Genes, Viruses, Microbes and IBD
Crohn’s disease is common and miserable to suffer from, yet its actual cause is still under some debate as no clear understanding has yet been fully elucidated. It is known that there are some gene variations and that the environment has an impact. A paper out in Cell suggests, based on a mouse model that it may be a virus that makes the difference between health and inflammation. demonstrate that a viral infection, a toxic insult to the gut, commensal bacteria, and a Crohn’s disease susceptibility gene collude to cause inflammatory disease in the mouse gut.[1]
To be clear, Cadwell and co-workers are not arguing that Crohn’s disease is caused by infection with norovirus (as used in this study) or by any other single microbe. The environmental factors that predispose to and protect from Crohn’s disease remain uncertain, but the balance among commensal and pathogenic gut bacteria and viral infections is likely to be part of the story. These studies make an urgent and compelling case for characterising the human virome as well as the microbiome and defining its effects on physiology and gene expression. In addition, further explanations to help us to understand how the virome interacts with polymorphisms in the host genome and how numerous toxins in the environment alter this complex interplay will need to be unravelled.
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More Evidence to Support Vit D as an Anti Viral Compound
Last year I wrote a number of posts relating to mechanisms related to mucosal immune defences, in particular the innate immune defences and how we as Nutritional Therapists may advise our patients of evidence based strategies. This paper out in the open access journal Plos One adds further validity to the vitamin D recommendations I proposed.
Declining serum concentrations of 25-hydroxyvitamin D seen in the fall and winter as distance increases from the equator may be a factor in the seasonal increased prevalence of influenza and other viral infections.[1]
This paper in PLOS Biology describes how almost 200 adults had their serum 25-hydroxyvitamin D levels measured, without knowing what was been investigated.
One hundred ninety-eight participants, 85 men and 113 women, with an age range of 20–88, were enrolled in the study.
The researcher found that people with fair skin, lean body mass and who supplemented with vitamin D had the highest levels of 25-hydroxyvitamin D. People who achieved 38ng/ml or higher 25-hydroxyvitamin D level had a remarkable 50% reduction in the risk of developing acute respiratory tract infections and a significant reduction in the number of days ill (p<0.0001).
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Atishoo – that’s D’ one!
Vitamin D Vs Influenza A
Lets face it, right now we are still recovering from the various revelations about the novel variant H1N1 or swine flu non event (in terms of pandemic effects) to be looking to see if we can manage the more common seasonal influenza. Plus spring is in the air and we all know that colds and the flu viruses seem to be less vigorous during the time of the year we actually see the sun!
However a rather neat randomised trial to see if Vitamin D supplementation had any prevention effect in school children adds further weight to the evolving understanding of its innate immune activation potential.[1]
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CFIDS Virus XMRV- Link Challenged
Controversial link. A previous study of chronic fatigue syndrome pointed to a retrovirus found in cancerous prostate cells
Last October 2009 the journal Science published a paper suggesting that a virus could be linked to CFIDS as well as prostate cancer. This was commented on in this site. Initial enthusiasm for this potential pathogen explanation for the chronic and debilitating condition has taken a couple of knocks as two papers have questioned the link. Scientists in the initial study found DNA traces of a virus in the blood cells of two-thirds of 101 patients with CFIDS, compared with 4% of 218 healthy controls. XMRV is a rodent retrovirus also implicated in an aggressive prostate cancer, though why it might cause or be associated with CFIDS remains unclear.
This naturally seemed to provide a plausible association with an infectious agent that would mesh with the common development of the condition following a viral infection.
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H1N1 – Questions About Profit Incentive
Swine flu has killed 12 799 people worldwide since it first emerged in Mexico in March 2009, the World Health Organisation said on the 8th January 2010.
The latest data posted by the United Nations health agency marked an increase of 579 deaths from the previous update published nine days ago.
The Americas continues to report the biggest number of casualties with at least 6,880 deaths while in Europe, at least 2,554 people have died from the A(H1N1) virus
Is it a False Pandemic Though?
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Novel Influenza H1N1 has Dramatic Risks for Pregnant Women
Like previous epidemic and pandemic diseases, 2009 pandemic influenza A (H1N1) may pose an increased risk of severe illness in pregnant women. To see if there were clinical experiences that matched this assumption a Californian investigation by their Department of Health reviewed demographic and clinical data reported from April 23 through August 11, 2009, for all H1N1-infected, reproductive-age women who were hospitalised or died. These included non-pregnant women, pregnant women, and postpartum women (those who had delivered ≤2 weeks previously).[1]
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H1N1 – 3 Key Questions
Question 1 – How does it kill?
H1N1 is a unique virus and unlike seasonal flu which damages the upper airway cells, H1N1 Novel Influenza damages the terminal air sacs called alveoli. These are found in the lower part of lungs.
Secondly a co-infection with bacteria such as S.aureus or Streptococcus pneumoniae has presented in about one third of recorded deaths to date. The others appear at this stage to have succumbed to the virus alone. There does however, tend to be other underlying health problems such as diabetes, overweight, cardiovascular problems etc. The damage to the lung tissues involves the rupture of the alveoli allowing blood to fill the spaces usually reserved for gas exchanges.
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Gastric Complications For Patients with H1N1 (Swine Flu)
The incidence of gastric events in normal seasonal flu is very low, almost never. The H1N1 swine Flu virus has differentiated itself from the seasonal flu not only in its speed of migration around the world, but also in the development of gut related events.
A new article in the International journal GUT [1] explains how a well set up investigational group based in Chile – a country well exposed to the virus, followed the first 500 confirmed patients who were infected with the influenza A (H1N1) 2009 virus back in May 2009.
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CFIDS and Prostate Cancer What’s The Viral Link?
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CFIDS is no stranger to controversy and the latest paper published on line by Science seems to raise more controversial thoughts. The researchers led by Judy Mikovits have implicated a contagious, rodent derived retrovirus (defn: A type of virus that contains RNA as its genetic material. The RNA of the virus is translated into DNA, which inserts itself into an infected cell’s own DNA. Retroviruses can cause many diseases, including some cancers and AIDS) named xenotropic murine leukemia virus -XMRV.
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H1N1 (Swine Flu) What Does it Mean This Winter?
The European Centre for Disease Prevention and Control recently surveyed H1N1 (Swine Flu) epidemiological 2009 data for 28 countries, finding that 51% of all deaths have been among people aged 20-49 years, and only 12% were among people over 60 years of age.
This is striking, as it is a near-perfect reverse of normal flu trends, and mirrors what was seen, demographically, in 1918. While the President’s Council of Advisors on Science and Technology have tried to factor in such trends, it is extremely difficult to know how influenza dynamics, illnesses and death rates may vary if transmission and illness is primarily among young adults.
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