Viruses live in a twilight zone, somewhere between life and its ingredients.

The word “virus” conjures up the terror of death on invisible wings. It raises images of hospital wards filled with patients dying of Spanish ’flu; poliomyelitis victims in iron lungs; health workers dressed in full-body suits against the deadly Ebola virus; or babies with microcephaly that could be linked to Zika virus. These are all dreadful human diseases, but they tell only a very small part of the story. Viruses infect all life forms—not just humans, and most viruses don’t even cause disease. Viruses are part of the history of life on Earth; precisely what part they play is a mystery that is slowly being unraveled.

The Oxford English Dictionary defines a virus as “an infective agent that typically consists of a nucleic acid molecule in a protein coat, is too small to be seen by light microscopy, and is able to multiply only within the living cells of a host.”

We think of germs as things that make us sick, and that includes both viruses and bacteria, so what’s the difference between bacteria and viruses? Bacteria, in common with other living cells, can generate their own energy, and translate the DNA sequences of their genes into proteins. Viruses can do neither.

Many important questions—some very fundamental— still remain open.

Are viruses alive? This question has plagued philosophers of science, though few virologists have tackled it. Some have explained that viruses are alive only when they are infecting a cell, and when they are outside a cell as an encapsidated particle, or “virion,” they are dormant, something like the spore of a bacterium or fungus. To answer this question, one first has to define life. Some argue that since viruses cannot generate their own energy, they are not alive. Whether or not we consider viruses to be alive, no one would dispute that they are an important part of life.

Are viruses the fourth domain of life? Darwin first conceived the idea of a tree of life, to reflect how organisms are related to each other. Since the 1970s life has been thought of as having three domains: bacterial, archaeal, and eukaryotic. The bacteria and the archaea each make up a kingdom of life, and the eukaryota are divided into several more: eukaryotes include animals such as ourselves, as well as plants, fungi, and algae. Bacteria and archaea are single-celled organisms that do not have a nucleus, and may be closer to the root of the tree of life. Eukaryotic cells are much larger and have distinct nuclei in which the genetic material resides and is replicated. Where do viruses fit on this “tree” of life? With recent discoveries of giant viruses, some proposed that viruses should be considered a separate domain of life. However, viruses can infect all other forms of life (including other viruses), and when we look at the genes that make up viruses and other organisms, we find that virus genes are everywhere, integrated into the genomes of all organisms. So rather than being a separate domain of life they are scattered throughout the tree.

Progress in the study of viruses accelerated in 1915 when one Frederick Twort discovered that bacteria, too, could be infected by viruses. Like many great discoveries, this was an accident. Twort was trying to figure out a way to grow vaccinia (cowpox virus), and he thought that bacteria might provide something essential for the virus to grow. He grew the bacteria in petri dishes, and in some of his cultures he found small areas that had become clear. No bacteria survived in these areas; something was killing them. Like the virologists before him, Twort showed that this agent could pass through very fine porcelain filters and infect and kill fresh cultures of bacteria.

Viruses teeter on the boundaries of what is considered life. On one hand, they contain the key elements that make up all living organisms: the nucleic acids, DNA or RNA (any given virus can only have one or the other). On the other hand, viruses lack the capacity to independently read and act upon the information contained within these nucleic acids.

Viruses live in a twilight zone, somewhere between life and its ingredients.

The different molecular strategies that viruses use to evolve within and between hosts, and to provide a view of the complexities of short term and long-term evolution, with their implications for viral disease.

Viruses exist in one of two general states, which you could think of as their ‘life’ cycle. In one state they are drifting around, either in solution or in the air, mainly just hanging around and ‘hoping’ to bump into the right sort of cell.

DNA viruses are likely to have co-evolved with their hosts while the DNA world was developing.

DNA virus evolution, includes the simplest and the most complex of the DNA viral genomes known.

