When sadness reeks in and you feel as if you are all by yourself, think again. That is because you are never alone. As a matter of fact, millions of microorganisms reside in our body day in and out. They are the normal flora. Our body is a world of microscopic living entities that inhabit our body without essentially causing a disease. Rather, they live in us in harmonious mutualism. Thus, our body is not ours alone. Hence, we can say we are not absolutely sterile from the moment we are born.
Typically, the body has about 1013 cells and harbors about 1014 bacteria.1 The multifarious yet specific genera of bacteria that predominate the body is referred to as the normal flora. In essence, the normal flora thrives in a host in a mutualistic lifestyle. The microbes take advantage from living stably in the body. In return, they confer benefits to the human host. For instance, their presence helps prevent other more harmful microbes from colonizing the host. Some of them biosynthesize products that the human body can use. Nevertheless, an immunocompromised host could suffer in cases when these bacteria became overwhelming in number, and thereby cause detectable harm, like infections or diseases.
Normal flora in the gut
Microbes that normally thrive in the gut are greater in density and diversity compared with those in other body parts. Nevertheless, they vary in density depending on the location in the gastrointestinal tract. For instance, the stomach harbors about 103 to 106/g of contents whereas the large bowel of the large intestine has about 109 to 1011/g of contents. The normal flora in the stomach has fewer normal microbial inhabitants due to its acidity. The ileum of the small intestine contains a moderate microbial number, i.e. 106 to 108/g of contents.1
Some of the various bacterial species of the normal gut flora includes the anaerobes, Enterococcus sp., Escherichia coli, Klebsiella sp., Lactobacillus sp., Candida sp., Streptococcus anginosus and other Streptococcus sp.. Some of these bacteria aid in the production of bile acid, vitamin K, and ammonia since they possess the necessary enzymes.
Certain normal gut bacteria can become pathogenic. They could cause a disease when opportunity presents such as when changes in their microbiota favor their growth. Be that as it may, a healthy individual would not be usually harmed by their presence. Thus, question arises — why our immune armies do not, by and large, act against the normal flora as aggressively as they would in the presence of more harmful pathogens.
Karen Guillemin, a professor of biology and one of the authors of a paper that appeared in a special edition of the journal eLife, was quoted3: “One of the major questions about how we coexist with our microbial inhabitants is why we don’t have a massive inflammatory response to the trillions of the bacteria inhabiting our guts.”
Guillemin and her team of scientists reported that they uncovered a novel anti-inflammatory bacterial protein they referred to as Aeromonas immune modulator (AimA). Accordingly, AimA is a protein produced by a common gut bacterium, Aeromonas sp., in the animal model, zebrafish. The researchers found that AimA alleviated intestinal inflammation and extended the lifespan of the zebrafish from septic shock.2 Furthermore, they described it as an immune modulator that confers benefits to both bacteria and the zebrafish host.
The newly-discovered protein seems to be the first of its kind. Nevertheless, it is structurally similar to lipocalins, a class of proteins that, in humans, modulate inflammation. Based on their findings, the removal of this protein caused more intestinal inflammation in the host and the destruction of the normal Aeromonas gut bacterium. The reintroduction of AimA reverted to “normal”, i.e. the host, relieved from inflammation and Aeromonas’ typical density, restored. AimA appears to represent a new set of bacterial effector proteins. And, Guillemin referred to them as mutualism factors.3
Guillemin and her team postulate that many more of these mutualism factors exist even in humans, and yet to be found. These mutualism factors may have therapeutic potential for use in modulating inflammation especially in medical conditions such as sepsis and certain metabolic syndromes.
— written by Maria Victoria Gonzaga
1 Davis, C. P. (1996). Normal Flora. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston. Retrieved from [link]
2 Rolig, A. S., Sweeney, E. G., Kaye, L.E., DeSantis, M. D., Perkins, A., Banse, A. V., Hamilton, M.K., & Guillemin, K. (2018). A bacterial immunomodulatory protein with lipocalin-like domains facilitates host–bacteria mutualism in larval zebrafish. eLife. [link]
3 University of Oregon. (2018, November 6). Novel anti-inflammatory bacterial protein discovered: Newly discovered protein alleviates intestinal inflammation and septic shock in an animal model. ScienceDaily. Retrieved from [link]
Porphyromonas gingivalis is a bacterium commonly associated in periodontitis a chronic inflammatory disease in the oral cavity. Periodontium is composed of periodontal ligament, cementum, alveolar bone and gingiva. Porphyromonas gingivalis is a gram-negative bacterium that contains toxic components. It is characterized by the presence of edema and destruction of tissue supporting the teeth. In which periodontal bacteria enters into circulation that leads to bacteremia and system dissemination of bacterial products. Moreover, Porphyromonas gingivalis can promotes systemic effects through expression of inflammatory mediators like pro-inflammatory cytokines. As a consequence it is confirmed to be associated with systemic diseases such as diabetes, respiratory disease and cardiovascular disease.
