C. elegans Gives Hope to Overcoming Obesity Epidemic

 

Scientists at the University of Virginia have recently identified 17 genes associated with obesity. High calorie diets covered in high-fructose corn syrup and sugar drive our obesity epidemic. Genes also play a major role in obesity by determining how our bodies metabolize food for energy. Hundreds of genes associated with obesity have been identified by genomicists, but the specific genes that cause or prevent obesity are unknown. O'Rouke and her colleagues studied C. elegans which share more than 70% of their genes with humans. These worms have been used to decipher how common drugs work. The team fed some worms a regular diet and some were fed a high-fructose diet. They screen 293 genes associated with obesity. From their obesity model, they identified 14 genes that can cause obesity and 3 genes that can prevent it. They discovered blocking 3 genes that prevented the worms from becoming obese led them to have better neuro-locomotory function and live longer. In lab mice, blocking one of the genes prevented weight gain, lowered blood sugar levels and improved sensitivity to insulin. This gives hope to anti-obesity therapies to reduce the obesity epidemic. 

Hopefully in the near future these discoveries can be implemented in humans. Worms, which seem completely different from humans, provide essential information about our own DNA. More than 40% of Americans are affected by obesity, so these findings are a huge step forward in helping this problem.

New Discovery In HSV Research

Herpes simplex virus (HSV) is an infectious disease that lasts forever if you get it. Like chicken pox, it is a virus that an extremely significant population of the world (two thirds of the world are infected with HSV1) gets at some point in their life. Again, like chickenpox, when you are initially infected with the virus that causes HSV, you normally get symptoms (like cold sores, lesions, serious eye conditions). However, after the initial symptoms subside, you are still infected with the virus, it just remains dormant in your body- meaning you still have the virus in your body, but you show no symptoms of it.

HSV has been much of a mystery to scientists since its’ discovery, however, there has been recent progress by NIH and Princeton scientists with this virus. They have identified a new HCF-1 protein complex that plays an additional role in initiating viral infection and reactivation. They found that- in mice- they could reactivate latent HSV by using compounds of these HCF-1 protein complexes. This is important because this research means that we can potentially reveal additional targets for the development of new therapeutics. In other words, with these new and continuing discoveries, we can hopefully minimize the spread of not only HSV itself, but also figure out better ways to keep the virus dormant (so that symptoms don’t ever occur if you are infected) since that would also help decrease the spread of the virus.

https://www.sciencedaily.com/releases/2017/04/170412132354.htm

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC136956/

Mutated Strain of Ebola is More Deadly

Ebola outbreaks happened throughout multiple areas, but the most deadly one was the outbreak within West Africa in 2014.  There were 11,310 victims.  Researchers now believe that they have identified the reason for this flare-up of victims.  Two different groups of researchers studied this problem and reached the same conclusion.  The original Ebola strain mutated and caused the virus to be able to enter human cells more easily than before.  The exact mechanisms of the mutated virus are unknown and new research needs to be conducted on that, but the same conclusion can still be reached; people with the mutated virus have a higher risk of death.

Viruses are known to mutate at a high rate, and Ebola is no different.  But this specific mutation, the GPA82V mutation, caused a lot more harm than most.  This mutation had not died out in areas where the original strain had.  GPA82V mutation is believed to change the gene that codes for Ebola's glycoproteins.  This causes the entrance into human cells to be much easier.  

When the mutated strain was injected into primates and bats, there was an increase in the amount of cells infected.  The mutated strain killed four times as many.  On the contrary, when the more harmful strain was injected into both cats and dogs, no effect was seen.  Scientists believe that the mutated strain originated in bats and that it only effects certain species.  Since primates are very closely related to humans, it is concluded that the mutated strain would impact us in basically the same way.  Research shows that it does effect humans equivalently, but not enough data was obtained to have a clear conclusion.  This article is very startling.  If this mutated strain cannot be understood and stopped, it can easily spread to regions throughout the world.  The strain mutated fairly quickly since the initial outbreak of Ebola and deadlier strains can emerge soon.  

H.I.V. Arrived in the U.S. Long Before ‘Patient Zero’

There is a legend that Patient Zero, Gaetan Dugas, a French Canadian flight attendant supposedly picked up H.I.V. in Haiti or Africa and spread it to many men before he died in 1984. He is also sometimes blamed for almost all AIDS cases in the United Sates, from Zaire to Haiti to New York in 1969-1971. A new genetic analysis of blood samples that were stored declared that Dugas is innocent. The analysis showed that Digas’s blood that was sampled in 1983 contained a viral strain that was already infecting men in New York before he went to gay bars in New York in 1974.  Dugas was originally the focal point of the epidemic because he kept a diary about his travels and he gave names to investigators. The researchers also reflected on the fact that they originally believed that the epidemic could be blamed on just one person, but now looking at it, it seems like it is not plausible because the epidemic was too widespread in Africa.

            Dr. Jacques Pepin is an infectious disease specialist at the University of Sherbrooke in Quebec showed that H.I.V. was carried from Kinshasa to Haiti in the 1960s. It was probably carried by one the Haitian civil servants that was recruited by the United Nations to work in the Beglian Congo. He also explained that Haiti was a sex-tourism destination for gay men, which is another way that the virus could have travelled to New York. More blood samples that were stored away in 19798 and 1979 from New York and San Francisco were analyzed. They showed that all of the New York samples all derive from one Haitian strain and the San Francisco strain were so closely related that they probably both derived from one person, or multiple people introducing the strain in New York. The myth of patient zero is being put to an end because of the new genetic studies that have been under analysis. Before reading this article I was confused on who Patient Zero actually was, and it came to a surprise that it was all blamed on one person, because as mentioned above, the researchers on this case thought that was absurd as well. It is crazy to think that the researchers are coming across this information now after so much time has passed after the discovery of H.I.V. and after publishing all of the data that they already had about Patient Zero. 