Viroids are unique systems for the study of RNA structure, function, and evolution. They are the minimal RNA replicons characterized so far — their genome is 10-fold smaller than that of the smallest known viral RNA — and in a certain sense are at the frontier of life. Despite being exclusively composed by a single-stranded and highly structured circular RNA of only , viroids contain sufficient information to infect some host plants, to manipulate their gene expression for producing progeny, and, as a consequence, to incite in most cases specific diseases . In striking contrast to viruses, which encode proteins that mediate their own replication and movement, viroids depend essentially on host factors for these purposes and can therefore be regarded as parasites of their host transcription machinery

The detailed clinical features of five patients with COVID-19 are aligned with the quantitative severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral RNA load from nasopharyngeal and other selected sampling sites. Previous studies in patients with SARS, Middle East respiratory syndrome (MERS), and COVID-19 generally provide insufficient detail to allow examination of the relationship between individual patient clinical course and viral RNA load.

Variation is intimately linked to their disease-causing potential. Paramount to the understanding of RNA viruses is the concept of quasispecies, first developed to describe the early replicons thought to be components of a primitive RNA world devoid of DNA or proteins.

Virologists now understand that virus populations are not made of a single member with a defined nucleic acid sequence. Rather, they are dynamic distributions of nonidentical but related members called a quasispecies. It was given this name because the classical definition of species – an interbreeding population of individuals – has little meaning for viruses.

The consequence of a quasispecies is that most viral infections are initiated not by a single virion, but a population of particles. The progeny produced after this infection results from selective forces that operate inside the infected host. The virions that go on to infect a new host have passed through another set of external selective forces. A steady-state population of a viral quasispecies consists of a vast number of particles.

Biology, and evolution in particular, are based on reproduction or multiplication and on variation. Reproduction; pure has the property of self-enhancement and leads to exponential growth. Self-enhancement in chemical reactions under isothermal conditions is tantamount to auto catalysis.

Nevertheless, based on the assumption that viral RNA load correlates with high levels of viral replication, there are important insights to be gained from this time-course analysis. Currently, our understanding of the relationship between viral RNA load kinetics and disease severity in patients with COVID-19 remains fragmented. Patients with COVID-19 with more severe disease requiring intensive care unit admission had high viral RNA loads at 10 days and beyond, after symptom onset. Unfortunately, it is unknown when in the course of their disease these patients deteriorated. Patients who developed late respiratory deterioration despite the disappearance of nasopharyngeal viral RNA. It would be interesting to know whether viral RNA load in lung tissue, or a surrogate sample such as tracheal aspirate, mirrors the decline in nasopharyngeal shedding. Nevertheless, this observation suggests that these late, severe manifestations might be immunologically mediated and has obvious implications for the potential to use immune-modulatory therapies for this subset of patients. This finding is consistent with recent reports that corticosteroids were beneficial for acute respiratory distress syndrome, and possibly those with COVID-19. With more detailed data such as those provided by Lescure and colleagues, the use of viral RNA load to suggest potential clinical strategies to treat COVID-19 could be exploited.

I never thought I’d write about a pandemic but now that I am pandemic stricken, I am researching about it leaving aside my rare genetic cancer vHL. Why am I pandemic stricken? It’s because a woman unaware of the viral world and how it works out of apathy said I should die right now, else who will account for it if my brother gets ill? What guts! 

She was a patient with few symptoms but high viral RNA load in the nasopharynx early in the course of disease.

Unaware of the viral RNA kinetics of patients despite the disappearance of nasopharyngeal viral RNA she was shedding.

Experts have also strongly suggested that solely relying on testing as a safeguard can make people ‘lax’ and take other safety measures, such as mask-wearing and social distancing lightly, which could be the two biggest factors which can spike up infections. Remember, the tests are a preventive measure and only effective, as long as you put in place other security measures. But she put my life at a risk by subtly killing me. 

 In the recent weeks of the surge in cases, one of the most peculiar and constant query has been about those who have COVID-19 symptoms but continue to test negative in RT-PCR tests. Sometimes, even though CT scan reports display patches in lungs due to coronavirus, the RT-PCR test report remains negative. According to experts, RT-PCR is the gold standard for COVID detection, however, as per reports from across the country, at least 1 in 5 patients may end up getting a false negative report. Why is that happening?