Potential effects of Porphyromonas gingivalis
Neurodegenerative diseases have been recognized as the major cause of cognitive and behavioral damage. It is known that peripheral infections could activate microglial cells within the nervous system enhancing development of neurodegeneration. Thus, the inflammatory molecules in the brain could be enhanced by periodontitis that increase inflammatory levels promoting the development of Alzheimer’s disease. In this particular research Porphyromonas gingivalis infection may impair cognition by elevating expression of pro-inflammatory cytokines. It is also shown that the infected mice displayed impaired memory and learning abilities. Elevated levels of pro-inflammatory mediators in the blood can lead to direct or indirect transport to the brain.
Periodontal infection caused by Porphyromonas gingivalis promotes neuro-inflammatory response via releasing pro-inflammatory cytokines. In which inflammation induces alterations in neurovascular functions causing increased in blood brain barrier permeability and aggregation of toxins. In brain trauma, infection and presence of endogenic abnormal protein aggregates can activate secretions of TNF-α. That plays a pivotal role in the development and functions of central nervous system. Moreover, aging is also associated to chronic inflammation which exerts additional stress to the brain nerve cells. Additionally, during systemic inflammation the functions of the blood-cerebrospinal fluid barrier were also significantly affected.
Therefore, Porphyromonas gingivalis periodontal infection may induce age-dependent brain inflammation. Also periodontitis can cause memory impairment which has a similar effect on the development of Alzheimer’s disease. Furthermore, aging is the major risk factor of Alzheimer’s disease and is correlated with elevated glial responsiveness. And in due course might increase the brain’s susceptibility to injury and disease.
Source: Prepared by Joan Tura from BMC Immunity and Aging
Volume 15:6, January 30, 2018
Aflatoxins produced by a certain molds that are poisonous carcinogens which grow mostly in soil, hay, decaying plants and grains. It can affect livestock and human as natural contaminants in foods like peanuts and corn meal. There are four types of aflatoxins these are B1, B2, G1 and G2 in which all are teratogenic, carcinogenic and immunosuppressive. Its toxic effect might be due to the generation of free radicals resulting into lipid peroxidation that damage biological system. On the other hand yogurt is produced from the bacterial fermentation of milk. In which bacteria produces lactic acid that acts on milk protein to give yogurt its texture and tart flavor. However, yogurt contains plenty of probiotic bacteria that offer benefits as microflora in the intestines. It also helps boost immune response and suppress carcinogenesis since fermented dairy products contain live lactic acid bacteria.
Selenium-fortified yogurt protects against aflatoxin toxicity
Yogurt has been known as therapeutic to various disorders including lactose intolerance, indigestion, intoxication, gastroenteritis, kidney, liver disorders and cancer. Selenium added to yogurt considered as the basic trace elements vital for normal growth and development in humans and animals. It also acts as anti-oxidant as well as improves nutritional values. Additionally, selenium has both enzymatic and structural functions that protect harmful reactive oxygen and minimized the production of hydrogen peroxide from aflatoxins. Ingestion of aflatoxins leads to weight loss due to the change in digestive enzymes activity that causes malabsorption of nutrients.
Aflatoxins will impair the biosynthesis of protein which results to the degranulation of the endoplasmic reticulum. It also caused liver fibrosis and poses health risk to humans and livestock. In this research , a positive results shows that selenium-fortified yogurt suppress the level of aflatoxins in rats. It also proved that with selenium contents inhibit the activity of enzymes related to carcinogenesis. Since yogurt improves intestinal mucosa and microflora that influence intestinal barrier. These yogurt bacteria inhibit the peroxidation of lipids by foraging reactive oxygen.
Therefore, consumption of nuts infected with aflatoxins caused toxicity mainly at the kidney and liver. But intake of selenium-fortified yogurt can definitely suppress against aflatoxins toxicity. In general, application of probiotic bacteria and selenium is vital and viable therapeutic approach to improve safety in food industry. Indeed, it is recommended to eat fresh nuts to avoid aflatoxins along with selenium-fortified yogurt to lessen its toxicity.
