasp to moth, were now protecting their new hosts from baculoviruses. · Together, they showed that one of the viral genes in the beet armyworm prevents baculoviruses from reproducing in insect cells. Another stops baculoviruses from entering the cells in the first place, blocking infections entirely. · Herrero speculates that the wasps might have originally used these genes to stop baculoviruses from prematurely killing their hosts before their grubs could develop. When the genes made their way into the caterpillars, they played exactly the same role, but on behalf of a different owner. Where they once preserved the caterpillar’s life so the wasp could later kill it, now they just preserve its life, full-stop. Parasitic Wasps Infected with Mind-Controlling Viruses http://phenomena.nationalgeographic.com/2015/02/10/parasites-within-parasites/ · The wasp, a species called Dinocampus coccinellae, lays an egg inside the ladybug Coleomegilla maculata. After the egg hatches, the wasp larva develops inside the ladybug, feeding on its internal juices. When the wasp ready to develop into an adult, it crawls out of its still-living host and weaves a cocoon around itself. · s I wrote in the article that accompanied that photograph, the ladybug then does something remarkable: it becomes a bodyguard. It hunches over the wasp and defends it against predators and other species of parasitic wasps that would try to lay their eggs inside the cocoon. Only after the adult wasp emerges from its cocoon does the bodyguard ladybug move again. It either recovers, or dies from the damage of growing another creature inside of it. · In the Proceedings of the Royal Society, a team of French and Canadian researchers now lay out the evidence for this strange state of affairs. As they studied this manipulation, they reasoned that the best place to look for clues was inside the heads of parasitized ladybugs. They discovered that the brains of these hosts were loaded with viruses. When the scientists sequenced the genes of the virus, they found it was a new species, which they dubbed D. coccinellae Paralysis Virus, or DcPV for short. · The scientists found DcPV in the wasps as well–but not in their brains. In female adult wasps, the virus grows in the tissues around their eggs. Once a wasp egg hatches inside a ladybug, the virus starts replicating inside it, too. The larva then passes on the virus to its host, and the ladybug develops an infection as well. · The virus makes its way into the ladybug’s head, where it attacks brain cells and produces new viruses in pockets inside the cells. Many brain cells die off during the infection. · The researchers hypothesize that the virus is responsible for the change in the ladybug’s behavior. To get the ladybug to guard the wasp, the virus may partially paralyze its host, so that it becomes frozen over the parasite. Because the paralysis isn’t complete, the ladybug can still lash out against predators. But these may just be wild spasms in response to any stimulus. The bodyguard effect may grow even stronger as the infection robs the ladybug of the signals from its eyes and antennae. Closed off the world, its sole purpose becomes protecting its parasite. · The fate of a parasitized ladybug–to die or to walk away–may depend on how it handles a DcPV infection. In some cases, the virus may be fatal–possibly by triggering a massive immune response that kills not just the virus but the ladybug itself. In other cases, the ladybug’s immune system may eventually be able to clear the virus out of its system, letting its nervous system heal. · In either case, the bodyguard paralysis lasts long enough to protect the wasp while it develops into an adult. Whether the ladybug lives or dies doesn’t matter to the wasp–or to the virus. The new wasp carries a fresh supply of DcPV. If it’s a female, it will be able to use the virus to infect both its own young, and its ladybug slave. First ‘virophage’ could take the fight to viruses https://www.newscientist.com/article/dn14480-first-virophage-could-take-the-fight-to-viruses/ · A newly discovered type of virus that spreads at the expense of other viruses, could be used to combat viral infections, say researchers. · Didier Raoult and colleagues from the University of the Mediterranean, France, say that the virus, called Sputnik, spreads by hijacking the replication machinery of the mamavirus – itself a new strain of the giant mimivirus. · The team says Sputnik is the first member of a new class they call “virophages” because of similarities with bacteriophages or phages – viruses that infect bacteria – and is the first time a virus has been seen to propagate at the expense of a viral host · Not only does Sputnik cut the spread of mamavirus in amoeba, Raoult’s analysis also shows it has looted genes from other viruses. This could help researchers understand the genetic evolution of harmful viruses, and potentially, use virophages to destroy them. However, the team is cautious. · “It’s too early to say we could use Sputnik as a weapon against big viruses or to modify them,” says co-author Bernard La Scola, also at the University of the Mediterranean. “But phages are used to modify bacteria, so why not?” · Sputnik resembles satellite viruses – such as the one that causes hepatitis D. These can only replicate in and infect