• Even though RT-PCR is gold standard, we have known from Day 1 that there’s a 30 per cent chance of it to be inaccurate. Moreover, when the testing kits are developed, the scientists pick up those parts of virus which are least prone to mutate, therefore this could be a reason behind the false-negatives.
•  The second reason for this could be that the viral load in your body is so less that its not getting detected in the RT-PCR test, as per experts.
• The sample collection, transportation as well as the overburden of the cases, wherein the labs are not able to complete the analysis of the sample, plays a major role in the quality of tests, Dr Mahajan explained.

Next, repeat your RT-PCR test in 2-3 days, and take advise of your doctor to get a CT scan, says Dr Ray.

Blood tests at times are a good marker of inflammation and they can also give you and your doctor an idea of what is going on in your body, in particular, the C-reactive protein and the D dimer. Both of them are said to be a good testing ground for understanding what is happening in your body.

The test was not done in my case because I have Trouble swallowing food and medicines, Here I'd like to state The cranial nerves associated with the swallowing process are the trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), accessory (XI) - usually not considered - and hypoglossal (XII). 

It should be emphasized that the structures involved in the swallowing process are pairs, both anatomically and/or functionally, due to the dual-side innervation. 

Anatomically unique, the tongue, palate, pharynx, and larynx are functional pairs, each side having independent innervation.

Hence it might be extremely hurtful as I get pain in the pharynx and larynx and often tongue gets paralyzed. Voice becomes hoarse after speaking a bit.

"Ur antibody level is low..which can occur 

1.early in disease

 2.low viraemia 

3.immunocompromised state"

Said Dr. Ishita B Sen

Nuclear Medicin

Director & Head

Dr. Ishita B Sen is a Nuclear Medicine Physician with 20 years experience, having worked in various hospitals across Delhi – NCR., She takes special interest in Nuclear Oncology and Radionuclide Therapy Sende

She also treats Covid.

The transplanted liver has been affected

Making Mum cry in the temple everyday for the daughter she had saved through 15 surgeries. How dare the woman out of spite attack and pass on her disease knowing that her daughter’s immune system has been turned off since liver transplant. Now who should account for my extra illness? Will I recover with my immune system turned off.

Even blocked my writing penchant. This blog is very useful for me. It contains what I encounter in life and also I can send my history of disease to the doctors via this blog.

I will die but never steal. I believe in karma. And let me ask the readers who was bullying whom and subtly killed her?

Ma had symptoms before 28th April and from 28th she started Augmentin Duo 625 then Dr Ishita Sen prescribed Azythromycin because of headache and congested nose. Even with my immune system turned off I didn't get any symptoms.

 Only after Madam fancy hit me and said without a mask I should die right now within 3 days I got High D dimer and CRP but no antibody. Antigen couldn't be tested because it might hurt my throat. Bilateral trigeminal nerve, vagus, Hypoglossal, Glossopharyngeal, facial, auditory are all compressed by tumours.

As per the rent, we have lived in lousy houses and he started paying rent only for this house he himself chose because of the court notice by which the landlord evicted us while I had kidney cancer. Before that everything was arranged by literally begging. Begging continues because he said he can't keep his promise to Father and can't pay for my treatment/ food/ electricity and water bill. Only rent. Avoiding responsibilities he's doing a favour to mother and sister. This transmutation of slow-witted Arindam Bhattacharjee to Arri became more pronounced after marriage.

My mother is sitting and crying in front of the temple inside the house that despite her precautions and maintaining distance I got Covid and I have uncertainty

She called him through my phone and told him a "kulangar", or black sheep, and disgrace.

She was crying that if anything happens to me she won't live without me which hurt me a lot.

Who is Arri? He's called Arri by his cinematographer friends and he tries producing an anglicised impact by calling Mom. It's all about style and glamour.

But he's not the brother I grew up with. When he was beaten up by the shady uncle who said filthy words like " bastard, scoundrel and rascal". He said my parents haven't taught me to use filthy language. 

