REPORT Coronavirus: what is it and how does it spread ?


A coronavirus was first isolated in 1937 from an infectious bronchitis virus in birds that has the ability to seriously devastate poultry stocks.

Coronaviruses were given their name based on the crown-like projections on their surfaces. “Corona” in Latin means “halo” or “crown.”

These viruses are responsible for between 15 and 30 percent of common colds.

Over the last 70 years, scientists have found that coronaviruses can infect mice, rats, dogs, cats, turkeys, horses, pigs, and cattle.

Coronaviruses are enveloped viruses with a positive-sense RNA genome and with a nucleocapsid of helical symmetry.

The SARS epidemic has boosted interest in research on coronavirus biodiversity and genomics.

Before 2003, there were only 10 coronaviruses with complete genomes available.

After the SARS epidemic, up to December 2008, there was an addition of 16 coronaviruses with complete genomes sequenced, and in September 2012, a novel coronavirus was found in UK.

These include two human coronaviruses (human coronavirus NL63 and human coronavirus HKU1), 10 other mammalian coronaviruses [bat SARS coronavirus, bat coronavirus (bat-CoV) HKU2, bat-CoV HKU4, bat-CoV HKU5 bat-CoV HKU8, bat-CoV HKU9, bat-CoV 512/2005, bat-CoV 1A, equine coronavirus, and beluga whale coronavirus] and four coronaviruses (turkey coronavirus, bulbul coronavirus HKU11, thrush coronavirus HKU12, and munia coronavirus HKU13).

Coronaviruses are divided into three groups:

  • group 1 coronaviruses (alphacoronavirus),
  • group 2 coronaviruses (betacoronavirus),
    • Two subgroups in group 2 coronavirus (groups 2c and 2d)
  • group 3 coronaviruses (gammacoronavirus).
    • two subgroups in group 3 coronavirus (groups 3b and 3c)

The diversity of coronaviruses is a result of the infidelity of RNA-dependent RNA polymerase, high frequency of homologous RNA recombination, and the large genomes of coronaviruses.

Among all hosts, the diversity of coronaviruses is most evidenced in bats and birds, which may be a result of their species diversity, ability to fly, environmental pressures, and habits of roosting and flocking.

The present evidence supports that bat coronaviruses are the gene pools of group 1 and 2 coronaviruses, whereas bird coronaviruses are the gene pools of group 3 coronaviruses.

With the increasing number of coronaviruses, more and more closely related coronaviruses from distantly related animals have been observed, which were results of recent interspecies jumping and may be the cause of disastrous outbreaks of zoonotic diseases.

3D Structure of Coronavirus
3D Structure of Coronavirus

Human coronaviruses (HCoV) were first identified in the 1960s in the noses of patients with the common cold.

Common human coronaviruses, including types 229E, NL63, OC43, and HKU1, usually cause mild to moderate upper-respiratory tract illnesses, like the common cold.

Most people get infected with these viruses at some point in their lives.

The first two human coronaviruses (HCoV) were identified: HCoV-229E and HCoV-OC43. These two human coronaviruses were studied extensively from approximately 1965 to the mid-1980s.

HCoV-229E is a member of the group I coronaviruses, and HCoV-OC43 is a member of group II.

Besides the human coronaviruses, there are several group I and group II animal coronaviruses that infect cattle, pigs, cats, dogs, mice, and other animals.

There is one additional branch, the group III coronaviruses, which are found exclusively in birds.

By infecting healthy volunteers, researchers learned that infection with HCoV-229E or HCoV-OC43 results in a common cold, and since then, HCoVs have been considered to be relatively harmless respiratory pathogens.

This image was roughly disturbed when severe acute respiratory syndrome (SARS)-CoV was introduced into the human population in the winter of 2002 to 2003 in China.

SARS-CoV causes a severe respiratory illness with high morbidity and mortality. The virus originated from a wild-animal reservoir, most likely bats, and was transmitted to humans via infected civet cats.

The epidemic was halted in 2003 by a highly effective global public health response, and SARS-CoV is not currently circulating in humans. However, the SARS outbreak brought coronaviruses back into the limelight, and a renewed interest in this virus family resulted in the identification of two more human coronaviruses.