Source: Prepared by Joan Tura from BMC Agriculture and Food Security
Volume 7:21, June 2018
Amidst the battle for supremacy, our army of immune cells relentlessly wages war against various pathogens, especially superbug bacteria. Despite the pool of ample winnings, our body still experiences defeat from time to time. We succumb to diseases as the war reels its favor towards the tenacious pathogens. Of course, we cannot allow our immune defense to be utterly defeated. Otherwise, we’d be dead. As bacteria advance by taking over much space and nutrients inside our body, we get external help through antimicrobial chemicals that scientists continue to contrive. Unfortunately, antibiotic resistance has surfaced and turned certain strains of bacteria into a superbug – one that has become resistant to the effects of antibiotics.
Chemical warfare prior to the rise of a superbug
Antimicrobial chemicals, particularly antibiotics, came into existence as chemicals that were strategically designed and produced with the intent of killing pesky bacteria. In 1928, penicillin was discovered, which led to its use as the first natural antibiotic capable of undermining a spectrum of bacteria, if not by killing, by inhibiting their growth. Its role as a wonder drug against various bacteria caused Alexander Fleming to receive a duly recognition by winning a Nobel prize award for its discovery. Soon, more antibacterial agents came up to our defense. Antibiotics, such as penicillin and cephalosporin, destroy bacterial cell wall whereas polymyxins target bacterial cell membrane. Rifamycin, quinolones, sulfonamides, and the likes interfere with the enzymes essential to bacteria. Once again, we gained an upper hand.
Bacteria resisting: the rise of a superbug
While we thought we finally came up with a powerful weapon, the bacteria conjured up an amazing strategy to work in their favour — antibiotic resistance. Some of them started to morph. They evolved and mutated into new strains referred to as superbug. They became capable of resisting the drugs’ antimicrobial effects. One of their strategies is to produce β-lactamases that destroy the structure of β-lactam antibiotics (e.g. penicillin and cephalosporin). The bacteria that evolved into superbug organisms did not just live; they thrived. They multiplied and passed on to the next generation the features that could withstand a number of antibiotics.
DNA uptake by superbug bacteria
Apart from the vertical gene transfer of genes, antibiotic resistance could also be transferred through horizontal gene transfer. It is a mechanism whereby genes are taken up or transposed from one species to another, and one of the possible explanations for the rise of superbug bacteria. DNA uptake by a bacterial cell was captured for the first time in a video by a team of scientists from Indiana University. In the video1, it shows how a bacterial cell takes up DNA fragments from dead bacterial cells through its pilus. Like a harpoon, the pilus was used by the bacterium, Vibrio cholera, to catch and reel a stray DNA fragment, and then bring it inside the bacterial cell via the same pore on its cell wall. It, then, incorporates the DNA into its own genome. Accordingly, this is probably one of the mechanisms for a bacterium to turn into a superbug.
First video evidence of DNA uptake by Vibrio cholera.
(Video credit: Ankur Dalia, Indiana University, uploaded on YouTube by Group IU Biology News)
A researcher from the team, Courtney Ellison, recounted, “The size of the hole in the outer membrane is almost the exact width of a DNA helix bent in half… If there weren’t a pilus to guide it, the chance the DNA would hit the pore at just the right angle to pass into the cell is basically zero.” It appears that the pilus takes a crucial role in horizontal gene transfer. If left to chance the DNA fragment would not easily get inside the cell since the pore was too small for it to fit. Through horizontal gene transfer, those that were once sensitive to the antibiotic could later become superbug bacteria as well. As Ankur Dalia, another researcher from the same team, pointed out, “Horizontal gene transfer is an important way that antibiotic resistance moves between bacterial species….” The video that the research team captured for the first time could explain how antibiotic resistance can be acquired from one superbug bacterial species to another.
The battle is far from over. The antibiotic resistance already raised global concerns as it has rendered certain antibiotics ineffective. Pathogenic superbug bacteria have successfully armed themselves with genes that could neutralize antibiotic effects. Fortunately, scientists do not waver in determining the strategies that superbug bacteria exploit. The recent discovery of the way by which bacteria employ to make them antibiotic-resistant superbug strains could lead to better therapeutic strikes that could counter them, hopefully, with ample success.
