Carlos Alberto Orozco Flores
Andrea Wong Ortiz
Alisson Coral luna Gris
Home is where the microbes are, millions and millions of microbes. Every single household has a different microbial community, and every time we pack up our stuff and move someplace else, our microbiological auras move too, according to a study published in Science this week. These microbes can populate new homes within just a single day.
“We know that certain bacteria can make it easier for mice to put on weight, for example, and that others influence brain development,” says Jack Gilbert at Argonne National Laboratory in a news release. “We want to know where these bacteria come from, and as people spend more and more time indoors, we wanted to map out the microbes that live in our homes and the likelihood that they will settle on us.”
Gilbert and colleagues from the Home Microbiome Project studied seven families—that’s 18 people, three dogs, and one cat—and their homes over the course of six weeks. The researchers collected daily swabs and sequenced the genomes of bacteria colonizing the skin of each family member, pet, and household surface—from doorknobs and light switches to countertops and floors.
The researchers identified 4 million DNA sequences and 21,997 distinct genomes (or operational taxonomic units, OTUs) from 1,586 different samples. Not surprisingly, the microbial communities on hands, feet, and noses reflected those on the home surfaces: Doorknobs looked like hands and floors looked like feet, microbially speaking. Homes with indoor-outdoor dogs or cats had more plant and soil bacteria.
By tracking the transfer of OTUs, the team found that people act as sources of bacteria more often than household surfaces. In one case, the potentially pathogenic Enterobacter first appeared on a person’s hands, then the kitchen counter, and then another person’s hand.
And it all happens fast. When someone leaves the house for a few days, that person’s aura quickly diminishes. And when three of the families moved to a different house or apartment—including one family that moved from a hotel room to a house—it took less than a day for the microbial signature of the new abode to look just like that of the old digs.
“People always say, ‘Ewwwww, someone else was in this room and it has their microbes all over it.’ That’s irrelevant,” Gilbert tells National Geographic. “You are constantly overwriting the microbes in the world around you with your own.”
Compared to other people, those living in the same home have more microbes in common with each other: Roommates share some, couples share more, and parents with young children share the most. However, individuals do have somewhat unique microbial signatures, no matter where we move, inside our noses.
Home microbiome signatures might one day be used as a forensic tool to catch criminals. Given an unidentified sample from a floor in this study, “we could easily predict which family it came from,” Gilbert says. And theoretically, he tells New Scientist, the technique could detect a new relationship or uncover a cheating partner.
Our Microbial Auras Follow Us Everywhere We Go. (n.d.). Retrieved August 31, 2014, from http://www.iflscience.com/health-and-medicine/our-microbial-auras-follow-us-everywhere-we-go#yIexFwmfI4bu7TyZ.99
HIV stands for Human Immunodeficiency Virus.
It is a virus that attacks the human immune system. Someone infected with the virus can live with HIV or be HIV positive for many years without becoming ill or showing symptoms. During this time however, HIV remains in the body damaging the immune system and the person remains infectious; able to spread the virus to others if a few simple precautions are not follwed.
A vaccine has been found that blocks the monkey equivalent of HIV. The discovery works in the opposite way to normal vaccines, but its relatively simple structure may lead to an effective oral vaccine for humans.
Simian immunodeficiency viruses (SIVs) are close relatives of HIV which infect various non-human primates, such as chimpanzees and sooty mangabeys. Unlike HIV, these viruses do not usually cause disease in their hosts; however, rhesus macaques are vulnerable to SIV and develop a disease that is pathologically similar to humans infected with HIV. These monkeys are therefore a useful model for HIV/AIDS research.
In both rhesus monkeys and humans, the virus predominantly infects and replicates inside cells of the immune system, in particular a type of white blood cell called a CD4+ T cell. These cells are normally a crucial part of our resistance to disease and thus their depletion leaves infected individuals susceptible to infections with other pathogens.
Macaques given the new vaccine produce a previously unknown type of regulatory CD8 white blood cell that prevents infected CD4 cells from becoming activated. Since resting (non-activated) CD4 cells are largely non-permissive for viral replication, this failure to activate blocked SIV from being able to make new viral particles. Subsequently, the monkeys were protected from a challenge infection with SIV.
The vaccine involved a combination of inactivated SIV and bacteria. The first trials used BCG, often used as a vaccine against tuberculosis. However, researchers at Paris-Descartes University replicated the effect with gut bacteria used in probiotic supplements—if the same technique works in humans you might get your cravings for unhealthy food fixed at the same time as being protected against infection.
Trials are being planned to see if people without HIV have the same immune response. A more advanced trial would see HIV infected individuals undergoing treatment given the vaccine. If their response suggests the vaccine is working then they could be taken off antiretroviral treatment to see if the virus remains suppressed.
Jean-Marie Andrieu, lead author of the Frontiers in Immunology paper that announced the finding, says the idea of suppressing a response to HIV—rather than stimulating it as most vaccines do—is an old one. However, no one expected it to work so well after other paths either failed or were too expensive for widespread use.
BCG was chosen because it is known to bind to dendritic cells infected by HIV, while the immune system recognizes gut bacteria as not being a threat and avoids attacking them. It seems that either acted as a passport for the inactivated SIV.
Of the 29 monkeys given the vaccine, 15 appear to have complete and long-lasting protection against SIV. Oral administration, besides being much easier, appears to be more effective than vaginal or rectal application. Injections had the least success.
