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Krishna: There are several factors that control the severity. Some you can avoid, some you can’t!

First let me explain what factors affect the infection ….

Initially it was thought that only older people 're at risk. But now reality shows even young people could have fatal consequences.

There can be a few reasons for this (1).

1. Even young people, because of their careless life styles, can have diabetes, BP and heart conditions. These factors increase the chance of severity. So keeping all these conditions in check is very vital to reduce the severity.

2. The amount of virus (microbial dosage or inoculum, the number of viral particles that cause infection) that infects an individual may have crucial outcomes. Small numbers of viral particles are more likely to be contained effectively by the body’s defenses. Then, infection may cause no symptoms or only mild disease. Get a huge dose which can lead to increased viral growth, and your outcome may be worse. A person with a high viral load has more virus particles than one with a low load. Either your immune system can't cope as it would be overwhelmed or can cause severe fatal reactions. Viral load is a deciding factor here. So to keep the viral load small you will have to maintain physical distance, wear a well fit mask, and maintain hygiene.

3. For some genetic susceptibility may be involved: in other words, there are individuals whose genetic makeup leaves them more vulnerable to the virus as it spreads through their bodies. Viruses often gain access to host cells via surface proteins, which vary in presence and nature from person to person. Someone with no such surface proteins may be resistant to infection. In the case of HIV, for example, some people lack the receptors needed for viral infection and are not susceptible to the virus. So your genetic make up is responsible for the danger here. You can’t do anything about this factor.

4. The route by which a virus enters the body also influences infection outcome. It’s possible that virus inhaled in the form of aerosolized droplets triggers different immune defenses than does virus acquired by touching contaminated surfaces and then touching one’s face. The nose and the lung differ in local defenses, so the route of infection could significantly affect the outcome.

5. The virulence of the virus. Viruses differ in virulence — their capacity to damage host tissues or immunity — even when they are all the same species. This is why flu seasons vary in severity from year to year. The varieties of a virus such as coronavirus differ depending on small genetic characteristics and how these affect the interaction with human hosts. As the coronavirus spreads from person to person, it may undergo unique changes in its genetic structure that enhance or attenuate its capacity to do harm. Strains that are more virulent could lead to more severe disease. How deeply into the lungs the viral particles penetrate is also a factor. You can’t do anything about this either.

6. Which infections the immune system has fought in the past. People’s immune status — especially their history of prior infectious diseases — crucially determines how they respond to a new infection. The immune system remembers previous encounters with microbes, and that affects how it fights and responds to new ones. In the case of dengue, infection with one type of the virus can make the individual more susceptible to infection with a different type of the same virus. In other situations, a recent infection with a virus can affect susceptibility to an unrelated new infection. For example, having had the flu before coronavirus infection could change the course of Covid-19 disease in unpredictable ways. When a person’s immune system has no memory of an infectious agent, it may be unable to rapidly respond, and this may allow the invader to escape detection, giving it more time to cause damage. Keep your body healthy and fit by eating nutritious food and exercising you can control the intensity ‘somewhat’.

7. Age and gender (2) also influence the outcome. There are substantial differences in the immune system between males and females and these have significant impact on the outcome from a wide range of infectious diseases. One key difference is that women have two X chromosomes per cell whereas men have one. “A number of critical immune genes are located on the X chromosome”, according to specialists, in particular the gene for a protein called TLR7, which detects single-stranded RNA viruses like the coronavirus. “As a result, this protein is expressed at twice the dose on many immune cells in females compared to males, and the immune response to coronavirus is therefore amplified in females’. Can you control these? NO! { One of my male colleagues joked recently that he wants to go for a gender change! :) But I told him, even that superficial change won’t help him now}.

8. Getting vaccinated, when that option is available, is the best way to avoid it or reduce the intensity to a large extent because vaccination keeps your immune system ready to fight the infection.

Taken together, these variables create a complex picture. The amount of virus, our genes, the route of infection, the variety of the virus and our immunological history combine to produce outcomes ranging from asymptomatic infection to death. And because these parameters can vary so much from infected person to infected person, it’s impossible to predict who will have the severe form and who will have the mild form and who will live and who will die. You can’t have a single mantra to everybody. Therefore, despite accumulating evidence that most who acquire the coronavirus will not develop severe disease, the uncertainty of who is at grave risk enhances the pandemic’s terror.

So don't be so confident and careless. Try to avoid it in the first place by taking the precautions experts advice.


  1. Qs people asked me on science and my replies to them - Part 179
  2. Why are men more likely to get worse symptoms and die from covid-19?



Q: How can we protect old people from infections if vaccines don't work properly for them?

Krishna:  Yes, a vaccine against any deadly disease like Covid-19 may not work well in older people who are most at risk of becoming seriously ill and dying from the disease. In such cases immunising others around them, such as children, youngsters other adults is the best way to protect very old people. 