Yet he came to look after Mum because of her illness and was constantly shouting beyond the door that I should open the door. Why? They were wearing PPE suits and have travelled from Bombay to Delhi he will be carrying the pandemic virus. When Ma opened the door he shouted: "Bastard, rascal" to Mum. 

Arindam Bhattacharjee screaming in a wild way broke the shield with which mother protects me saying we are asking him to leave from the house of which he pays the rent.

 He only pays rent and not bearing or accepting his responsibilities towards his mother and ailing sister.

I called him to help me look after Mum because at 68 she developed mild Covid from the society being a hotspot or by collecting the deliveries of medicines or food kept in the bag hanging on the door. Perhaps some delivery men might be Covid positive and she collected stuff after an hour but aSARS-CoV-2 remained viable in aerosols throughout the duration of in experiments (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per litre of air. This reduction was similar to that observed with SARS-CoV-1, from 104.3 to 103.5 TCID50 per millilitre. Because from 18/3/2020 we are under voluntary isolation and just Mum collects the deliveries hanging on the bag outside the door after the person has gone for over alll

Now to continue with Covid 19

SARS-CoV, which causes severe acute respiratory syndrome (SARS). The incubation period for SARS is usually 2 to 7 days trusted Source, but it can be up to 10 days in some people.

MERS-CoV, which causes Middle East respiratory syndrome (MERS). The incubation period for MERS-CoV is between 2 and 14 days trusted Source, with 5 to 6 days being average.

The bottom line

Most people who develop COVID-19 start noticing symptoms within 2 to 14 days after being exposed to the novel coronavirus known as SARS-CoV-2. On average, it takes about 5 days to develop symptoms, but this may change as we learn more about the virus.

It would be interesting to know whether viral RNA load in lung tissue, or a surrogate sample such as tracheal aspirate, mirrors the decline in nasopharyngeal shedding. Nevertheless, this observation suggests that these late, severe manifestations might be immunologically mediated and has obvious implications for the potential to use immune-modulatory therapies for this subset of patients.

In a pandemic, prevention of disease transmission is key. 

It has been noted implications for transmission from patients with few symptoms but high viral RNA load in the nasopharynx early in the course of disease.

This finding is consistent with recent reports that corticosteroids were beneficial for acute respiratory distress syndrome, and possibly those with COVID-19. With more detailed data such as those provided by Lescure and colleagues, the use of viral RNA load to suggest potential clinical strategies to treat COVID-19 could be exploited.

I am on corticosteroid inhalers and nebulizers.

It is noteworthy that the presence of viral RNA in specimens does not always correlate with viral transmissibility. In a ferret model of H1N1 infection, the loss of viral culture positivity but not the absence of viral RNA coincided with the end of the infectious period. In fact, real-time reverse transcriptase PCR results remained positive 6–8 days after the loss of transmissibility. For SARS coronavirus, viral RNA is detectable in the respiratory secretions and stools of some patients after onset of illness for more than 1 month, but live virus could not be detected by culture after week 3.The inability to differentiate between infective and non-infective (dead or antibody-neutralised) viruses remains a major limitation of nucleic acid detection. Despite this limitation, given the difficulties in culturing live virus from clinical specimens during a pandemic, using viral RNA load as a surrogate remains plausible for generating clinical hypotheses.

Virus crystals add a bit of disorder, and they will “wake up” and regain their infectious properties.

The process of transformation of viral components into organized solid particles is known as crystallization. A virus crystal consists of many thousand viruses and because of it’s purity we can understand their characteristics, pathogenic activity, mutational levels, nucleic acids, capsid properties.

Viruses sit on a fine line of what constitutes life. To some extent, the discussion is philosophical in that definitions are chosen and the subject either meets those criteria or not, and some criteria are a bit more arbitrary than others.

Some have argued that viruses in infectious virion form are life, at the stage when infecting a cell and redirecting its machinery to make more virus particles. 