HCoV-NL63, a novel member of group I, was discovered in a child with bronchiolitis in The Netherlands. HCoV-HKU1, a novel group II virus from an adult with chronic pulmonary disease in Hong Kong, was described in 2005.

The renewed interest in coronaviruses since the outbreak of SARS-CoV has revealed that at least four human coronaviruses circulate worldwide, generally causing relatively mild respiratory symptoms.

However, in young children, immunocompromised patients, or otherwise-weakened persons, these viruses can cause more-serious respiratory tract disease that requires hospitalization.

Symptoms include:

  • sneezing
  • a runny nose
  • fatigue
  • a cough
  • in rare cases, fever
  • a sore throat
  • exacerbated asthma

Information on the 2019-nCov infection is scarce at present.

In the past, respiratory conditions that develop from coronaviruses, such as SARS and MERS, have spread through close contacts.

However, while some viruses are highly contagious, it is less clear with coronaviruses as to how rapidly they will spread.

Symptoms vary from person to person with a 2019-nCov infection.

It may produce few or no symptoms.

However, it can also lead to severe illness and may be fatal.

Common symptoms include:

  • fever
  • breathlessness
  • cough

It may take 2–14 days for a person to notice symptoms after infection.

As of January 31, 2020, the virus carries a death rate of 10%, according to a study of 99 people with 2019-nCov.

Human coronaviruses can sometimes cause lower-respiratory tract illnesses, such as pneumonia or bronchitis.

This is more common in people with cardiopulmonary disease, people with weakened immune systems, infants, and older adults.

Among humans, infection most often occurs during the winter months as well as early spring.

It is not uncommon for a person to become ill with a cold that is caused by a coronavirus and then catch it again about four months later.

This is because coronavirus antibodies do not last for a very long time. Also, the antibodies for one strain of coronavirus may be useless against other strains.

Other human coronaviruses

Two other human coronaviruses, MERS-CoV and SARS-CoV have been known to frequently cause severe symptoms.

MERS symptoms usually include fever, cough, and shortness of breath which often progress to pneumonia. About 3 or 4 out of every 10 patients reported with MERS have died.

MERS cases continue to occur, primarily in the Arabian Peninsula.

SARS symptoms often included fever, chills, and body aches which usually progressed to pneumonia.

No human cases of SARS have been reported anywhere in the world since 2004.

In September 2012, a novel coronavirus (NCoV) was discovered in the Middle East in a 49 year-old Qatari man with travel history to Saudi Arabia prior to onset of illness.

From April 2012 to February 2013, a total of 13 people from Jordan, Saudi Arabia, Qatar, and the United Kingdom were confirmed to have an infection caused by the novel coronavirus, and 7 of the infected have died.

There are no specific treatment for illnesses caused by the novel coronavirus.

Medical care is supportive and to help relieve symptoms.

Before this novel coronavirus 2012, the human coronaviruses (HCoV) OC43 and 229E are common causes of upper respiratory tract infections.

Severe diseases were rare, however, until the emergence of the severe acute respiratory syndrome (SARS)-CoV in 2003.

Since then, other novel CoV (NL63 and HKU1) have been described, and they have caused respiratory infections worldwide.

The ACE2 molecule, which is used as a receptor by HCoV-NL63 and SARS-CoV, has recently been associated with respiratory disease.

The fact that ACE2 is also involved in protection against lung damage is intriguing and suggests opportunities to treat complications during respiratory tract infections.

The fact that SARS-CoV and HCoV-NL63 use the same receptor, while their pathogenicities and disease courses are utterly different, calls for detailed comparisons of the immune responses, inflammation processes, and in vivo replication characteristics of these two viruses.

The identification and characterization of novel respiratory viruses is of obvious clinical importance.

Diagnostics can be improved, and new therapies can be developed.

An antiviral strategy that would target all human coronaviruses, e.g., broad-spectrum inhibitors of the Mpro enzymes, is promising.

For HCoV-NL63, several compounds that efficiently inhibit distinct steps of the viral replication cycle have been described.

A short interfering RNA (siRNA) targeting the S gene of HCoV-NL63 is one of these potent inhibitors.

