The Global Fool

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Prenatal Exposure to Pollutants: Influence on the Immune Response
Nov30

Prenatal Exposure to Pollutants: Influence on the Immune Response

By Roberta Attanasio The development of the immune system during fetal and neonatal life is negatively influenced by exposure to toxic chemicals, resulting in compromised immune function later in life. An example is fetal exposure to arsenic, which has deleterious effects on the immune response to influenza virus infection in adulthood. Now, results from a new study provide additional evidence for the role that exposure to toxic chemicals early in life plays in shaping the immune response to the influenza virus.   The study (by researchers at the University of Rochester) focused on a mouse model and the chemical 2,3,7,8-tetrachlordibenzo-p-dioxin, or TCDD for short. TCDD, a known carcinogen, is a persistent environmental contaminant usually present in a complex mixture of dioxin-like compounds. It’s a by-product of industrial processes such as pesticide and metal production, waste incineration and wood combustion, and acts via the aryl hydrocarbon receptor, which is present in all cells. The aryl hydrocarbon receptor is a ligand-activated transcription factor that controls the expression of a diverse set of genes.  The researchers designed their mouse study to expand previous epidemiological findings from human studies. These findings showed correlation between maternal exposure to pollutants that bind the aryl hydrocarbon receptor and the decreased ability of the offspring to combat respiratory infections and produce antibodies. In other words, the epidemiological findings indicated that mothers exposed to these pollutants while pregnant may give birth to babies with impaired immune function.  An effective immune response requires the coordinated action of several cell types. CD4+ T cells, one of these cell types, exist in different subsets. It has been known for several years that, by binding the aryl hydrocarbon receptor, some chemicals influence the different subsets of CD4+ T cells, thus resulting in the observed impaired immune function. However, it was not known whether or not prenatal exposure to these chemicals could cause changes in the different CD4+ T cell subsets. The researchers that carried out the new study wanted to know whether or not fetal exposure to an aryl hydrocarbon receptor ligand (in this case TCDD) directly alters CD4+ T cell differentiation and function later in life. Thus, they exposed pregnant female mice to TCDD and then infected the adult offspring with the influenza virus. The results show that the offspring of the exposed pregnant mothers had a reduced frequency of different subsets of CD4+ T cells when compared with mice born to untreated mothers. In addition, exposed mice produced considerable lower levels of a specific class of antibodies against the influenza virus than control mice.   Then, the researchers transferred CD4+ T cells from the exposed offspring into unexposed mice. They found that, following cell transfer, the unexposed mice responded to influenza virus...

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Chlorovirus ATCV-1, a Green Algae Virus, May Slow Human Brain Activity
Nov03

Chlorovirus ATCV-1, a Green Algae Virus, May Slow Human Brain Activity

By Roberta Attanasio Chlorella viruses, or chloroviruses, infect green algae, single-celled organisms present throughout the world in freshwater ecosystems such as lakes and ponds. Now, it seems that chlorovirues also infect humans, causing changes in cognitive functions — the processes by which information is perceived, registered, stored, retrieved, and used. In other words, chloroviruses influence the ability to acquire and use knowledge. These novel findings — published on line in the scientific journal Proceedings of the National Academy of Sciences (October 27, 2014) — confirm that viruses may be able to jump from one kingdom (plants) to another (animals), something that has been shown only in very few instances.  For the study (Chlorovirus ATCV-1 is part of the human oropharyngeal virome and is associated with changes in cognitive functions in humans and mice), the researchers used throat swabs collected from 92 adults without a psychiatric disorder or serious physical illness. The researchers found that 40 of these adults carried the genetic material of one of the chloroviruses — Acanthocystis turfacea chlorella virus 1, or ATCV-1 for short. They also found that the presence of ATCV-1 was associated with a modest but measurable decrease in cognitive functions. Such a decrease was not associated with age, sex, race, socioeconomic status, cigarette smoking, travel history, or place of birth. However, this first set of findings did not show “causality” — the ability of ATCV-1 to cause the observed decline in cognitive functions. Thus, the researchers infected mice with the virus. After several months, as expected, the infected mice exhibited signs of cognitive impairment. Moreover, the researchers found that, in both humans and mice, exposure to ATCV-1 was associated with decreases in performance on tasks calling for visual spatial abilities, which are important for everyday life — for example, when using a map or merging into high-speed traffic. Robert Yolken, one of the study’s authors, said in a press release: “This is a striking example showing that the ‘innocuous’ microorganisms we carry can affect behavior and cognition. Many physiological differences between person A and person B are encoded in the set of genes each inherits from parents, yet some of these differences are fueled by the various microorganisms we harbor and the way they interact with our genes.” The researchers speculate that the immune system might be involved in the cognitive decline associated with the presence of ATCV-1. In mice infected with the virus, they found changes in several pathways involved in antigen processing and immune cell functioning. These changes were located in the hippocampus, the region of the brain involved in emotions, learning and memory formation. About 35% of the mice mounted an immune response following infection. The researchers propose that a type of chemical messengers called proinflammatory cytokines...