Over the decades, biology has shifted from a study of cells in Petri dishes, or monks growing peas, to a more abstracted investigation into information science and related fields and subjects: mathematics, entropy, statistics, physics. That perspective started with scientists like Schrödinger, Turing, and Von Neumann, and it continues in the modern day with work by Dawkins, England, and others.

Viruses have and continue to shape the evolution of life around them. In a way, they are frozen information, and the definition of life may be changed over time, as we gain a more broader picture of how things work.

In 2015, the Wuhan Institute of Virology (WIV) was upgraded to the National Biosafety Laboratory (Level 4), the first of its kind in China, at a cost of 300 million Yuan ($44 million). The lab was involved in the research of coronaviruses (CoVs) and the causative agents of the severe acute respiratory syndrome (SARS) outbreak in 2003. In 2015, Li et al. published reports about the species of bats acting as natural reservoirs for SARS-like CoVs (SL-CoVs), and pointed out the genetic diversity of the viruses in bats, highlighting the possibility of them infecting the humans. The transmission from palm civets to humans occurred when the civets came into human contact in the live animal markets. As the pools of CoVs in bats were limited, the likelihood of a future emergence of this viral outbreak was never anticipated.

However, when it was proven that a chimeric virus containing the SHC014 spike in a SARS-CoV backbone causes robust infections in both human airway cultures and mice,a warning was issued that the starting materials required for SARS-like emergent strains were already circulating in animal reservoirs. A research team in China that spent 5 years in the Shitou caves of Yunnan sampling from the bats issued a similar warning and raised alerts for a potential disease outbreak if adequate precautions were not taken. By December 2019, the first cluster of cases of infection with a novel CoV was reported in China.

Naturally, the origins of the epidemic were investigated. The WIV published reports stating that the new strain of CoV had bats as the “probable” source.All the studies of Shi Zheng Li, the lead virologist from the institute, on bat-related CoVs were centered in the southern, subtropical areas of Yunnan. However, the outbreak occurred in Wuhan, which is almost 900 km from Yunnan. Samples from the infected patients were compared with those from the bats, but none of them matched. If not from bats, where did this novel strain of CoV come from? The Government of China conducted an investigation and reported a wildlife market, 10 miles away from the virology institute, as the epicenter. Though the Chinese government discredited the possibility of a lab origin based on the genetic studies, the distance of the epicenter from the bat caves raises questions.

The theory of lab origin gains credibility from seemingly unrelated, but nevertheless solid and tangible facts. The institute called for research job openings on November 18, 2019, and December 24, 2019. These urgent advertisements tell us about the kind of research taking place in the labs and also underline the fact that the Chinese knew about the possibilities of novel strains even before the outbreaks that warranted research. The lab then generated a chimeric virus from the SARS-CoV using the reverse genetics approach and reported the potential for human emergence. The leak could have happened from this lab.

On February 6, 2020, scientists from the South China University pointed out that the intermediate host, the horseshoe bat, was not available in the wet market and did not live in the Wuhan area. The only place the bats existed in the locality was the research facility, which is just about a 100 yards from the Wuhan wet market. The horseshoe bats are found only in the Yunnan province. However, they are neither consumed as food in the city, nor are they ever traded in the markets. The paper also states that in the Wuhan Center for Disease Control and Prevention located 280 m from the market, the extraction and sequencing of the DNA and RNA from caged animals could have been a potential source of the pathogen. This center is also adjacent to the Union Hospital, where the first groups of doctors were infected during this epidemic. Curiously, the lead author has now retracted the paper saying that it was based on mere speculations and not on solid proof.

Not surprisingly, two papers posted on the websites of the Fudan University and the China University of Geosciences met a similar fate. They were removed following a new policy mandating government approval for publishing academic papers about COVID-19.These clampdowns support the theory of a lab leak. The theory gets bolstered by the classified cables from the US embassy in China in January 2020.It was reported that the labs were conducting high-risk studies with a lack of appropriately trained technicians and investigators. There were concerns of undue risks being taken. Similar concerns were raised about the nearby Wuhan Center for Disease Control and Prevention lab. It appears that the leaks cannot be ruled out entirely.