— written by Maria Victoria Gonzaga
1 Indiana University. (2018). IU scientists watch bacteria ‘harpoon’ DNA to speed their evolution. Retrieved from https://news.iu.edu/stories/2018/06/iub/releases/11-scientists-watch-bacteria-harpoon-dna-to-speed-their-evolution.html
Leptospirosis is a corkscrew shaped that is known as one of the most widespread bacterial zoonoses in the world. Symptoms range from mild flu to severe multi-organ failure and fatal pulmonary hemorrhagic syndrome. In which the key factors of these diseases are from stray animals, poor sanitation, rodents, heavy rainfall and flooding. Many regions have been increasingly exposed to leptospirosis infection due to climate change, global warming, poverty and high urban density. Rodents are the main animal reservoir in urban settings mainly involved in pathogenic transmission. Moreover, a high prevalence in rodent population occurs in major cities such as in Baltimore, Tokyo and Copenhagen. In Italy sporadic cases of leptospirosis have been often related to river flooding. This study focused on molecular survey of rodents in the city of Palermo, Italy.
Human leptospirosis cases
Two cases in 2009 of leptospirosis in Palermo during spring and fall seasons and there were 22 locations monitored. A rodent is the main reservoir for leptospirosis related to heavy rainfall and flooding in urban streets and riverbanks. During street floods individual were potentially in contact with water contaminated by infected rodent urine. So, the risk of infection is high but because of good hygienic conditions and economic wellness severe symptoms is rare. It is also possible that periodic exposures to serovars leave the immune competent population more resistant to infection. Other cases also in Northern Italy an elderly woman has a fatal infection after river flooding occurs.
Based on molecular testing leptospirosis are positive in all species of wild rodents living in almost all areas in the city. Mice and rats are the natural source for this pathogenic infection. The main common problem in Palermo, Italy is the urban street floods from heavy rains and waste accumulation. In which the city is represented by almost ten thousand stray dogs feeding on garbage. Previously, a patient was in contact with contaminated water in street flood after violent cloudburst. Waste collection also is one of the problem in Palermo that eventually facilitates the increased of rodent population.
High prevalence of leptospirosis occurs in mild wet climate, flooding of urban streets and socio-economic problems. Other Italian cities has presence of simultaneous risk factors for leptospirosis, and thus, a major concern from this underestimated zoonosis should be considered by public health authorities and clinicians particularly for elderly and immune-compromised individuals. However, severe symptomatic cases are referred to hospitals and the true prevalence of infection is probably not evaluated.
Source: Prepared by Joan Tura from Journal of Infection and Public Health
Volume 11, Issue 2, March–April 2018, Pages 209-214
Epstein-Barr virus — the virus causing the kissing disease or mononucleosis — is eyed as a risk factor for contracting seven other major diseases. This is what the research team at Cincinnati Children’s Hospital Medical Center reported. The Epstein-Barr virus is contracted by kissing or by the oral transfer of saliva. Apparently, once the Epstein-Barr virus infects the body it stays there forever.
Epstein-Barr virus and mononucleosis
The Epstein-Barr virus belongs to the herpes family, Herpesviridae. It contains DNA that bears 85 genes and is surrounded by a nucleocapsid. Apart from the nucleocapsid, the virus is further bounded by a protein tegument and an outermost layer of a lipid envelope. The envelope has glycoprotein projections, which are crucial for the virus during its infection of the host cell.1 B cells, the immune cells producing antibodies, are ought to destroy them. However, the Epstein-Barr virus can outwit them by a slick mechanism. The virus invades the B cell, reprograms it, and makes it “follow” its “commands”. The virus is known for causing mononucleosis or the kissing disease. The common symptoms include fever, fatigue, sore throat, rash, and swollen lymph nodes, especially in the neck.
Epstein-Barr virus and the seven major diseases
According to the study led by three scientists, John Harley, Leah Kottyan, and Matthew Weirauch, the Epstein-Barr virus infection has been implicated to seven unrelated serious diseases.2 Previous studies by Dr. Harley and his team have already connected Epstein-Barr virus with the increased risk of developing systemic lupus erythematosus years ago. Recently, however, they found that the virus could also augment the risk of developing other serious diseases, such as multiple sclerosis, type 1 diabetes, inflammatory bowel disease, celiac disease, rheumatoid arthritis, and juvenile idiopathic arthritis.3 A person contracting the Epstein-Barr virus has a greater risk of developing them. This is because the virus produces a protein, Epstein–Barr virus nuclear antigen 2 (EBNA-2), that interacts with the human DNA, especially at genetic risk variants. 2 A genetic risk variant pertains to a variant in the DNA genome that has a potential to cause disease(s).