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Food-Borne Parasites: The “Top Ten” List
Jul01

Food-Borne Parasites: The “Top Ten” List

By Roberta Attanasio Food-born parasites affect the health of millions of people all around the world, causing huge social costs. However, we don’t know much about these parasites — where they come from, how they live in the human body, and how they make us sick. Today (July 1, 2014), the Food and Agriculture Organization of the United Nations (FAO) released, along with the World Health Organization (WHO), a report — Multicriteria-based ranking for risk management of food-borne parasites — as a first step in tackling the problem. Parasites are organisms that derive nourishment and protection from other living organisms known as hosts. Parasites that are present in food cause food-borne infectious diseases. They are classified biologically as protozoa (single-celled organisms) or helminths (better known as tapeworms, flatworms and roundworms).  Infectious diseases caused by food-borne parasites have not received the same level of attention as other food-borne biological and chemical hazards. Nevertheless, they cause a high burden of disease in humans, may have prolonged, severe, and sometimes fatal outcomes, and result in considerable hardship in terms of food safety, security, quality of life, and negative impacts on livelihoods. It is difficult to know how widespread these parasites are globally — in many countries it is not compulsory to notify public health authorities of their presence. In Europe, more than 2,500 people are affected by food borne parasitic infections each year. In 2011 there were 268 cases of trichinellosis and 781 cases of echinococcosis recorded in the EU. In Asia, there is no precise national data but parasitic diseases are known to be widely spread and are recognized as major public health problems in many countries. In most African nations there is no data at all on the prevalence of food borne parasites in humans because there of a general lack of surveillance systems. In the United States, Neurocysticercosis, caused by Taenia solium, is the single most common infectious cause of seizures in some areas of the US where 2 000 people are diagnosed with neurocysticercosis every year. Toxoplasmosis is a leading cause of food-borne illness and death. The FAO-WHO report was developed following a request by the global food standards body, the Codex Alimentarius Commission (Codex), to review the current status of knowledge on parasites in food and their public health and trade impacts. FAO’s food safety and quality unit and WHO responded by jointly organizing a global call for information on the problem. Twenty-two nations and one regional body responded, followed by an assessment and analysis by 21 experts on the impact of food-borne parasites. From this work, an initial list of 93 parasites was developed. The list was then narrowed down to the 24 most damaging parasites based on the...

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Global Threats: The Alarming Rise of Antibiotic Resistance
May02

