Humidity > Influenza Virus

Photo, James Gathany Photo credits: CDC

Photo, James Gathany
Photo credits: CDC

Each year in the winter influenza or “flu” season rolls around and this sickness runs rampant throughout the country. This virus, and many in general, are quite scary because of how easily they can be spread through the air ie. via coughing. Researchers of the National Institute for Occupational Safety and Health (NIOSH of the CDC) have recently linked higher humidity and transmission particle size to more inactivation of influenza (and less spread).

Influenza is an RNA virus that affects mammals and birds causing a small scale pandemic every year in the United States. Viruses tend to mutate very quickly, therefore, it is hard to find a single band-aid to blanket cure this bug. Most people can spread the virus between -1 and 6 days after showing symptoms. Airborne transmission is most likely when this virus appears since many people are in closed quarters attempting to stay warm at home with others during winter.

To test the rate at which influenza stays infectious in different humidities, researchers set up coughing and breathing test dummies in an isolated room. The sneezing dummy released about 4.5×103 virus/liter of air into the room, where 4.6% of that virus was seen to be infectious upon discharge. Of that, upwards of 77.2% of the virus retained infectivity at lower relative humidity (7-23%), while only 14.6% retained infectivity at higher relative humidity of 43%. As a grounding point, average in home humidity during winter is just above 20%, while summer humidity indoors is just below 60%.

Next, the rate of loss of infectivity was measured comparing low and moderate humidity (20% and 45%). Within 15 minutes, 52% of the virus’ infective ability was lost at 45% humidity compared to 20% humidity.

Together these two showed more virus lost its ability to infect new people/etc. at higher relative humidities.

Finally, transmission particle size was measured to see if it had bearing on influenza’s spread and infection at differing humidities. Three particle sizes were used, <1 µm, 1-4 µm, and >4 µm. At the two extremes, <1 & >4 µm, 94% infectivity was seen as lost in the first 15 minutes after coughing virus into the air. However, the 1-4 µm range of particles only showed 29% decrease in infectivity of the virus after 15 minutes. All sizes did, however, show increased loss of infectious ability with more time passed.

It seems as though humidity has great bearing on the inactivation/spreading ability of the influenza virus. At higher humidities, 45% +, the influenza virus showed very little strength in infecting new hosts. This was doubly true when the particle size they rode on was really small or really big.

The best way to minimize your chance to get influenza each year without getting a flu shot?…move to a state with really high humidity in the winter.

Reference:
John D. Noti, Francoise M. Blachere, Cynthia M. McMillen, William G. Lindsley, Michael L. Kashon, Denzil R. Slaughter, Donald H. Beezhold. High Humidity Leads to Loss of Infectious Influenza Virus from Simulated Coughs. PLoS ONE, 2013.
http://dx.doi.org/10.1371/journal.pone.0057485

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Heart failure preventive induces heart failure in mice

Photo courtesy of Cardiomegaly

Who says too much growth and nutrition is a bad thing? The human heart does first and foremost. Past research has set out to prove limiting the amount of fatty acid derivative entering the mitochondria of the heart is protective in that it prevents cardiac hypertrophy and heart failure. However, researchers of the Sanford-Burnham Medical Research Institute believe carnitine palmitoyltransferase 1 (CPT1) inhibition (lowered ß-oxidation) actually exacerbates cardiac hypertrophy and induces heart failure. This study proved their assumptions correct using CPT1b+/- knockout mice.

CPT1b is the main isoform of CPT1 found in the heart and works to assist long chain acetyl-CoA’s (from fatty acid metabolism) entrance into the mitochondria for ß-oxidation. ß-oxidation is an important contributor of energy to the heart as so is glucose oxidation (70:30 energy contribution).

Cardiac hypertrophy is a thickening of the heart resulting in a decrease in the volume of its chambers. This can occur naturally in athletes or due to a physiological impairment in non-athletes.

