Sunday, April 12, 2020

What makes this novel coronavirus the scariest so far for humans

If you do not know what you are fighting, you are unlikely to know how to fight it. When it comes to the coronavirus, however, the more we get to know about the virus, the more we realise how badly the odds are stacked against us.

Viruses, to begin with, have not been easy to take on. Their invisibility gives them a wide edge even before the fight begins, which is before they enter our bodies. Covid-19, which we have been trying to scrub off our hands, clothes, paper and poly bags, is one-thousandth the width of an eyelash.

Viruses, it seems, can bide their time to attack humans with the patience of a monk. Till the time viruses do not get a human body, they are not even technically alive. They can remain in that state for eternity. In 2014, a virus frozen in permafrost for 30,000 years was still able to infect an amoeba after being revived in a laboratory. Coronavirus is far from frozen.

This coronavirus that causes Covid-19, the SARS-Cov-2, is a novel virus. There is not one thing which scientists can say with certainty about its behaviour. We do not know of the exact way in which it is entering us. Droplet infection is definitely a way. So let’s look at how it works.

Droplet infection

When an infected person sneezes or coughs, she releases droplets in the air. A person who happens to inhale these droplets becomes the next victim. The virus can also stick to surfaces and stay put, waiting for its next target. This is called a fomite-mediated transmission.

Many experts have been assigning varying periods for which the virus can survive on a surface - on cardboard for up to 24 hours, and on plastic and stainless steel for up to three days. The shocker on that front came when US public health institute Centers for Disease Control and Prevention found that the virus on surfaces of the Diamond Princess cruise ship was potent up to 17 days after passengers disembarked. So, it can’t be conclusively said as to how long Covid-19 can stay alive on surfaces.


What happens when the virus finds its way into our system?
Once in our body, the virus spreads to the back of the nasal passage and to mucous membranes in the throat. The viral particles attach themselves onto the outer walls of the host’s cells.

The genetic material that the virus has, then breaches the cell membrane of the host cell. The novel coronavirus then hijacks the cell and comes to life. The virus uses the hijacked cell to make more copies of itself.

Numerous copies are created. These copies then break out of the cell the virus attached itself to, and begin infecting other cells in the body.

It would not be unfair to say that the only purpose the virus has in mind is to make copies of itself and multiply its race.

Peter Kolchinsky, virologist and author of The Great American Drug Deal, in a Twitter thread brings out the sly nature of the virus strikingly – also scarily. He says viruses, they may not be technically alive, but are evil geniuses.

Before a cell dies, it can churn out millions of copies of the virus. Professor Hugh Montgomery, director of the Institute for Human Health and Performance at University College London, has illustrated that 10 infected people can pass on the novel coronavirus to 59,000 people.

The R-naught, which is basically the rate at which an infected person can pass on the infection for most viral infections is 1.3 to 1.4 people. This means an infected person can infect another 1.3 or 1.4 people. The R-naught for Covid-19 is three.

So what makes Covid-19 more infectious than others?

So, now we know that viruses like to multiply and for that, they need a human cell. They need to enter a human cell to produce more of their kind. The SARS-Cov-2 isn’t too good at entering cells. But it has other advantages that make it more dangerous than other viruses.

A Lancet research has shown that the novel coronavirus sneaks in by attaching itself to a protein called ACE2. ACE2 is present on the surface membrane of human cells.

So what does the ACE2 do lying on the surface of the cells? Its job is to bind to a hormone (ACE2 hormone). This combination guides the body’s stress response. The ACE2 hormone plays a role in constricting blood vessels. When blood vessels are constricted, blood pressure rises.

When the SARS-Cov-2 sneaks in, it finds that the part that creates antibodies that help identify foreign elements in the body quickly, doesn’t know what this coronavirus looks like.

SARS-Cov-2 then assumes control of the cell’s genetic reproduction tools and begins to fulfil its life’s mission – which is to create more of its kind. This relentless duplication allows the virus to burst through the cell membrane.

It is the ACE2 which could be making the virus deadlier for those suffering from diabetes or high blood pressure. Such patients are given ACE inhibitors to limit the constriction of blood vessels.

So such people have more ACE2 receptors in the body and hence the SARS-Cov-2 can multiply faster in their bodies.

What about healthy individuals?

ACE2 is found in abundance in our body otherwise too. They exist on our tongue and oesophagus, the part of the digestive tract that connects the throat to the stomach. They are also on the heart, kidney and gastrointestinal tract.

This is perhaps the reason why many patients report a loss of appetite and diarrhea if suffering from a coronavirus infection.

Most worryingly, ACE2 receptors are present on the alveoli in our lungs.

What happens to the lungs when SARS-Cov-2 reaches them?

The alveoli is the most vulnerable part of our lungs. The alveoli are responsible for the exchange of oxygen and carbon dioxide molecules to and from the bloodstream. And this is the reason why Covid-19 patients are reporting coughs and/or trouble in breathing.