their host if another virus is present. A key difference, though, is that Sputnik significantly reduces the viral load of the other virus. · However Geoffrey Smith, a virologist at Imperial College London, says this may not be surprising since both viruses are dependent upon the host cell for metabolites and will compete for them. He adds: “Bacteriophages replicate only in bacteria and that’s all they need, so the use of the phrase ‘virophage’ is inappropriate.” Viruses Have Their Own Version of CRISPR https://www.theatlantic.com/science/archive/2016/02/giant-viruses-have-immune-systems-that-protect-them-from-smaller-viruses/471387/ · With all the buzz around CRISPR, the gene-editing technique that has instigated many an ethical debate and one acrimonious patent dispute, it would be easy to mistake it for a recent human invention. It’s not. Bacteria invented CRISPR billions of years ago, as a defense against marauding viruses. The bacteria grab pieces of a virus's genetic material and incorporate these fragments into their own DNA. In doing so, they memorize the identities of past enemies. They can then use the viral sequences to guide their own defensive enzymes. · Now, it seems that some viruses use the same trick. Bernard La Scola and Didier Raoult from Aix-Marseille University have found that some giant viruses have a CRISPR-esque immune system, which they use to defend themselves from other smaller viruses. It seems that the defenders steal the genes of the attackers, and use those ‘memorized’ sequences to tailor their own countermeasures. · This is the latest in a string of discoveries that show how unexpectedly crazy the viral world really is. In the last 13 years, scientists have found giant viruses that outsize bacteria, viruses that parasitize other viruses, and now viruses with immune systems that defend themselves against more viruses. · The story began in 1992, when La Scola and Raoult studied amoebas contaminating the water of a cooling tower in Bradford, England. The amoebas were infected by a microbe, which was so large that the researchers initially assumed it was a bacterium. Only later, in 2003, did they realize it was a virus—a huge one, around four times bigger than, say, HIV or the influenza virus. They called it mimivirus. · An entire world of giant viruses soon came to light: Mamavirus in a Parisian cooling tower, Pithovirus in 30,000-year-old Russian ice, and Megavirus and Pandoravirus in Chilean coastal waters. Most of these also infect amoebas, manufacturing new copies of themselves by setting up viral factories in their hosts. And these factories can themselves be corrupted by viruses. · In 2008, La Scola and Raoult noticed that amoebas infected by Mamavirus often carry a second smaller virus. This pipsqueak is a parasite that hijacks Mamavirus’s factories, using them to make copies of itself at the expense of its bigger cousin. When it’s around, the giant virus reproduces slowly, assembles abnormally, and produces daughters that are poorer at infecting amoebas. The team described the smaller virus as a ‘virophage’—an ‘eater of viruses’, a virus that sickens other viruses. · That first virophage was called Sputnik, after the Russian for ‘fellow traveler.’ More were then discovered, including Maverick virus from coastal waters, Organic Lake virophage from an Antarctic lake, and Sputnik 2 found in the inflamed eye of a French teenager. · The latest member of the virophage club is Zamilon, after the Arabic for “neighbor.” Raoult and La Scola found in 2014, and they noticed that it can only parasitize some branches of the Mimivirus family tree. Of the three such branches, one—lineage A—is immune to Zamilon. · Raoult suggested that these giant viruses defend themselves from Zamilon with some kind of CRISPR-like immune system. In other words, they contain stolen copies of Zamilon’s DNA, and using these pilfered sequences, they deploy DNA-slicing enzymes to disable the virophages. “Bernard disagreed, so we competed among ourselves to find the answer,” says Raoult, laughing. · He made three predictions. First, the A-group mimiviruses should contain DNA that matched the Zamilon virophages (which they resist), but not the Sputnik ones (which they don’t). Second, these immunizing sequences would be absent in the other two Mimivirus lineages that were not resistant to Zamilon. Third, the stolen Zamilon sequences would be accompanied by enzymes for unwinding and cutting DNA. All three predictions were true. “The war between giant viruses and virophages is similar to that between bacteria and viruses,” says Raoult. · The giant virus’s defense system, which the team calls MIMIVRE, isn’t exactly the same as CRISPR, but it is very close in form. It’s a wonderful example of convergent evolution, where two groups of living things independently come up with the same solutions to the same problems. · “[Some giant viruses] can get sick from a viral infection and can produce a "immune" response to the infection,” · It’s clear where Raoult stands. “Giant viruses are not ordinary viruses,” he says. He thinks of them just another type of microbe, a group of microscopic living organisms, much like bacteria. They have their own immune system—MIMIVIRE. And they have their own parasites—virophages. Even their parasites have parasites.
  7. RogueSolace

