Covid-19: How to contain the contagion before it is too late

Viruses are extremely tiny (80-300 nanometers) non-living inert beings. Almost a speck. They come into existence only when inside the cell of a carrier — animal or human. Here, they hijack the host’s cellular machinery to reproduce millions of their copies. Once they have reproduced and their mission accomplished, these viruses break free by killing the host cell to infect neighbouring cells and repeat the cycle. This is unlike the bacteria, which can divide by themselves. And come to think of it, the viruses have brought the planet to a grinding halt and caused the unthinkable today.

Coronaviruses are a group of viruses that can cause respiratory tract infections. The current variant strain (SARS-Cov-2), is a relative of SARS virus (SARS-CoV) which caused the epidemic in 2002. The SARS-CoV-2 virus causes the Covid-19 infection — the name given to denote the epidemic breakout in the year 2019. Each time I follow up on the live tickers to see the statistics, the numbers make me numb and uncertain of our collective future. On March 17, 2020, Italy registered 349 coronavirus fatalities in a single day and 2,158 total deaths so far. Globally, nearly 8,000 people have died because of the virus as of March 19, 2020.

According to research, the fatality is way higher than the numbers given by the World Health Organization. As per the statistical analysis by Tomas Pueyo, if France claims 1,400 cases, the numbers on the ground could range between 24,000 to 1,40,000. And this makes the case as to why countries should proactively take up extreme measures to contain the contagion.

Countries responding to the pandemic

As in case of any new animal to human transition of virus (zoonotic disease), it is difficult for doctors to determine if they are observing a novel strain of the virus. If reports are to be believed, the 55-year-old Hubei resident, who contracted coronavirus on November 17, 2019, could have been the 'Patient Zero'. The whistle-blower doctor Li Wenliang, who wrote on social media about the possibility of an outbreak, was summoned and admonished by Wuhan police for "making false comments on the Internet". He later died after contracting the Covid-19 infection. Although China was criticised initially for its slow response, the country soon resorted to extreme measures to minimise the spread.

Italy seems to be ground zero for the coronavirus spread in Europe. Italian hospitals are running at 200 per cent capacity, and are already reporting lack of beds and ICUs. This is affecting the routine functioning of hospitals and clinics, which cannot deal with patients coming in to be treated for other ailments. Another ethical issue that the doctors are facing is to choose between patients to provide intensive care and ventilation facilities. This is based on the chances of survival — implying that a younger patient will have a higher chance of getting intensive treatment. When the first time my Italian friends told me this as speculation, it was hard to imagine. Barely two days later, this was reality.

In Italy, the entire country is under lockdown and only one person from each family can visit stores to buy groceries. Aerial footage with deserted roads appears surreal and straight out of apocalypse movies. Italy’s coronavirus victims face death alone, and the local priest in the village of Zogno has decided to ring the death knell just once a day, to keep from ringing it all day long. An Italian newspaper printed 10 pages of obituaries, as the death rates do not die down.

The situation in many countries only seems to be aggravating.

According to Public Health England (PHE) briefing, as many as 80 per cent of the population is expected to be infected with Covid-19 in the next 12 months, and up to 15 per cent (7.9 million people) may require hospitalisation. UK’s response has been surprisingly callous, where they were counting on ‘herd immunity’. This is a strategy that counts on letting a large number of people (60 per cent of the population) catch the disease and hence develop immunity to it, to stop the virus spreading. This will soon prove to be disastrous. Though, geographically separate from Europe, the UK is fairly connected owing to many Europeans living in the country. Also, dense cohabitation in many parts like London can spread the contagion. Despite these real risks, it was only on March 16, 2020, that the UK decided to implement a lockdown until March 31 akin to Italy.


Due to their history with the SARS epidemic, Hong Kong and Singapore defied initial WHO orders and upped travel restrictions as early as February 1, 2020. These countries are setting examples of epidemic preparedness for other nations.

Due to its proximity to Europe, Israel has been proactively taking measures to contain the infection. Banks, pharmacies, supermarkets and public transportation remains operative so far,  as compared to the complete lockdown in Italy and Spain, but the restrictions might get tighter. My friend who flew from Switzerland has been under two-weeks home quarantine as a precautionary measure. The same is the case with over a lakh people who flew back to Israel from various countries. Israel has developed mobile apps to track Covid-19 positive patients to minimise the spread. A few days ago, a person who defied quarantine was arrested in Tel Aviv by Israeli Police.