An Indian paper published in January, which has now been retracted, theorized genetically altered insertions in the genome of the novel CoV similar to the genetic sequences of human immunodeficiency virus (HIV) and Ebola. They found it quite unlikely for a virus to have acquired such unique insertions naturally in a short duration. These artificially engineered changes were thought to increase the range of host cells that the 2019-nCoV can infect. This paper was taken down amidst criticism, but research from the Nankai University in Tianjin reports similar findings.This can be considered evidence for the virus being man-made.

Lastly, the doctors who were the first responders were allegedly clamped down by the government. Li Wenliang who sounded the alarm on the Wuhan CoV on WeChat was taken to the police station where he was warned against spreading rumors. Unfortunately, he succumbed to the disease subsequently. These doctors were advised by the government, “not to mislead the public” and to “refrain from publishing any unauthorized information.” They were also told to “resist all kinds of rumors and clarify and guide false opinions and discussions.”

For a pragmatic view on the issue, it is imperative on our part to look at arguments against the lab origin of COVID-19. Rhinolophus affinis bat and Malayan pangolins (Manis javanica) contain CoVs similar to the SARS-CoV-2. However, the receptor-binding domains (RBDs) of viruses isolated from these two sources were markedly different from the human SARS-CoV-2 RBDs, which have a lower affinity to the angiotensin-converting enzyme 2 (ACE2) receptors. Theoretically, this may indicate a process of natural selection in the animal host before transfer.Secondly, this adaptation may have occurred after the zoonotic transfer into the humans. A progenitor of SARS-CoV-2 after infecting humans may have acquired genomic features through adaptation during undetected human-to-human transmission.

Retrospective serological studies could answer these questions. Lastly, the optimal RBD sequence for the human receptors as predicted using computer models, significantly differs from the RBD sequences with high binding affinity isolated from the humans. If artificial engineering was the source, this particular RBD sequence would not have been preferred as it did not have a high binding affinity as predicted in the computer models. This underscores the possibility of natural selection.

Nevertheless, many evidences seem to give credence to the theory of a man-made virus that has leaked from the lab into the community. Although it seems unethical to point fingers at this time when efforts are required elsewhere, one cannot be contented with the community origin theory put forward by the Chinese government when the evidences say otherwise. It is imperative on the part of the health-care community to get to the bottom of this in order to prevent future occurrences of man-made pandemics, simply because we may never have a chance otherwise.

It’s worrying that persistently high nasopharyngeal viral RNA load, and the detection of viral RNA in blood and pleural fluid, with severe multi-organ dysfunction.

Development and effective administration of antiviral therapy to critically ill patients throughout the course of disease is likely to remain important. Vigilance regarding the strict implementation of transmission precautions is required throughout the prolonged course of COVID-19 in patients who are critically ill, and ancillary staff responsible for collecting and disposing of bodily fluids or waste, who are at high risk during an outbreak, should be properly protected and trained.

The invention of vaccination at the end of the eighteenth century led to huge changes in the treatment of infectious diseases. Smallpox was just one of the dreadful diseases common at the time, killing millions of people, and leaving survivors horribly disfigured. English country doctor Edward Jenner noticed how certain kinds of people were resistant to the disease—notably milkmaids who had contracted cowpox, a very mild disease, from the cows they milked. Jenner’s insight was that cowpox could protect against smallpox, and that injecting people with extracts from cowpox pustules might confer the same immunity to smallpox previously enjoyed by milkmaids. The word “vaccine” comes from “vaccinia,” derived from the Latin word for a cow— and the proper name for the infectious agent of cowpox. Jenner published his work in 1798, but he had no idea that smallpox (or cowpox) was caused by viruses. Vaccination caught on, and other vaccines were developed before anyone knew that viruses existed. The pioneering French scientist Louis Pasteur, for example, developed a vaccine for rabies. He first “killed” the rabies infectious agent by heating. This was the first vaccine in which a dead version of the infectious agent was used to protect against subsequent infection by the live agent. Unlike Jenner, Pasteur knew of the existence of bacteria. He realised that the rabies agent was smaller even than these tiny organisms, but remained ignorant of its true nature.