Bacteria Resistant to Last Resort Antiobiotics

Antibiotics, super drugs of our age, have been suddenly decreasing in effectiveness around the world, as bacteria continue to adapt. Earlier this month, scientists in South China have identified enterobacteriaceae, found in pigs and humans, containing a powerful gene resistant to last-resort antibiotics. This mcr-1 gene gives bacteria a successful resistance to polymyxins (colistin and polymyxin B). Mcr-1 was once identified on a bacterium's single chromosome from a mutation. Now, the gene is located on bacterial plasmid, which is circular DNA more easily transmitted from bacteria through conjugation. Consequently, resistance to polymyxins and other antibiotics is rapidly increasing.  

Experiments and research show bacteria with this resistance originated in animals, pigs to be exact, but now are effecting humans as well. Animal feed contains strong antibiotics for product preservation and animal health. This exposure of antibiotics has promoted bacterial resistance in pigs, as bacteria develop and adapt to survive. The same enterobacteriaceae are now effecting people in China. This could cause widespread epidemic, and no drug could stop the bacteria from affecting massive population around the globe. 

Bacterial resistance to antibiotics is a major concern. Dr. Bruce Hirsch, an infectious disease specialist, sums up our responsibility to prevent major crisis and antibiotic resistance. He states, "If you don't need antibiotics, don't take them…you are only giving bacteria more practice." Let us be wise. 

Original Article: New Gene for Antibiotic Resistance

Other Article: Experiment

Close Isn't Always Good

Ever heard of the word myopia? If you aren’t able to read this text from a distance, chances are you have it. The curse of nearsightedness is currently plaguing humans as a whole. In the past 30 years, cases of myopia in children have risen from 25% to 44%. In some parts of the world the numbers have hit 80%.

Until recently, the cause of myopia was widely thought to be environmental factors like profusely reading or using cell phones. So then why would this ever pertain to genetics you might ask? Recent discoveries in this field of study show that only 30% of the cause of myopia is environmental factors leaving a 70% contribution from the genetics of an individual. Those carrying a variant of the gene APLP2 are five times more likely to develop myopia if they profusely read or use cell phones. (Other technology also counts) Educating parents seems to be the only way to see these numbers drop in the future. Dr. Tkatchenko was quoted saying, “the critical period for myopia development is during elementary and middle school, so when kids are in school, make sure they also spend at least two hours outdoors each day.”

Anyone wanting a more in depth explanation of this phenomenon can watch this video!

A New Strain of Ebola Discovered

 

     On November 7, 2014, in the Democratic Republic of Congo, a new strain of the Ebola virus was found.  Although this strain is not the same strain found previously in Central Africa, it does however display the rapidness this virus can emerge, and ultimately spread.  Researchers incollaboration with WHO experts, such as IRD, the Institut Pasteus, the CRNS, the CIRMF in Gabon and the INRB in the Democratic Republic of Congo.  The CIRMF has performed whole genome sequencing of the virus responsible using a high-throughput sequencerthat is unique to Sub-Saharan Africa.  Ultimately, this finding confimrs that these two strains are not related but however are two strains of Ebola. Moreover, it is said that the Congolese strain is very similar to those that "ravaged" in the DRC and Gabon between 1995-1997.

     These results display that the Congolese outbreak is due to a local viral strain, which has ultimately been controlled.  This epidemic occurred on July 26, 2014 when a woman became ill after encountering a dead monkey in the forest where she then cut the monkey opened.  There have been 70 cases have been confirmed, which included 42 deaths awith a fatality rate of 60%.  Due to the Congolese health authorities isolating patients, protecting the medical staff, instructing the populations to avoid all body contact, the epidemic appears to be contained in Central Africa. 

     I found this article to be interesting and informative.  I was not aware of the finding of a new strain of Ebola, that is unrelated to the strain found in West Africa.  The discovery of a new strain of Ebola is extremely imperative to the health and medical field as well as research because it can be understood the rapid alternation of genes and growth this epidemic may have.  Hopefully, in the near future, this epidemic can be understood and isolated. 

Main article: http://www.sciencedaily.com/releases/2014/11/141107111003.htm

Scientists Shed More Light on Ebola Virus Through Experimentation on Mice

          There is a laboratory located in Hamilton, MT which is said to be one of the safest in America. This is the location where Scientist are trying to dismantle the problem of Ebola. Through experimentation with Ebola-infected mice, it has been discovered that the host genes play an important role in deciding if the virus is fatal or not. What does this mean? In some people the virus could actually be restricted, saving the lives of who are infected.

                                          From: http://www.bbc.com/news/world-africa-28749615
       
           The Ebola virus deals immensely with the genetics behind the host it deals with, not necessarily due to the virus itself. Some of the infected people suffer from bleeding, shock, and some resist the virus entirely. After implementing the virus into the mice, the scientists found that 19% of them were not infected at all meaning there was no major sign of physical deterioration, they looked "normal". Less than half of the group of mice died, with 11% showing partial resistance. However, their was 70% that were severely infected. Many suffered from liver inflammation, loss of blood, swollen spleens, and many more symptoms.

         The conclusions the scientists came to were astonishing. The severity of Ebola infection was directly correlated to their specific gene patterns.The mice were a specific inbred of mice that had been developed to study influenza and were replicated in order to study the Ebola virus. I feel this experiment needs more studies done on it. Those mice could have built up an immunity from the previous side effects of the influenza virus. However, this experiment is definitely on the right track in solving this epidemic, which is adamant in Africa.
Article: http://www.medicalnewstoday.com/articles/284708.php
Related Article: http://jid.oxfordjournals.org/content/178/3/651.short