India in stage I/II

India’s response to the situation has been commendable from the start, in terms of containment. When reports of a high incidence of pneumonia from China came through, surveillance at airports was intensified, especially for those returning from China. The first case was reported on January 30, 2020, in Kerala. Just to give a comparative outlook, Ohio in the USA got the test kits on March 5, 2020. The three cases in Kasargode, Thrissur and Allepey were put into quarantine and all the patients subsequently recovered.

The second wave of positive cases came to light on March 5 with a group of Italian tourists. The tourists and people who came in contact with them have since been receiving treatments and are under quarantine. Indian government airlifted 645 Indians as early as January 31 and February 1, 2020, from the worst-affected Wuhan Province in China and placed them in quarantine in Delhi before releasing them. India has been sending medical staff to the worst-affected countries including Italy and Iran in recent times. Here in Israel, we are continuously been updated on emails and WhatsApp groups by the Indian Embassy on the continuously changing situation.


Media has been abuzz on India testing very few people per million population, as compared to other countries. And these concerns are genuine too. To understand it better, the current testing is limited to people with travel history (Stage I) and people who came in contact with those (Stage II). Mass gatherings are cancelled and there is awareness being spread among the people. The problem is only the symptomatic carriers are being checked due to current limitations of being able to conduct only 6,000 tests per day. However, more test kits are being procured.

The potent virus

No one is spared by the virus, irrespective of gender, geography, caste or economic class. From American actor Tom Hanks and his wife Rita Wilson to Canadian President Justin Trudeau’s wife Sophie Trudeau, all have tested positive for the virus. And the virus seems very resilient too.

Recent research established that the virus can stay as aerosol (droplets in the air) for hours and on surfaces for days. Another recent study showed that the virus tested positive in stool samples of 10 patients, even though the nasopharyngeal tests were negative. This demonstrates the potential of faecal transmission of the virus beyond it spreading through contact and transmission through the air. Face masks should be worn only by patients or those taking care of the sick. Regular detergents and hand sanitisers are good enough to break/dissolve the virus structure. Expensive detergents with antibiotics will not do anything different from their basic counterparts. Antibiotics kill bacteria and not viruses. As for sanitisers, at least 60 per cent alcohol content is necessary to break the virus apart. DIY sanitisers that are made at home should be disregarded. The same applies to the media channels/ organisations spreading such news and risking the health of millions.


Mild symptoms following the viral infection include dry cough, fever with shortness of breath and diarrhoea. Roughly two to five per cent cases are fatal, which progress from pneumonia-like symptoms to multiorgan failure. At risk are those with compromised immune systems including the elderly, or those with co-morbidities such as cardiovascular disease, diabetes, cancer or hypertension. There were times when our parents asked us to be home on time when we were growing up. Now, the tables have reversed and we should request our parents and grandparents to quarantine themselves as much as possible to safeguard their health from the viral threat.

Asymptomatic carriers

On average it takes two to 14 days for the symptoms to appear. During this stage, the person is an asymptomatic carrier — that is, the person is not showing full-blown symptoms but is transmitting the virus nonetheless. It is almost like the 2011 movie Contagion is playing out in the real world. It is trending on Netflix and can be a good reference to understand the transmissions globally. Malayalam movie Virus can also be enlightening. After all, Kerala braved Nipah virus which has a fatality rate of 40-75 per cent against two to four per cent for Covid-19 infection. While South Korea is testing everyone, Italy is testing only the people with symptoms. The scary part is that the age group of 20 to 29 years do not show any symptoms and appear fine. However, they are transmitting the disease in large numbers. Hence social distancing for two weeks can help contain the spread to a large extent.

Governments are doing their best, but personal responsibility and sensibility is the need of the hour.

The case of ‘Patient 31’ from South Korea gives a deeper understanding, makes one realise the gravity of the situation and the need for social distancing. The patient travelled to crowded places in capital Seoul, met with an accident on February 6, 2020, in Daegu, admitted herself to Saeronan Hospital, attended the Shincheonji Church services on February 9, 2020, and February 16, 2020.