Inhalation of a cocktail of siRNAs targeting all the different coronaviruses or perhaps all respiratory viruses may be an effective and simple therapy to block viral replication in the lungs.


Different types of human coronaviruses vary in the severity of illness they cause and how far they can spread.

There are currently seven recognized types of coronavirus that can infect humans.

Common types include:

  • 229E (alpha coronavirus)
  • NL63 (alpha coronavirus)
  • OC43 (beta coronavirus)
  • HKU1 (beta coronavirus)

Rarer, more dangerous types include MERS-CoV, which causes Middle East Respiratory Syndrome (MERS), and severe acute respiratory syndrome (SARS-CoV), the coronavirus responsible for SARS.

In 2019, a dangerous new strain started circulating, but it does not yet have an official name.

Health authorities are currently referring to it as 2019 Novel Coronavirus (2019-nCov).

Coronavirus – 2019-nCov


There has not been a great deal of research on how a human coronavirus spreads from one person to the next.

However, it is believed that the viruses transmit using secreted fluid from the respiratory system.

Coronaviruses can spread in the following ways:

  • Coughing and sneezing without covering the mouth can disperse droplets into the air, spreading the virus.
  • Touching or shaking hands with a person that has the virus can pass the virus from one person to another.
  • Making contact with a surface or object that has the virus and then touching your nose, eyes, or mouth.
  • On rare occasions, a coronavirus may spread through contact with feces.

People in the U.S. are more likely to contract the disease in the winter or fall.

The disease is still active during the rest of the year.

Young people are most likely to contract a coronavirus, and people can contract more than one infection over the course of a lifetime. Most people will become infected with at least one coronavirus in their life.

It is said that the mutating abilities of the coronavirus are what make it so contagious.

To prevent transmission, be sure to stay at home and rest while experiencing symptoms and avoid close contact with other people.

Covering the mouth and nose with a tissue or handkerchief while coughing or sneezing can also help prevent the spread of a coronavirus. Be sure to dispose of any used tissues and maintain hygiene around the home.

Can wearing a face mask protect you from the new coronavirus?

No, a regular surgical mask will not help you steer clear of the virus.

Surgical masks offer “limited protection” against contracting illness.

While face masks can be helpful in stopping the spread of germs in certain situations — like when people are in close quarters on a train or packed into a waiting room.

In some Asian countries, such as Japan and China, it’s not uncommon to see people wearing surgical masks in public to protect against pathogens and pollution.

A more specialized mask, known as an N95 respirator, can protect against the new coronavirus, also called 2019-nCoV.

The respirator is thicker than a surgical mask, but it’s not recommend for public use, that’s because it’s challenging to put these masks on and wear them for long periods of time.

Risultato immagini per N95 respirator"

If you decide to use a N95 respirator, you should only use an N95 mask that is certified by the National Institute for Occupational Safety and Health (NIOSH). Look for the NIOSH logo and the test and certification (TC) approval number on the mask or packaging.

Masks that are not certified by NIOSH may not provide adequate protection to you.

How to Make Sure the Mask Fits

Do a user seal check, including both positive and negative pressure checks, to verify that you have correctly put on the mask and adjusted it to fit properly.

  • Negative pressure check
    • Place both hands completely over the mask and inhale sharply. Be careful not to disturb the position of the mask. The mask should pull into your face. If air leaks around your face or eyes, adjust the nosepiece and straps and repeat the positive pressure check.
  • Positive pressure check
    • Put your hands over the mask and breathe out sharply. If your mask has an exhalation valve (like the one pictured above) be sure to cover the exhalation valve when you exhale. No air should leak out of the mask if it fits properly. If air leaks out, re-adjust the nosepiece and straps and repeat the negative pressure check.

When to Throw Out the N95 Mask

As the N95 mask gets clogged, it becomes more difficult to breathe.

When this occurs, throw it out and use a new one.

Discard the mask if it is wet or dirty on the inside, if it is deformed, or if the filter is torn.

A deformed mask may not fit properly. An N95 mask cannot be cleaned or disinfected.