Sometimes it is possible to protect a vulnerable group by targeting another group and this, for example, is being done with influenza. Giving the nasal spray flu vaccine to children who do not often get severe flu protects their grandparents. Immunising health and care workers – who are likely to be the first to get the vaccine – would also help protect older people who have the most contact with them.

One thing that’s apparent, even in healthy older people, is that there’s more inflammation all around the body.

According to experts, something else might be needed alongside the vaccine for older people, such as the steroid drug dexamethasone, which can block the inflammation caused by the virus and has been shown to save lives in Covid-19. 


In a new article, scientists provide an exhaustive, evidence-based review of how COVID-19 droplets from infected patients spread through the air and describe how health care professionals can protect themselves. This Pulmonary Perspective is published online in the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine.

In "Coughs and Sneezes: Their Role in Transmission of Respiratory Viral... they describe the various types and sizes of virus-containing droplets present in sneezes and coughs, the locations in the respiratory systems where they deposit, and how certain medical procedures and devices may spread these droplets and the risks for health care professionals.

Research recommendations for reducing the transmission of respiratory tract infections, which are consistent with guidelines from the Centers for Disease Control and Prevention, include :

  • Avoid procedures that irritate airways and provoke violent coughing and try to reduce exposure to infectious aerosol.
  • If possible, health care providers should stay six feet away from infected patients, especially when the patient is coughing or sneezing.
  • When using a mechanical ventilator, institute barriers to filter the virus or reduce virus dispersion by placing a filter at the exhalation port of the ventilator or connecting a filter to the oxygen mask.
  • For spontaneously breathing patients, placing a surgical mask on the patient's face or using tissue to cover his or her mouth, especially during coughing, sneezing or talking, may reduce the dispersion distance or viral load.
  • Employ PPE for health care providers.
  • While, ideally, infected patients should be in single rooms to prevent droplet dispersion, it is acceptable for two patients with the same infection that is spread by respiratory droplets to be in the same room.

Coughs and sneezes create respiratory droplets of variable size that spread respiratory viral infections. Because these droplets are forcefully expelled, they are dispersed in the environment and can be exhaled by a susceptible host. While most respiratory droplets are filtered by the nose or deposit in the oropharynx, the smaller droplet nuclei become suspended in room air and individuals farther away from the patient may inhale them.

These finer particles are carried by the airstream into the lungs, where their site of deposition depends on their size and shape and is governed by various mechanisms. The respiratory transmission of the SARS-CoV-2 virus that causes COVID-19 is mainly by respiratory droplets. Appropriate protective measures are necessary to prevent virus transmission in various settings.



Studies Report Rapid Loss of COVID-19 Antibodies

The results, while preliminary, suggest that survivors of SARS-CoV-2 infection may be susceptible to reinfection within weeks or months.

Apair of studies published this week is shedding light on the duration of immunity following COVID-19, showing patients lose their IgG antibodies—the virus-specific, slower-forming antibodies associated with long-term immunity—within weeks or months after recovery. With COVID-19, most people who become infected do produce antibodies, and even small amounts can still neutralize the virus in vitro, according to earlier work. These latest studies could not determine if a lack of antibodies leaves people at risk of reinfection.

One of the studies found that 10 percent of nearly 1,500 COVID-positive patients registered undetectable antibody levels within weeks of first showing symptoms, while the other of 74 patients found they typically lost their antibodies two to three months after recovering from the infection, especially among those who tested positive but were asymptomatic. 

In contrast, infections caused by coronavirus cousins such as SARS and MERS result in antibodies that remain in the body for nearly a year.

The first study, published June 16 on the preprint server medRxiv, screened for antibodies in almost 1,500 coronavirus patients in Wuhan, China. The researchers compared their levels to three other groups: nearly 20,000 members of the general population; more than 1,600 patients hospitalized for reasons other than COVID-19; and more than 3,800 medical workers, whom the authors assumed had “inevitably” been exposed to the virus in its early days, meaning they should have developed antibodies.

They found that while almost 90 percent of COVID-19 patients had antibodies, roughly 1 percent to 5 percent of individuals in the others groups had them as well. The authors conclude in their paper that the remaining 10 percent of infected patients with no detectable antibodies, combined with the lack of antibodies in healthcare workers, suggest that “after SARS-CoV-2 infection, people are unlikely to produce long-lasting protective antibodies against this virus.”

In the second study, published June 18 in Nature Medicine, researchers compared the immune responses of 37 asymptomatic but positive patients to an equal number with severe symptoms living in the Wanzhou District in China. They found that asymptomatic individuals reacted less strongly to infection, with 40 percent having undetectable levels of protective antibodies in the two to three months after the infection compared to 13 percent of the symptomatic patients. 