The inflammation in the lungs, and their reduced efficacy, can cause them to fill with fluids, pus and dead cells, and cause an infection, leading to pneumonia.

According to The Guardian, pneumonia caused by the novel coronavirus appears to be more severe than most cases of the disease. It also affects a larger portion of the lungs.

Delayed symptoms

One person in South Korea, known as Patient 31, transmitted the virus to over 1,100 people as she went about her life. Similar cases are being reported from across the world.

It takes about five days to two weeks for symptoms to show in an infected person. All this while, the person can pass on the infection to other people without anyone knowing.

People can be asymptomatic for different reasons. One reason is that the person’s immune system is strong. The body is not completely defenceless against the virus.


One person in South Korea, known as Patient 31, transmitted the virus to over 1,100 people as she went about her life. 


Our immune system comes into action the moment we contract a new infection. Infected cells do not surrender without giving a fight to the virus. The system tries to limit the spread of the virus by eliminating infected cells. This human body, which is at war with a virus inside, is also a carrier. The person who houses this body could suffer mild infection or may show no symptom at all.

SARS and MERS, two other diseases caused by the coronavirus, made people so badly sick and so rapidly, that they couldn’t go undetected. So, while the virus wasn’t visible, it was possible to see which body was carrying the virus. The mildness with which Covid-19 is treating some of us is perhaps its biggest weapon.

Spread through body fluids

The virus has also been found in blood and stool specimens. It is, however, unclear whether it can spread through any bodily fluids.

We do not know if the coronavirus, like the Human Immunodeficiency Virus (HIV), can spread through blood transfusion or while having sex. Now, HIV didn’t spread through kissing, but this novel coronavirus could very well, since it could bind itself to the ACE2 receptors on the tongue.

Social distancing, with your mask on, so far seems to be the best remedy to avoid infection.

As more data emerges, hopefully, silver linings on tackling it will also come forth.


This is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.     

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Sunday, July 07, 2019

Common Plant Compound Found To Reverse Lung Damage Associated With COPD


“Given the high costs, both direct and indirect, associated with COPD, there is an urgent need to identify novel approaches to treat the disease,” said a professor of medicine.

The COPD Epidemic

Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term that includes chronic bronchitis, emphysema, bronchiectasis, and asthma. But it most commonly describes two often overlapping and life-threatening lung diseases: emphysema and chronic bronchitis. COPD is a progressively worsening, debilitating lung disease that adversely affects breathing by obstructing airflow and causing lung tissue damage.

COPD is the third-leading cause of death in the United States and the fifth leading cause of death worldwide. The National Heart Lung and Blood Institute (NHLBI) estimates that an additional 12 million people have COPD but haven't been diagnosed.


The National Emphysema Foundation states that 3.1 million Americans have emphysema while 11.2 million have been officially diagnosed with COPD.

Chronic Bronchitis: According to the clinic, chronic bronchitis is characterized by chronic inflammation of the lining of the bronchial tubes, which are the primary vehicle for air transport in (oxygen) and out (CO2) of the lungs. Common symptoms include: shortness of breath (“dyspnea”), thickening and narrowing of the airway lining, constant coughing to remove copious amounts of difficult to expel phlegm, wheezing and fatigue. Chest infections are common.

Emphysema: Emphysema involves the gradual destruction of the small, air sacs (alveoli) located at the tip of the smallest air passages (bronchioles). Over time, the walls of the air sacs are destroyed, resulting in “holes,” leaving fewer and larger air sacs that diminish the gas exchange in the lungs – leading to dyspnea, fatigue and early death.
Bronchiectasis: Bronchiectasis (brong-ke-EK-tah-sis) is a chronic lung disease that is characterized by scarred and damaged airways, which causes them to widen and become flaccid. Although it can be a congenital defect, it’s more often an “acquired” disease caused by a severe lung infection, repetitive infections, or an injury.


The damaged airways can no longer efficiently clear mucus and become inflamed. Eventually, they lose their ability to clear out mucus. Mucus builds up. Unwanted bacteria multiply leading to chronic infections, which results in more airway damage and decreased oxygen flow to the vital organs. Typical symptoms include chronic coughing to remove excess phlegm, fatigue, and shortness of breath.

Asthma: Asthma (AZ-ma) is a chronic lung disease that causes inflamed narrowed airways. Asthma symptoms include wheezing, chest tightness, shortness of breath, and coughing. More than 25 million people in the US have been diagnosed with asthma and approximately 7 million are children. Over time, chronic inflammation can destroy the surface layer of the airways.

According to an associate clinical professor of immunology, “the surface layer acts as a kind of filter, but once it’s gone, all of the pollutants and allergens have direct access into the lungs.”