In this study, CPT1b+/- mice were subjected to transverse aorta constriction (TAC) induced pressure-overload and analyzed for accompanying cardiac problems. Basically cardiac thickening was forced on the wild type/control mice and the CPT1b+/- mice.

At baseline, no cardiac abnormalities was seen in either mouse cohort. After inducing TAC, most CPT1b+/- mice died after two weeks, while their wild type companions survived. Additionally, higher rates of cardiomyocyte (heart cell) apoptosis was seen in the knockout mice than wild type. Following, triglyceride levels were measured in the post-mortem hearts of mice. Again, the  CPT1b+/- mice showed higher levels of lipids (Oil-red-O staining) than the normal mice.

CPT1b deficiency in hearts has been shown to exacerbate hypertrophy and heart failure, increase cellular suicide, and raise lipotoxicity. Therefore, caution should be taken with clinical prescription of drugs inhibiting cardiac CPT1.

Reference:
Lan He, Teayoun Kim, Qinqiang Long, Jian Liu, Peiyong Wang,Yiqun Zhou, Yishu Ding, Jeevan Presain, Philip A. Wood, Qinling Yang. Carnitine Palmitoyltransferase-1b (CPT1b) Deficiency Aggravates Pressure-Overload-Induced Cardiac Hypertrophy due to Lipotoxicity. DOI: 10.1161/CIRCULATIONAHA.111.075978
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484985/

Restoring insulin creation in diabetes type I sufferers

Type I diabetes is very manageable by taking daily doses of exogenous insulin. However, researchers of the University of South Dakota pulled together a method utilizing G-protein coupled receptor 119 (GPR119) and dipeptidylpeptidase-IV (DPP-IV) to regenerate lost ß-islet cells of diabetics and restore insulin production in the body.

ß-cells are the insulin generators of the body, but in type I diabetes patients, they don’t exist or don’t work. GPR119, when activated by an agonist such as PSN632408, stimulates ß-cell replication, increases GLP-1 secretion, reduces food intake, and decreases body weight gain. If hyperstimulated in type I diabetes sufferers the level of insulin reached would be closer to that of normal body levels, which is why this was a target of this study. Contrarily, DPP-IV works to degrade or breakdown GLP-1, which is a protein that stimulates insulin release from ß-cells, enhances ß-cell proliferation, and prevents ß-cell programmed cell death.

In the study, diabetic mice with blood glucose levels of 400 to 500 mg/dL were treated with PSN632408 and/or sitagliptin for 7 weeks. The former acted as a GPR119 agonist and the latter as a DPP-IV inhibitor. After treatment ended, the three different treatment groups obtained the following percentages of normoglycemia (blood glucose < 200 mg/dL) mice:

– PSN632408, 32% mice with normoglycemia
– Sitagliptin, 36% mice with normoglycemia
– PSN632408 & sitagliptin, 59% mice with normoglycemia

The average drop in blood glucose was 257 mg/dL after seven weeks. The treatment actively reversed type I diabetes in these mice.

Further tests showed increased levels of GLP-1 (7.6±0.4 pmol/L in control mice, 14.8±1.0, 35.9±8.6, 44.2±10.5 pmol/L in mice treated with PSN632408, Sitagliptin, or both respectively), ß-cell replication, and ß-cell regeneration.

Mice treated with a GRP119 agonist and DPP-IV inhibitor showed increased ß-cell regeneration and overall insulin production. As mice have similar GRP119/DPP-IV pathways to humans, these results are very exciting for the diabetes scene.

Drinking (or painfully auto-injecting) daily insulin may no longer be necessary for diabetics if the GRP119 agonist/DPP-IV inhibitor treatment is approved for clinical use.

Reference:
Ansarullah, Yan Lu, Martha Holstein, Brittany DeRuyter, Alex Rabinovitch, Zhiguang Guo. Stimulating β-Cell Regeneration by Combining a GPR119 Agonist with a DPP-IV Inhibitor. PLoS ONE, 2013. http://dx.doi.org/10.1371/journal.pone.0053345