    @Mass and I combining rp experience 😊

     

    IMG_3891.GIF

  8. Community Opinions and the Sort

    I'm going to respectfully disagree. While they may be auto targets for some, it makes no sense on the level people take it in game. Large goverments are not just going to be gone. They're going to be those trying to bring aid and relief. Even to people who hate them, the supplies they provide are important when there is no manufacturing locally. My issue is not pvp thats productive to the story, its pvp that feels constant, especially when it makes little sense. There was very little actual reason for the UN to be hit that hard. A major rp source was taken away, and people are complaining that the rp is gone. Rather ironic to me. Its not just military, its nearly any attempted settlement. Thats where I have the problem. Nearly all the rp hubs we have get turned into warzones. Even Severograd and Tortuga. While there may have been 'protection' every person I ran into who had been there told me ic to stay away, and ooc'stay away, its cancer. People go to have some kind of rp, but the rp is shit.' Thats not me, that is what near constant feedback I got from others was. It feels like people are only looking for whats quality to them. As people are given feedback and get mad about it, they never actually change anything. Only claim its whining or make excuses. Just because its good for some people, doesn't make it good for everything overall. What would happen if UN, pubs, hospitals, etc. actually were not attacked , stolen from, and forced to close on a constant basis? We would actually have spread out areas that people could actually do shit in. It doesn't mean PVP would have to stop entirely or in someways even stop at all. Just change in how they go after places. If places are actually going to be beneficial to you, like a hospital, it makes no sense to fucking try to control it and tear it down. It makes more sense that you would befriend and even protect these places because they are resources where you can get things you need.
  9. Community Opinions and the Sort

    I would also like to point out, as I have in other posts... that again, people essentially decide we cant have nice things unless they get to be overlord, which no ones really going to just be okay with The UN camp was the biggest rp hub at the beginning, pushing both lore and promoting rp. it worked as always for a time, then * rumors ic and people spreading stupid and false info * people trying to sell drugs and start fights * repeated griefing even though the UN kept several tents out for supplies for everyone * CDF, VDV, UN repeadedly being put into fights with each other WHEN THE POINT OF THE UN IS TO KEEP CONFLICT FROM ESCALATING. But no lets just all attack them anyways. * Repeatedly be starting fights when people knew server pop is low so they can get away with it * pretty much everyone attacked the camp, especially any doctors, congratulations, you committed a war crime in which irl all forces in the area (local, military, international, even dealing w infected) would have hunted you down and imprisoned you. Except we cant regulate that kind of thing in this game, because its a game * people got pissed while real life UNs job is to protect civilians at all costs. via lore this unit was sent in to protect the researchers. CDF and VDV were supposed to work together to protect civilians. Yet no one understood or acknowledged that, so it was always the UN getting shit for things like not guarding the public, when the only reason they even had public camps was to be nice. Via the lore for this game they didn't have to do shit for civilians, they did anyways * and were eventually hunted down (I was there the whole time of this) * then the hospital itself was attacked which was a massive war crime, that ended in an extensive injuries to several people that had to go underground for nearly a month to heal physically * except they were chased to the NATO compound which was also getting the shit beaten out of it on a daily basis * when the UN did its evacuation, as expected, it was attacked and several helicopters I believe shot from the sky. Which basically means no one's gonna fucking send any more reinforcements because people decided that attacking helicopters with help and civilians was a great idea * Repeatedly being attacked over and over and over, by both individuals and groups So people are basically shooting themselves in the foot and then whining. A lot of groups have tried to do RP hubs and as you see, where are they? They're mostly nonexistent due to all of this bs.
  10. Community Opinions and the Sort

    I was at the pub, living there. In the council of people who made decisions for the overall group. We didn't leave because we wanted to, or because there was interest lost in the area. There were no firefights. Because @FieJaxon managed to diffuse the situation before it happened, or we got word of incoming and evacuated the town before we could be initiated on, several times.
  11. RogueSolace

    Good photos

    27750618_1473957912716371_6562167612586013084_n.jpg

    27867915_1473958052716357_7138071428404209255_n.jpg

    27655176_1473958202716342_3123422515717430491_n.jpg

  12. RogueSolace

    Good photo

    27540176_1473957339383095_523680386901153801_n.jpg

  13. RogueSolace

    Good photo

    27751534_1473957809383048_2786580794073071346_n.jpg

×