COPD Causes, Prognosis, and Disease Management

Allopathic mainstream medicine believes the most common causes of COPD are smoking, genetic factors (alpha-1 antitrypsin disease) and long-term environmental exposures to toxic chemicals, fumes, or dust in the workplace.

Conventional medicine considers COPD to be incurable, progressive, irreversible and fatal. Most allopathic doctors believe lung tissue can never be regenerated. Palliative care or disease management is the standard treatment for COPD patients. Smoking cessation is a primary treatment goal.

Big Pharma medications used to manage COPD symptoms with toxic chemical inhalers, dangerous steroids (anti-inflammatories), oxygen, and mucous thinning drugs. In severe cases, surgical interventions including lung transplants are resorted to.

Studies Reveal Lung Tissue Can be Regenerated

Research performed successfully reversed emphysema in experimental rats. The researchers used a derivative of vitamin A: all-trans-retinoic acid (ATRA).

Twelve days of daily ATRA injections enabled the mice to grow healthy new alveoli. the Dr. said, “It appeared that the treatment regenerated the adult rat’s ability to produce alveoli, the small air sacs where oxygen and carbon dioxide move between the lungs and the bloodstream. The production of alveoli normally ends in childhood.

Interestingly, a 2003 study demonstrated why cigarette smoking is considered to be the primary cause of emphysema.

Previous studies by lead researcher, revealed that rats fed a diet deficient in vitamin A developed emphysema. In the 2003 study, it was discovered that rats exposed to cigarette smoke became vitamin A deficient. A common carcinogen found in cigarettes called benzopyrene had previously been linked to vitamin A deficiency.

When the researchers fed benzopyrene to rats it predictably induced a vitamin A deficiency. Baybutt explained: “When the lung content of vitamin A was low, the score of emphysema was high.” He added, “So, the hypothesis is that smokers develop emphysema because of a vitamin A deficiency.”

To further solidify the link between smoking, vitamin A deficiency and emphysema, Baybutt and team fed the lung damaged rats a diet rich in vitamin A. The result was promising, to say the least. “We saw that the areas of emphysema were effectively reduced,” he said.

He feels that a vitamin A deficiency may be the culprit behind emphysema and cigarettes could merely be the vehicle. He also believes that there is a link between Vitamin A deficiency and lung cancer, as vitamin A has known anti-cancer attributes.

More Clinical Trials

According to a  article, “Vitamin ‘cure’ for emphysema”: British scientists announced that retinoic acid commonly used to treat acne reversed Emphysema damaged lungs in mice. In fact, the article claims that clinical trials with humans have begun in America.

Professor  said his team’s research “… saw quite dramatic results. It is potentially hopeful for emphysema sufferers, and for premature babies who often suffer from loss of alveoli because of treatments given to stimulate lung growth.” The researchers found that the compound stimulated alveoli to regenerate back to normal function.

Beta-Carotene or Vitamin A

Beta-carotene is one type of carotenoid. It’s a pigment found in plants that helps produce the vivid colors of certain fruits and vegetables, such as cantaloupe and carrots. When ingested, beta-carotene is converted by the body into vitamin A (retinol), which can then be used by the body for a variety of purposes, or it can simply act as an antioxidant scavenging free radicals.

The best way to safely increase vitamin A/Beta-Carotene levels is with Food. Experts warn that large or even semi-large oral doses of synthetic stand-alone supplemental vitamin A can be dangerous. Since vitamin A is a fat-soluble vitamin, it’s stored in the liver and large doses can damage the liver. The best way to ensure adequate levels of beta carotene or vitamin A is via your diet, not through pills.

In fact, smokers, former smokers, and those exposed to asbestos may have an increased lung cancer risk from taking supplemental, isolated beta-carotene. Also, several studies revealed that beta-carotene supplements could adversely affect the heart and may increase cancer risk.

Kitchen Table Medicine

Instead of waiting for Big Pharma’s synthetic, negative side–effect laden miracle drug to reverse lung tissue damage, why not make your own beta–carotene medicine from real food?

 The researchers recommend increasing the bioavailability of carotenoid-rich foods by eating them with fat at mealtime and/or chopping, pureeing, and cooking them in oil. Daily juicing of organic, fresh fruits and vegetables high in beta-carotenoids can be an efficient and delicious method for therapeutically boosting beta-carotene levels. One cup of raw carrots contains a whopping 9,135 mg of beta-carotene!

 Here’s a list of the top 10 foods highest in beat-acrotene.