A better way to avoid getting the coronavirus is :

  • Wash your hands thoroughly before touching eyes, mouth, mucous membranes in general;
  • Avoid touching your eyes after touching objects in public places;
  • Avoid close contact with people who are sick ;

Effects of Air Temperature and Relative Humidity on Coronavirus Survival on Surfaces

Environmental surfaces have been recognized as likely contributors to the transmission of nosocomial viral infections (25).

The question of whether hospital surfaces play a role in the spread of nosocomial viral infection took on particular urgency during the worldwide outbreak of severe acute respiratory syndrome (SARS).

SARS was a novel coronavirus infection, and local and institutional outbreaks were driven in part by nosocomial spread; cases of SARS were documented in health care workers, patients, and visitors in health care facilities (20).

During outbreaks in health care facilities, surface sampling for SARS coronavirus (SARS-CoV) revealed SARS-CoV nucleic acids on surfaces and inanimate objects (610).

This suggests that surfaces could be sources of virus transmission.

Assessment of the risk posed by SARS-CoV on surfaces requires data on the survival of the virus on environmental surfaces and data on how this survival is affected by environmental variables, such as air temperature (AT) and relative humidity (RH).

Because working with SARS-CoV requires specially trained personnel working under biosafety level 3 (BSL-3) laboratory containment conditions, there are significant challenges in studying this virus, and only limited data on its survival and response to environmental stressors are available.

The use of surrogate coronaviruses has the potential to overcome these challenges and expand the available data on coronavirus survival on surfaces.

In addition to SARS-CoV, there are two pathogenic human coronaviruses that are adapted to propagation and assay in cell culture, 229E and OC43, which could serve as surrogates for SARS-CoV in survival studies. However, previous studies suggested that the survival of 229E and OC43 on surfaces may be shorter than that of SARS-CoV (1035).

To evaluate surrogates that might serve as more conservative models of SARS-CoV on surfaces, animal coronaviruses were chosen as surrogates for this study.

Because SARS-CoV does not fall clearly into either of the two groups of mammalian coronaviruses, the following two potential surrogates representing the two groups were evaluated: transmissible gastroenteritis virus (TGEV), a diarrheal pathogen of swine and a member of coronavirus group 1, and mouse hepatitis virus (MHV), a respiratory and enteric pathogen of laboratory mice and a member of coronavirus group 2 (16).

The advantages of using these two viruses as surrogates are the fact that they can be readily propagated and assayed in cell culture systems and the fact that there is no human infection risk.

There has been some study of TGEV survival in aerosols (17), but the data on the environmental survival of this potential coronavirus surrogate for SARS-CoV are limited.

The use of surrogates for studying the environmental survival of SARS-CoV can increase our understanding of the survival and persistence of this virus on environmental surfaces, the possible role of such surfaces in the transmission of SARS-CoV and other coronaviruses, and the risk posed by contaminated surfaces in outbreak settings.

Therefore, this work was undertaken to determine the effect of AT and RH on the survival of the surrogate coronaviruses TGEV and MHV on hard nonporous surfaces.


This study was the first study to examine the individual and synergistic effects of AT and RH on coronavirus survival on surfaces. The results show that when high numbers of the surrogates TGEV and MHV are deposited, these viruses may survive for days on surfaces at the ambient AT and wide range of RH levels (20 to 60% RH) typical of health care environments.

TGEV and MHV may be more resistant to inactivation on surfaces than previously studied human coronaviruses, such as 229E (28).

SARS-CoV has been reported to survive for 36 h on stainless steel (35), but the reductions in the levels observed were greater than those seen for either TGEV or MHV at 20°C at any RH in this study.

However, the AT and RH conditions for the previous experiment were not reported, making comparisons difficult. Rabenau et al. (23) reported much slower inactivation of SARS-CoV on a polystyrene surface (4 log10 reduction after 9 days; AT and RH conditions not reported), consistent with some observations for TGEV and MHV in the present study.

There are some similarities with studies of another enveloped virus, human influenza virus, on surfaces in that at higher RH (50 to 60%), the inactivation kinetics are closer to those of TGEV and MHV (21).

In the experiments in this study, the relationship between inactivation and RH was not monotonic, and survival was greater at low RH, a finding reflected in the results of previous studies of coronaviruses and other enveloped viruses in aerosols.