Global Threats: The Alarming Rise of Antibiotic Resistance

By Roberta Attanasio For the last 70 years, we have been winning  most fights against harmful bacteria, using antibiotics as weapons. Now, we’re losing — our weapons don’t work any more, and the bacteria are fighting back. The alarming rise of antibiotic resistance is mostly due to overuse of antibiotics, both in medicine and in agriculture. In her book “The drugs don’t work“, Sally Davis, the UK chief medical officer, says that if we do not take responsibility now, in a few decades we may start dying from the most commonplace of operations and ailments that can today be treated easily. About a year ago (March 2013), she recommended to add antibiotic resistance to the UK government’s list of threats to national security. In addition, Davies recognized the global nature of the problem and called for coordinated action at the global level. Later last year (September 2013), the U.S. Centers for Disease Control and Prevention released a report (Antibiotic resistance threats in the United States, 2013) on the impact of resistant bacteria in the U.S. According to the analysis, each year at least 2 million people become infected with bacteria that are resistant to antibiotics and at least 23,000 people die as a direct result of these infections. Many more people die from other conditions that were complicated by an antibiotic-resistant infection.  The estimates are based on conservative assumptions and are likely minimum estimates — they are the best approximations that can be derived from currently available data. However, antibiotic resistance is a worldwide problem. Resistant bacteria can cross international boundaries and spread between continents with ease and at remarkable speed. World health leaders have described antibiotic resistant microorganisms as “nightmare bacteria” that “pose a catastrophic threat” to people in every country in the world. Thus, it is not surprising that a few days ago (April 30, 2014) the World Health Organization (WHO) released the first global report on antibiotic resistance. The report provides the first comprehensive picture of antibiotic resistance to date (with data from 114 countries) and reveals a global, serious threat to public health — it warns that infections caused by resistant bacteria double the risk of death and increase the rate at which infection spread, lengthening hospital stays and adding significant economic burdens to already stretched healthcare systems around the world. Infections by resistant bacteria are becoming “harder or impossible to control.” Keiji Fukuda, WHO’s Assistant Director-General for Health Security said in a press release “Without urgent, coordinated action by many stakeholders, the world is headed for a post-antibiotic era, in which common infections and minor injuries which have been treatable for decades can once again kill. Effective antibiotics have been one of the pillars allowing us to live...

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Climate Change: Influence on the Spread of Lyme Disease
Mar30

Climate Change: Influence on the Spread of Lyme Disease

By Roberta Attanasio Blacklegged ticks feed on blood — they attach to the skin of humans and many animals and, slowly, suck for several days. To get there, they patiently wait on the tip of grasses and shrubs using their lower legs to hold on, until a human or an animal passes by. Ticks can’t jump or fly, so they keep their upper pair of legs outstretched, ready to climb aboard. Once there, they insert their feeding tube into the skin and start to suck the blood — this is how they become infected by or transmit Borrelia burgdorferi, the micro-organism that causes Lyme disease. Lyme disease is one of the most common infectious diseases in the United States, and it also occurs in many regions of Europe and Asia. It’s at the center of ongoing disputes on how to cure it and on whether or not a chronic form of the disease exists.  Now, something else may add to the controversy — the influence of climate change on its spread. During their life cycle, ticks undergo profound transformations that require moisture in the air — eggs develop into larvae, which then become nymphs and, finally, adults. In addition, the ticks’ development from egg to larva depends on warm temperatures. Climate change, then, may make the ticks’ life harder or easier — if the climate becomes warmer, ticks will reproduce and spread more, thus increasing the risk of Lyme disease. The blacklegged tick (also dubbed deer tick) Ixodes scapularis spreads Lyme disease in the northeastern, mid-Atlantic, and north-central United States, whereas the western blacklegged tick Ixodes pacificus spreads the disease on the Pacific Coast. In the 1970s, populations of Ixodes scapularis expanded in the northeastern United States, thus leading to the diffusion of Lyme disease in this region. Now, Ixodes scapularisthe is expanding northwards, leading to the increased occurrence of Lyme disease in Canada. Results from a study published on March 14, 2014, in the journal Environmental Health Perspectives (Estimated effects of projected climate change on the basic reproductive number of the Lyme disease vector Ixodes scapularis) show that, as temperatures increased northward between 1971 and 2010, so did the sprawl of Ixodes scapularis. Thus, the authors of the study suggest that climate warming may be responsible for the emergence of Lyme disease in northeastern North America. On the basis of climate projections to 2070, the authors conclude that, in the future, higher temperatures may drive Lyme disease into new geographic regions while, at the same time, increasing the risk of diseases carried by ticks in climates currently suitable for their...

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