Epstein-Barr virus and future research
Dr. Harley and his team suspect that the EBNA2 protein from the Epstein-Barr affects a set of transcription factors. Accordingly, what the seven seemingly unrelated diseases share in common is a set of dysfunctional transcription factors, each affected by the EBNA2 protein.2 When the activity of transcription factors deviate from what they are supposed to do, the host cell (such as B cell) would not be able to carry out its normal function. This, in turn, could progress to certain diseases. With their recent finding, Dr. Harley and his team are optimistic that further intensive research could direct to finding better therapies and preventive methods such as vaccines against Epstein-Barr virus infection.
This recent finding suggests that contracting Epstein-Barr virus can lead to multiple diseases apart from mononucleosis. Therefore, this calls for more studies that aim at finding better cures and preventive measures. Currently, there is no vaccine against Epstein-Barr virus; being able to boost our immunity against the virus may help mitigate the risk to many other diseases, such as those mentioned above.
— written by Maria Victoria Gonzaga
1Odumade, O.A., Hogquist, K.A., & Balfour Jr., H.H. (2011). “Progress and Problems in Understanding and Managing Primary Epstein–Barr Virus Infections”. American Society for Microbiology. 24 (1): 193–209. doi:10.1128/CMR.00044-10
2 Harley, J.B., Chen, X., Pujato, M., Miller, D., Maddox, A., Forney, C., Magnusen, A.F., Lynch, A., Chetal, K., Yukawa, M., Barski, A., Salomonis, N., Kaufman, K.M., Kottyan, L.C., & Weirauch, M.T. (2018). “Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity.” Nature Genetics. DOI: 10.1038/s41588-018-0102-3
3 Cincinnati Children’s Hospital Medical Center. (2018). ‘Mono’ Virus Linked to Seven Serious Diseases. Retrieved from https://www.cincinnatichildrens.org/news/release/2018/mono-virus.
Based on new updates about E.coli outbreaks the CDC extends its warning to include all types of romaine lettuce. It avoids consumers to eat romaine lettuce growing from Yuma, Arizona. And discourage the consumer to buy at grocery store unless proven that it is not come from the same region. Mostly the packaging of the romaine lettuce does not indicate the growing regions. So it encourages consumers to throw away the romaine lettuce even if symptoms of E.coli infections did not occur. Restaurant also prevented to serve any salads containing romaine lettuce that came from Yuma, Arizona. Also the retailers not allowed selling any of it that came from the region.
What is E.coli?
E.coli is a gram-negative coliform bacterium that is facultatively anaerobic. It is enteric bacteria not normally thrive in the intestine of animals and human. Most E.coli strains are harmless and part of normal flora in the gut that offers benefits to the host. By producing vitamin K and preventing any pathogenic bacteria through symbiotic relationships. But some of its strain is harmful like E.coli 0157:H7 that cause serious illnesses. Like gastroenteritis, hemorrhagic colitis and urinary tract infections. The usual symptoms and sign of infections include diarrhea, abdominal cramps, vomiting and fever. Most likely children are more susceptible to infections that develop severe illnesses. This E.coli 0157:H7 produced shiga toxin that caused premature destruction of red blood cells which damaged the kidneys.
What went before?
E.coli outbreaks have sickened at least 53 people in 16 states according to the CDC. Last March 13, 2018 reported to have 31 people hospitalized since the onset of the outbreaks. Five people developed kidney failure but no death have been recorded. No recalls have been made because the CDC could not identify the specific grower that is responsible for the outbreaks. But official released a statement for the consumer to throw away all romaine lettuce even if sickness didn’t appear.
The outbreaks dates started from March 22, 2018 to March 31, 2018. On April 10, 2018, 18 more people from 9 states were added to this outbreak. As of April 12, 2018, another 35 people infected of E.coli 0157:H7 have been reported from 11 states. So far, Pennsylvania has the highest cases of infection followed by Idaho. Health officials advice consumers to avoid buying romaine lettuce up to date unless source known not come from Yuma, Arizona. Additionally, more hospitalization has been reported and in past few days more new cases added to CDC investigation.