I enjoyed The Stand by Stephen King where he states One man escapes from a biological weapon facility after an accident, carrying with him the deadly virus known as Captain Tripps, a rapidly mutating flu that – in the ensuing weeks – wipes out most of the world’s population. In the aftermath, survivors choose between following an elderly black woman to Boulder or the dark man, Randall Flagg, who has set up his command post in Las Vegas. The two factions prepare for a confrontation between the forces of good and evil.

Testing negative for COVID-19 is a big reassurance in times of the pandemic, especially after you have spent days suffering in isolation. Some places also require a negative COVID certificate before they allow people to travel or meet others safely. But, is a negative COVID test certificate a clear pass enough for a person to be around people?

A single negative report isn’t proof enough that it is safe for the person to mingle and be around other people. Treating one negative test being ‘safe’ from COVID-19 could be a big mistake. As much of a relief a negative COVID diagnosis can be, relying on a negative report alone may not be a reassurance that you won’t infect other people, or put others at risk.

A new study from the Scripps Research Institute in Florida suggests the new coronavirus has mutated into a variant that’s more infectious.The mutation — named “the D614G mutation” — occurred on the spike protein, the part of the virus that helps it bind and fuse to our cells. The D614G mutation makes it easier for the virus to infect our cells.The Scripps researchers aren’t the first to identify the tiny mutation on the spike protein.In March, researchers from the Los Alamos National Laboratory announced they detected the D614G mutation, and that it was likely responsible for most infections reported in Europe and the United States.In total, the researchers identified 14 strains of SARS-CoV-2 and released their findings to help those working on vaccines and treatments.That being said, the new dominant strain identified does seem to be more infectious in laboratory settings. Scientists are now trying to understand how the variation behaves in the body — which may be very different from lab settings.It’s still unclear whether the mutation causes a more severe illness or increases the risk of death.It’s also unclear whether the new mutation infects and sickens people differently. At this time, the illness and hospitalization rates caused by the new variation seems to be similar.More data is needed to understand the implications of the new mutations, like whether re-infections after recovery are possible, and whether the changes could affect the vaccines and treatments in development.

The accuracy of the test results depends on the timing. The virus has an incubation period of 5-12 days, but in some cases, it can take longer than that. So, if you probably have been exposed to someone with an active infection, you should treat the next two weeks as a quarantine period as well.According to a study, RT-PCR tests, for example, are most susceptible to delivering wrong results in the early days of infection onset (4-5 days). The risk multiplies with antigen testing.This is one reason why people are asked to go for RT-PCR testing if they get a negative on an antigen test.

The antibodies that protect against infection with Covid-19 fade over time, so it’s likely that vaccination will not provide a permanent defence. Covid could become an illness like flu, says Dr John Wright of Bradford Royal Infirmary – one that flares up in society at regular intervals, and that people have more than once.

Some viral infections such as measles, mumps or chickenpox only infect us once. They trigger an immune response that provides a lifetime of antibody protection. Some viruses such as flu are masters of disguise, mutating rapidly to escape the detection from our immune surveillance. Other viruses like the common cold, and other endemic corona viruses, have forgettable faces that fade from our immune memory and come back to visit us year after year.

The vaccine provides a degree of confidence. But it seems highly likely that as more variants emerge across the world, the genetic mutations in the virus will make it a moving target for our body’s defence system, and for vaccine manufacturers.

So how will this combination of immune challenges - infection and vaccination - affect risk of future infection? 

Investigate the risk of reinfection with new variants ?

But it seems highly likely that as more variants emerge across the world, the genetic mutations in the virus will make it a moving target for our body's defence system, and for vaccine manufacturers.

The moral of the real lifestory

Mr potato you are at a threat from your lovely love Madam fancy while I am dying Arindam Bhattacharjee and you are a killer of your mother and sister.