Researchers have recognized a fungus which can damage down plastics. The species could be a beneficial device as we strive to lessen the impact of waste fabric at the surroundings.
Researchers at the Chinese Academy of Sciences’ Kunming Institute of Botany have discovered a fungus that could doubtlessly assist us to deal with the trouble of non-biodegradable plastics. The fungus is ready to break down waste plastics in a depend on weeks that might in any other case persist in the environment for years.
Aspergillus tubingensis is commonly observed in soil, however, the have a look at observed that it is able to additionally thrive at the surface of plastics. It secretes enzymes which smash down the bonds between person molecules after which use its mycelia to break them aside.
Scientists at the University of York have harnessed the therapeutic effects of carbon monoxide-releasing molecules to develop a new antibiotic which could be used to treat the sexually transmitted infection gonorrhoea.
The infection, which is caused by the bacteria Neisseria gonorrhoeae, has developed a highly drug-resistant strain in recent years with new cases reported in the north of England and Japan.
There are concerns that gonorrhoea, which is the second most common sexually transmitted infection in England, is becoming untreatable.
Almost 35,000 cases were reported in England during 2014, with most cases affecting young men and women under the age of 25. The interdisciplinary team, from the University of York's Departments of Biology and Chemistry, targeted the "engine room" of the bacteria using carbon monoxide-releasing molecules (CO-RMs).
CO is produced naturally in the body, but there is increasing evidence that carbon monoxide enhances antibiotic action with huge potential for treating bacterial infections.
The scientists found that Neisseria gonorrhoeae is more sensitive to CO-based toxicity than other model bacterial pathogens, and may serve as a viable candidate for antimicrobial therapy using CO-RMs.
The CO molecule works by binding to the bacteria, preventing them from producing energy.
Scientists believe the breakthrough, published in the journal MedChemComm, could pave the way for new treatments.
Professor Ian Fairlamb, from the University's Department of Chemistry, said: "The carbon monoxide molecule targets the engine room, stopping the bacteria from respiring. Gonorrhoea only has one enzyme that needs inhibiting and then it can't respire oxygen and it dies.
"People will be well aware that CO is a toxic molecule but that is at high concentrations. Here we are using very low concentrations which we know the bacteria are sensitive to.
"We are looking at a molecule that can be released in a safe and controlled way to where it is needed."
The team say the next stage is to develop a drug, either in the form of a pill or cream, so that the fundamental research findings can be translated on to future clinical trials.
Professor Fairlamb added: "We think our study is an important breakthrough. It isn't the final drug yet but it is pretty close to it." "People might perceive gonorrhoea as a trivial bacterial infection, but the disease is becoming more dangerous and resistant to antibiotics."
The team worked with Professor James Moir from the University's Department of Biology. He added: "Antimicrobial resistance is a massive global problem which isn't going away. We need to use many different approaches, and the development of new drugs using bioinorganic chemistry is one crucial way we can tackle this problem, to control important bacterial pathogens before the current therapies stop working."
Chalita Suansane is a 21 year old Thailand native currently studying Microbiology at Mahasarakham University. Ever since Suansane was young, she was often curious and eager to learn new things, including a passion to explore living organisms that you cannot see by the eyes. On top of her studies, Suansane volunteers at ‘Baan Home Hug’ which is an orphanage that houses children who have inherited HIV from their parents, children who were abused, and children who have lost their family. If crowned, she would like to raise awareness and advocate for HIV/AIDS. Suansane would also like to let young women know that fulfilling your own passions, having self-respect, and being compassionate to others will make you confidently beautiful in your own way.
Most adults carry multiple herpesviruses. Following the initial acute infection, these viruses establish life-long infections in their hosts and cause cold sores, keratitis, genital herpes, shingles, infectious mononucleosis, and other diseases. Some herpesviruses can cause cancer in man. During the latent phase of infection, the viruses remain dormant for long periods of time, but retain the capacity to cause occasional reactivations, that may lead to disease. A study published on June 30th in PLOS Pathogens suggests that attacking herpesvirus DNA with CRISPR/Cas9 genome editing technology can suppress virus replication and, in some cases, lead to elimination of the virus.
The CRISPR/Cas9 system targets specific DNA sequences and induces clean cuts across both strands of the DNA. In mammalian cells, such cuts are flagged and quickly repaired by an emergency repair system called NHEJ (for non-homologous end-joining). NHEJ is efficient but not very accurate and often results in insertion or deletion of a few DNA bases at the repair site. Because DNA is read in codons of three bases at a time, such small changes in critical positions often destroy the function of the respective gene and its protein product.
Robert Jan Lebbink, from the University Medical Center in Utrecht, The Netherlands, and colleagues reasoned that CRISPR/Cas9 could target and mutate latent herpesvirus DNA in infected human cells and so potentially prevent herpesvirus-associated diseases. To test this, the researchers devised specific guide (g)RNAs—sequences that are complementary to vital parts of the viral genome and function as 'molecular addresses'. These gRNAs, combined with the 'molecular scissors' part of the CRISPR/Cas9 system, should induce specific cuts and subsequent mutations in the herpesvirus DNA, and so cripple the viruses.
In their systematic approach, the researchers looked at three different members of the herpesvirus group: herpes simplex virus type 1 (HSV-1) causing cold sores and herpes keratitis; human cytomegalovirus (HCMV), the most common viral cause of birth defects (when the virus is transmitted from mother to fetus); and Epstein-Barr virus (EBV) causing infectious mononucleosis and multiple types of cancer.
Working with lymphoma cells latently infected with EBV, the researchers showed that introduction of gRNAs that target specific EBV DNA sequences can introduce mutations at the targeted sites. Such mutations can eliminate essential functions of the virus as well as de-stabilize the viral DNA molecules. Consistent with this, the researchers report that by using two different gRNAs targeting an essential EBV gene, they can induce loss of over 95% of EBV genomes from the host cells.
During latent infection, HCMV genomes exist as circular DNA molecules in the nucleus of host cells. Upon virus reactivation, HCMV replication proceeds slowly. With appropriate gRNAs, the researchers found that CRISPR/Cas9 editing can efficiently impair HCMV replication. However, they also observed emergence of escape variants that bypass CRISPR/Cas9 editing, suggesting that simultaneous editing at multiple critical sites in the HCMV genome is necessary to avoid the development of resistant genomes.
Compared to HCMV, HSV-1 multiplies much faster. When the researchers tested various gRNAs targeting different essential HSV-1 genes in conjunction with CRISPR/Cas9, they found that many of them were able to reduce virus replication. When they combined two of those gRNAs, thereby simultaneously targeting two essential genes, they were able to completely suppress HSV-1 replication. On the other hand, they were unable to induce editing during the latent phase, i.e. when the viral DNA was not actively multiplying.
"We observed highly efficient and specific clearance of EBV from latently infected tumor cells and impairment of HSV-1 and HCMV replication in human cells", the researchers summarize. They go on to say, "although CRISPR/Cas9 was inefficient at directing genome engineering of quiescent HSV-1, virus replication upon reactivation of quiescent HSV-1 was efficiently abrogated using anti-HSV-1 gRNAs". Their results, they hope, "may allow the design of effective therapeutic strategies to target human herpesviruses during both latent and productive infections."
Author: Heather Buschman, PhD