Despite being advised by doctors to test herself for Covid-19, the woman went for a buffet with a friend in a hotel on February 15, and it was only by February 17 when her symptoms worsened that she got herself tested. The results were positive and she was identified as ‘Patient 31’ on February 18, 2020.

In just a few days, there were hundreds of people from the hospital (119 cases), Shincheonji Church (2,418 cases), and the hotel who were tested positive. The woman became responsible for 80 per cent of the total cases in South Korea.

No vaccine and no cure

Currently, there are no vaccines for prevention nor FDA-approved drugs for treatment.

The first vaccine trial began on March 16, 2020, based on Moderna’s messenger RNA vaccine — 70 days after the genetic makeup of the coronavirus was released. Another antiviral drug developed by Gilead Science is soon going to trials on infected patients with severe infection. This is a great scientific leap compared to how pandemics like the plague or Spanish flu panned out just a century ago.

In the meantime, people working from home or under isolation have become creative. Be it workouts at home, or like my friend in quarantine who is taking his singing skills seriously. Remember, Isaac Newton also worked from home during a pandemic and ended up discovering gravity.

Let us not be South Korea’s Patient 31. Let us help contain the contagion.

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

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Contagion

Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau.

The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson’s may spread in a similar way.

Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning.

But for more than a quarter-century, researchers have been unable to decide between two explanations. One is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer.

The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.

The studies, done independently by researchers at Columbia and Harvard, involved genetically engineered mice that could make abnormal human tau proteins, predominantly in the entorhinal cortex, a sliver of tissue behind the ears, toward the middle of the brain, where cells first start dying in Alzheimer’s disease. As expected, tau showed up there. And, as also expected, entorhinal cortex cells in the mice started dying, filled with tangled, spaghettilike strands of tau.

Over the next two years, the cell death and destruction spread outward to other cells along the same network. Since those other cells could not make human tau, the only way they could get the protein was by transmission from nerve cell to nerve cell.

Although the studies were in mice, researchers say they expect that the same phenomenon occurs in humans because the mice had a human tau gene and the progressive wave of cell death matched what they see in people with Alzheimer’s disease.

Two groups of researchers were inspired by the many observations over the years that Alzheimer’s starts in the entorhinal cortex and spreads.

Researchers knew that something set off Alzheimer’s disease. The most likely candidate is a protein known as beta amyloid, which accumulates in the brain of Alzheimer’s patients, forming hard, barnaclelike plaques. But beta amyloid is very different from tau. It is secreted and clumps outside cells. Although researchers have looked, they have never seen evidence that amyloid spreads from cell to cell in a network.

Still, amyloid creates what amounts to a bad neighbourhood in memory regions of the brain. Then tau comes in — some call it “the executioner” — piling up inside cells and killing them. If some cells take longer than others to succumb to the bad neighbourhood, that would explain the spread of the disease in the brain, and there would be no need to blame something odd, like the spread of tau from cell to cell.

The question of which hypothesis was correct — tau spreading cell to cell, or a bad neighbourhood in the brain and cells with different vulnerabilities to it — remained unanswerable. A Dr  said he tried for 25 years to find a good way to address it. One of his ideas was to find a patient or two who had had a stroke or other injury that severed the entorhinal cortex from the rest of the brain. If the patient developed Alzheimer’s in the entorhinal cortex — and it remained contained there — he would have evidence that the disease spread like an infection.

The solution came when researchers were able to develop genetically engineered mice that expressed abnormal human tau, but only in their entorhinal cortexes. Those mice offered the cleanest way to get an answer, said John Hardy, an Alzheimer's researcher at University College London who was not involved in either of the new studies.

There is another advantage, too,  the Dr  said. The mice give him a tool to test ways to block tau’s spread — and that, he added, “is one of the things we’re excited about.”

But if tau spreads from neuron to neuron,  it may be necessary to block both beta amyloid production, which seems to get the disease going, and the spread of tau, which continues it, to bring Alzheimer’s to a halt. He and others are also asking if other degenerative diseases spread through the brain because proteins pass from nerve cell to nerve cell.

Distorted protein

Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning.

But for more than a quarter-century, researchers have been unable to decide between two explanations. One explanation is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer.

The new studies provide an answer. And they indicate it may be possible to bring Alzheimer's disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.