Overall, these results are interesting but more research is needed, following large numbers of people over time.Only then will we clearly know how many people produce antibodies when infected with coronavirus, and for how long.

In addition to a lack of consistency among testing methods, individuals do not have a uniformly robust antibody response. This fact may make it difficult to develop a vaccine that works equally well for all people.

These reports highlight the need to develop strong vaccines, because immunity that develops naturally during infection is suboptimal and short-lived in most people. We cannot rely on natural infection to achieve herd immunity. 


But our common sense tells us that a ‘dying patient’ usually exhibits some, usually serious symptoms.

Even if someone is infected by the novel coronavirus and remains asymptomatic — free of coughing, fever, fatigue and other common signs of infection, that doesn't mean the coronavirus isn't taking a toll. The virus can still be causing mild — although likely reversible — harm to their lungs (2).

The asymptomatic individuals have a reduced inflammatory response characterized by low circulating concentrations of cytokines and chemokines, which are actually responsible for fatal reactions. Until you test them, it is difficult to identify them as COVID-19 corona virus carriers. The asymptomatic patients in China were hospitalized for observations (2). Fifty-seven percent of them showed lung abnormalities on a CT scan, a sensitive imaging technique that produces a three-dimensional picture of the lungs. Some showed "striped shadows," while others presented with "ground-glass opacities" — clear signs of inflammation in the lungs. It shows that even people with no outward signs of infection can be experiencing some temporary damage to their lungs. It was concluded that the coronavirus is often taxing a person's body more severely than their symptoms — or lack thereof — suggest. The same situation was observed in New York too.

Some people who appear asymptomatic at first do later develop classic symptoms such as high temperatures, fatigue and difficulty breathing. At present we can't predict how an individual's case will progress. There's no way to know who is going to stop with an asymptomatic infection and likely recover completely and who is likely to go on to more severe infection in normal healthy individuals as several factors influence the outcome (1).

Now can Covid-19 capable of killing an asymptomatic patient? It is unlikely as only mild cases don’t show any symptoms. Viral load will be so low in such patients that it doesn’t cause any serious immune reaction. And Serious cases show definite symptoms.

However, if you take co-infections or co-morbidities into consideration, that is a different ball game altogether.

Then there is a condition called ‘happy hypoxia’ or ‘silent hypoxia’. A healthy person would be expected to have an oxygen saturation of at least 95%. But doctors are reporting patients attending A&E with oxygen percentage levels in the 80s or 70s, with some drastic cases below 50%. These people describe themselves as comfortable. Although these people look normal, these patients are likely to have hypoxic cardiac arrests. Early hypoxia can rapidly progress to pneumonia and death. But these patients too show some mild symptoms like black lips, shortness of breath or fatigue or something else but might not notice them or take them seriously. People may not be aware of their more rapid breathing rate and don't seek help, yet blood oxygen levels continue to fall. In the meantime, the body slowly becomes somewhat adjusted to the lower levels of oxygen, much like what happens when a person travels to a higher altitude. By the time these patients get to the hospital with crippled lungs and crashing oxygen levels, it will be too late. So it is not noticing the ‘early symptoms’ that is responsible for the progress and subsequent death, not the absence of symptoms.

In the journal Academic Emergency Medicine, they reported that among 50 patients with low oxygen saturation, switching to a prone position (putting them on their sides and tummy) raised average saturation significantly.


  1. Qs people asked me on science and my replies to them - Part 195

Q: Why has science become helpless against COVID-19?

Science is an extremely slow process unlike other things. You just cannot think and do whatever you want with science because the consequences can be catastrophic.

Science needs to get validated to get established and validation takes hell of time.

Okay, we found what is causing COVID 19. Then we will have to test again and again what it causes ( various symptoms) and how it causes. That is years and years of work.

Then we will have to figure out how to stop all these processes that are giving us trouble. More years of work.

Drugs are being identified and vaccines are being developed. But the testing for tehir safety and efficacy takes several years (some 20–30 years in the former cases and atleast 2–3 years for the latter ones) but now they are speeding up the processes but in the process if we miss some dangers, it is the scientists that are blamed. We are doomed if we speed up, we are doomed if we go slow.

But still we are speeding up things. Labs are ‘working 48 hours per day’ all around the world! We noticed COVID 10 just six months back. You want results so soon? That is a disastrous expectation!

If we are unable to control the spread, it is because of non-cooperation from politicians, governments and the public. Scientists clearly stated all the points to manage the pandemic efficiently long back. But most people don’t even bother to follow what the scientists advice. Then you blame science for not restraining it?

Then we don’t have enough funds to work. People spend more on sports, religion, defence, and other things than on science. Then how can we manage with meagre funds to solve your problems?

You are misplacing your anger, and frustration.

If there is anything that can help the human kind now, it is science. Just give us money and time, we will show you the results.

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