Source: Prepared by Joan Tura from Center for Disease Control and Prevention
Honey is a viscous sweet substance produced by bees from the secretions of plant nectars. It is a product from some regions of Mexico as a sugar supplement and for therapeutic purposes. Honey contains fructose and glucose with low level of water activity and high osmotic potential in humidity. In Mexico apiculture contains high economic and social value wherein forty five thousand producers depend on it. That accounts for almost 19 million beehives placing Mexico as the fifth producing and third exporting country in the world. Microbial characteristics of honey are the built-in biota of bees from the nectar of different flowers that kept overtime. This particular research study evaluates the microbial community of honey produced in Mexico.
Microbial Biota of Honey
Microbial contamination of honey occurs during extraction and handling including dust, air, dirt, flowers and digestive tract of honey bees. Microorganisms commonly found include Bacillus spp., Clostridium spp., Corynebacterium spp., Pseudomonas spp. and some bacteria found in sugars and plants. The official standard in Mexico stated that no more than 1000 CFU/g of non-pathogenic bacteria and 100 CFU/g of molds and yeast are acceptable. Since Mexico is one of the main honey producers that comprised at least 86 thousand tons to be exported.
The study reveals that out of 1,920 samples of honey 40.5% exceeded the limits permitted by the regulatory board. For the yeast and molds 18.1% and 17% of the samples showed more than 100 CFU/g respectively. With regard to Clostridium 12% the samples contained more than 100 CFU/g due to the bees contamination, nectar and external sources. There have been observations also that bee gut contains 27% gram positive bacteria including several species of Clostridium. Although honey has high osmolarity and low water activity yet development of microorganisms found on several sources. However, microbial contamination caused by handlers, equipment and crossed contamination can be controlled by standard sanitation and good manufacturing practices.
Since it reveals that over 40% from the samples did not complies specification for the presence of aerobic mesophilic bacteria. It gives emphasis to local producers the proper handling and minimizing the sources of contamination so it can fit the standard. If honey is used for therapeutic purposes better quality is vital and fulfills quality parameters to remove pathogens. Mexican honey of great percentage has been exported that is why maintaining good hygienic practices during manufacturing is very important.
Sources: Prepared by Joan Tura from Revista Argentina de Microbiología
Volume 50, Issue 1 January–March 2018, Pages 75-80
Zika virus is mainly spread by mosquitoes particularly female that is active during daytime to feed blood in order to lay eggs. This Zika virus when contact with human infects epidermal cells following the lymph nodes down to the bloodstream. Pathogenesis of this virus is similar to dengue fever showing symptoms like fever, joint pain, red eyes and skin rashes. Diagnosis of Zika virus is through blood test, urine or saliva test. Many countries have been affected by this virus which leads to some deaths.That is why this particular research came about to know the important tool to confirmed the etiology of this disease.
Zika virus Infection
Infection of Zika virus is normally established through serum test in order to detect viral nucleic acid. Diagnostic test of this virus have limitations that is why comparing the sensitivity and specificity on different tools is important to get reliable results. Accuracy of any diagnostic method is vital since Zika virus represent public health concern that has been usually misdiagnosed. Results of the study reveal that Zika virus is highly detected in urine and semen.
The Zika virus strains circulating worldwide has low viremia period that is why it compromise diagnostic accuracy. Laboratory examination rely only upon detection of virus RNA through body fluids including serum, plasma and amniotic fluid. Because detection of RNA in blood is usually low on third to fourth day after the onset of disease. That is why it is very important to further characterize the virus dynamics in blood. Whether increase level of virus in is correlated with the severity of the disease or due to immune responses.
Indeed, further developments is needed to reduce the limitations of current diagnostic test. Evaluation and thorough examination for widespread implementation is significant for Zika virus to test accurately. Furthermore, crucial monitoring and preventive action is important to treat Zika fever. Hence, better assay is needed to enhanced diagnosis and surveillance of this virus.
Source: Prepared by Joan Tura from the Brazilian Journal of Microbiology
Volume 49, Issue 1, January–March 2018, Pages 144-147
It came as a surprise to me recently to realize how much is known about the immune responses of plants and, moreover, how much there is to know. There is, I found, detailed molecular information about how our botanical cousins defend themselves against the onslaught of infectious agents. Perhaps most surprising is that plants and animals share basic mechanisms of immunity. Here I am referring to innate immunity, being that plants — like the invertebrates — do not have the adaptive immunity of vertebrates. Did these arise before the two realms diverged about one billion years ago? Or, alternatively, are they the result of convergent evolution? (more…)