When the macaques were given an antibody to the CD8 cells their protection disappeared, but encouragingly, it returned when the antibodies were withdrawn.
If the same pattern is seen in humans, the vaccine would not only stop people getting HIV, but could work as therapy for those already infected.
Read more at http://www.iflscience.com/health-and-medicine/%E2%80%9Csurprising%E2%80%9D-oral-vaccine-stops-hiv-monkeys#Tx7evLoDxl3YF9UX.99
What Is HIV? (n.d.). Retrieved August 31, 2014, from http://www.can.org.au/Pages/HIV/What_is_HIV_.aspx
Growing living tissue and organs in the lab would be a life-saving trick. But replicating the complexity of an organ, by growing different types of cells in precisely the right arrangement—muscle held together with connective tissue and threaded with blood vessels, for example—is currently impossible. Researchers at MIT have taken a step toward this goal by coming up with a way to make “building blocks” containing different kinds of tissue that can be put together.
The team first puts embryoid bodies into microscale wells, which causes the cells to clump together to form spheres. Next they pour a light-sensitive hydrogel solution over the top of the cells. When this solution is exposed to light, it hardens, leaving behind a sphere of cells, half naked, half encased in a cube of gel. The process is repeated to encase the other half in a second type of gel. The result is a hydrogel block, half gelatin, half polyethylene glycol, with a sphere of embryonic stem cells inside.
Freeman, D. (2014, August 25). Scientists Create Working Organ From Scratch For First Time Ever. Retrieved September 1, 2014, from http://www.huffingtonpost.com/2014/08/25/organ-thymus-embryonic-cells-video_n_5709981.htm
Scientists have identified the developmental on-off switch for Streptomyces, a group of soil microbes that produce more than two-thirds of the world’s naturally derived antibiotic medicines.
Their hope now would be to see whether it is possible to manipulate this switch to make nature’s antibiotic factory more efficient.
The study, appearing August 28 in Cell, found that a unique interaction between a small molecule called cyclic-di-GMP and a larger protein called BldD ultimately controls whether a bacterium spends its time in a vegetative state or gets busy making antibiotics.
Researchers found that the small molecule assembles into a sort of molecular glue, connecting two copies of BldD as a cohesive unit that can regulate development in the Gram-positive bacteria Streptomyces.
“For decades, scientists have been wondering what flips the developmental switch in Streptomyces to turn off normal growth and to begin the unusual process of multicellular differentiation in which it generates antibiotics,” said Maria A. Schumacher, Ph.D., an associate professor of biochemistry at the Duke University School of Medicine. “Now we not only know that cyclic-di-GMP is responsible, but we also know exactly how it interacts with the protein BldD to activate its function.”
Streptomyces has a complex life cycle with two distinct phases: the dividing, vegetative phase and a distinct phase in which the bacteria form a network of thread-like filaments to chew up organic debris and churn out antibiotics and other metabolites. At the end of this second phase, the bacteria form filamentous branches that extend into the air to create spiraling towers of spores.
Small molecule acts as on-off switch for nature’s antibiotic factory. (n.d.). Retrieved August 31 , 2014, from http://www.biologynews.net/archives/2014/08/28/small_molecule_acts_as_onoff_switch_for_natures_antibiotic_factory.html
In an unexpected twist, a family of proteins that have been found to promote HIV-1 entry into cells also potently block viral release. Interestingly, these proteins were also found to inhibit the release of other viruses, including Ebola virus. These intriguing new findings provide us with novel insights into both viral infection and the development of AIDS, which could ultimately lead to new antiviral strategies. The study has been published in Proceedings of the National Academy of Sciences.
Viruses are unable to replicate by themselves and thus must hijack a host cell’s machinery in order to do so. To get inside host cells, HIV, or human immunodeficiency virus, needs to bind to receptors found on target cells. This triggers a series of events that ultimately lead to viral entry; once inside, HIV converts the cell into a factory for making more viruses.
Recent studies have identified a family of proteins, called TIM proteins, which play critical roles in facilitating the entry of various viruses including Ebola, West Nile and dengue viruses. Intriguingly, University of Missouri researchers have now discovered that these proteins not only promote HIV-1 entry into host cells, but they also prevent viral release.
For the study, scientists investigated the interactions between HIV-1 and TIM proteins using various molecular, biochemical and microscopic techniques. They found that as HIV-1 begins to bud from, or escape, the host cell, TIM proteins become incorporated into the virions and tether the particles to the cellular membrane. This is mediated through interactions with a lipid called phosphatidylserine (PS) that is found both on the cell membrane and the outside of the virus particles. Usually, PS is expressed on the inside of the cell, but viral infection causes it to flip to the outside, meaning that both PS and TIM are now present on the cell and viral surface. TIM and PS then bind to one another as HIV-1 attempts to escape from the cell, causing the particles to be retained at the cell surface.
Interestingly, the team also discovered that TIM proteins inhibited the release of other viruses including a mouse virus belonging to the same family as HIV (murine leukemia virus), and also Ebola virus.
While these discoveries extend our understanding of viral infection, lead researcher Shan-Lu Liu points out that it is not clear at this stage whether HIV’s interaction with TIM proteins is a positive or negative factor. “However, this discovery furthers our ultimate goal of understanding the biology of TIM-family proteins and potentially developing applications for future antivirus therapies,” he says.