Previous studies of TGEV and human coronavirus 229E in aerosols found that there was greater survival at low RH than at high RH (1517).

Greater survival of other enveloped viruses, including vaccinia virus, Venezuelan equine encephalitis virus, and influenza virus, at low RH has been observed previously (1112132627).

Overall, virus survival was enhanced by a lower AT. Similar relationships between AT and virus inactivation have been observed for enveloped viruses in liquids (729) and aerosols (1115).

The coronavirus data obtained in this study suggest that although the rates of viral inactivation are lower at lower ATs, there are still different effects of RH on viral survival at each AT.

At 40°C, the same protective effect of low RH was seen at 20% RH compared to that at 50% and 80% RH. Overall, however, inactivation was more rapid at all three RH levels at this high AT.

It may be that at 40°C AT effects are the predominant effects that cause viral inactivation and that RH levels play a lesser role than they do at lower ATs.

The results of the statistical analysis suggest that RH has a greater effect on viral inactivation than AT, but there are interactions between AT and RH.

The relationship between AT, RH, and virus inactivation is still not entirely clear and may vary depending on the virus type (119).

Multiple mechanisms may contribute to viral inactivation on surfaces. Some inactivation may take place when viral capsids accumulate at the air-water interface (AWI) of a solution, causing structural damage (303133).

Desiccation may also be an important contributor to inactivation on surfaces (1), as loss of water molecules triggers lipid membrane phase changes, cross-linking, Maillard reactions, and peroxide formation (9).

Virus inactivation on surfaces may involve both desiccation and interaction at the AWI, with the contribution of each depending on the RH. At a low RH, oxidation and Maillard reactions that occur during rapid desiccation may predominate.

Around 80% RH, the rate of loss of water molecules is slowed, the hydrophobicity of the AWI is decreased (19), and the main mechanism may be inactivation at the AWI.

Around 50% RH, inactivation at the AWI and desiccation may occur simultaneously; as water molecules are lost, lipid oxidation and Maillard reactions occur (the maximum rates of Maillard reactions occur when the RH is 50 to 80%) (9), possibly providing a partial explanation for why viral inactivation appears to be more rapid at 50% RH than at 20% or 80% RH.

At ambient ATs (around 20°C), coronaviruses can survive for 2 days while losing only 1 to 2 log10 infectivity, depending on the RH. Nasopharyngeal aspirates from infected individuals with SARS can have viral loads ranging from 105 to 108 genome templates/ml (8142234), suggesting that respiratory secretions from SARS patients may contain infectious virus.

If deposited on surfaces in these types of secretions, coronaviruses could potentially survive on surfaces in health care environments for days.

Evidence of SARS-CoV nucleic acids on surfaces and inanimate objects in hospitals has been reported (610).

However, there are no data on the occurrence of infectious SARS-CoV on these surfaces. The dose-response relationship and minimal infectious doses for infection of humans by SARS-CoV and other coronaviruses have also not been defined.

Given these gaps in our knowledge, the magnitude of the risk due to virally contaminated surfaces is uncertain and should be examined further.

The survival data for TGEV and MHV suggest that enveloped viruses can remain infectious on surfaces long enough for people to come in contact with them, posing a risk for exposure that leads to infection and possible disease transmission.

This risk may also occur for other enveloped viruses, such as influenza virus (34). The potential reemergence of SARS or the emergence of new strains of pandemic influenza virus, including avian and swine influenza viruses, could pose serious risks for nosocomial disease spread via contaminated surfaces.

However, this risk is still poorly understood, and more work is needed to quantify the risk of exposure and possible transmission associated with surfaces. Statistical analysis showed that TGEV and MHV do not differ significantly in their inactivation kinetics on surfaces, and both viruses may be suitable models for survival and inactivation of SARS-CoV on surfaces. However, more data on the survival rates and inactivation kinetics of SARS-CoV itself are needed before these relationships with other coronaviruses can be definitively established.

However, the findings of this study suggest that TGEV and MHV could serve as conservative surrogates for modeling exposure, transmission risk, and control measures for pathogenic enveloped viruses, such as SARS-CoV and influenza viruses, on health care surfaces.


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