#1: Sweet Potatoes

Beta-carotene per Cup MashedBeta-carotene per 100g
123% RDA (13308μg)48% RDA (5219μg)

Carrots

#2: Carrots

Beta-carotene per Cup CookedBeta-carotene per 100g
120% RDA (12998μg)77% RDA (8332μg)
A Bowl of Spinach

#3: Dark Leafy Greens (Spinach)

Beta-carotene per Cup CookedBeta-carotene per 100g
105% RDA (11318μg)58% RDA (6288μg)

More Dark Leafy Greens High in Beta-Carotene

-98% RDA in 1 cup of cooked kale
-96% RDA in 1 cup of cooked mustard greens
-79% RDA in 1 cup of cooked collards
-61% RDA in 1 cup of cooked beet greens
-59% RDA in 1 cup of cooked swiss chard
Half a Butternut Squash

#4: Butternut Squash

Beta-carotene per Cup CookedBeta-carotene per 100g
87% RDA (9369μg)42% RDA (4570μg)
A cantaloupe with a cantaloupe wedge

#5: Cantaloupe

Beta-carotene per CupBeta-carotene per 100g
33% RDA (3575μg)19% RDA (2020μg)
Lettuce

#6: Lettuce

Beta-carotene per CupBeta-carotene per 100g
23% RDA (2456μg)48% RDA (5226μg)
Sweet Bell Peppers

#7: Red Bell Peppers

Beta-carotene per Cup CookedBeta-carotene per 100g
19% RDA (2059μg)14% RDA (1525μg)
-3% DV in 1 cup of cooked green bell peppers.
Half an apricot

#8: Apricots

Beta-carotene per CupBeta-carotene per 100g
16% RDA (1696μg)10% RDA (1094μg)

More Fruits High in Beta Carotene

-15% RDA in 1 cup of pink grapefruit
-10% RDA in 1 cup of mangoes
-6% RDA in 1 cup of guavas
Broccoli Stalk

#9: Broccoli

Beta-carotene per Cup CookedBeta-carotene per 100g
13% RDA (1449μg)9% RDA (929μg)

Podded green peas

#10: Podded Peas 

Beta-carotene per Cup Cooked

 11% RDA (1216μg)

Beta-carotene per 100g
7% RDA (760μg)
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Thursday, February 11, 2016

Autopsy of patient suffering from MERS show how it affects the lungs

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A study of the first reported autopsy of a MERS patient revealed that patients with the Middle East respiratory syndrome (MERS) often show signs of acute kidney failure but lungs are the primary target organs of the new disease in humans. The MERS coronavirus (MERS-CoV) was first isolated from the sputum of a patient who died of respiratory and renal failure in Saudi Arabia in 2012. Since 2012, at least, 1,500 individuals have developed Middle East Respiratory Syndrome (MERS), resulting in more than 500 fatalities. 

Only now are results being reported of the first autopsy of a MERS patient, which was performed in 2014, but the study also said. Not only do these findings published in the American Journal of Pathology provide unprecedented, clinically-relevant insights about how MERS progresses, but they also challenge previously accepted ideas about MERS and the relevance of current animal models.

The 45-year-old male patient analysed by autopsy was one of a large patient cluster treated at a hospital in the United Arab Emirates in April 2014. The autopsy, performed 10 days after his death, showed that the lungs were the main target organs of MERS, with diffuse damage to the air sacs (alveoli) observed. Using immunohistochemistry, the researchers identified anti-MERS-CoV antibodies, in particular, cells in the lungs (pneumocytes and epithelial syncytial cells) and bronchial submucosal glands. 

‘Infection of bronchial submucosal glands is a likely source of viral shedding in respiratory secretions leading to human-to-human transmission,’ explained lead investigator Sherif Zaki from US Centres for Disease Control and Prevention, Atlanta. Patients with MERS often show signs of acute kidney failure, and MERS-CoV has been found in the urine of MERS patients. In this case, although certain signs of pathology were seen in this patient’s kidneys, immunohistochemistry showed no evidence of MERS-CoV. 

Such new insights suggest that MERS researchers and clinicians treating MERS patients should focus their infectious control strategies on the lungs. Similarly, no sign of MERS-CoV infection was found in the brain. In many ways, findings from this autopsy differ from observations made using animal models. ‘Although these experimental studies were able to suggest the target cells of the virus and histopathology of MERS, only some of the features of the animal models conform to the observations in the human autopsy,’ Walker noted.

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Thursday, April 26, 2012

Grapes helps to reduce the risk of Lung cancer



cid:96706231308C405D8F977546629D4B52@vpop
GRAPES                   LUNGS 
OUR lungs are made up of branches of ever-smaller airways that finish up with tiny bunches
of tissue called alveoli.  These structures, which resemble bunches of  grapes, allow oxygen
to pass from the lungs to the  blood stream. One reason that very premature  babies struggle
to survive is that these alveoli do not begin to form until week 23 or 24 of pregnancy.
A diet high in fresh fruit, such as  grapes, has been shown to reduce the risk of lung  cancer
and emphysema.
Grape seeds also contain a chemical called proanthocyanidin, which appears to reduce
the severity of asthma triggered by allergy.

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