Coronavirus COVID-19: what happens in airports and airplanes – what can we do?


Major airports have begun screening passengers for the coronavirus, and more than three dozen airlines have cut their flights to quarantine countries.

But these measures do not offer a solution to the problems of contagion for those who must board a flight.

Real life teaches us that you can avoid a person who sneezes in a large and airy space, but in a confined space, you are at the mercy of fate, in fact once we fasten the seat belt inside an airplane, you do not have the possibility to avoid the infection if you are affected by the viruses of your neighbor

So how do those viruses spread, specifically on airplanes and airports ?

And how serious is the coronavirus threat compared to the likes of influenza?

Let’s take a look.

How can the coronavirus spread?

Human coronaviruses spread just like the flu or a cold:

  • Through the air by coughing or sneezing;
  • Close personal contact, such as touching or shaking hands;
  • Touching an object or surface with the virus on it;
  • Occasionally, fecal contamination.

Respiratory illnesses can also be spread through the surfaces upon which the droplets land – like airplane seats and tray tables.

How long those droplets last depends both on the droplet and the surface – mucus or saliva, porous or non-porous, for example.

Viruses can vary dramatically in how long they last on surfaces, from hours to months.

There’s also evidence that respiratory viruses can be transmitted through the air in tiny, dry particles known as aerosols.

But, according to Arnold Monto, professor of epidemiology and global public health at the University of Michigan, it’s not the major mechanism of transmission.

“To be sustained, to allow true aerosols, the virus has to be able to survive in that environment for the amount of time it’s exposed to drying,” he says.

First of all we need to define the type of virus:

Non-enveloped viruses, such as coxsackieviruses, rotavirus, or poliovirus, can survive for extended periods on surfaces (910), while enveloped viruses, including H1N1 and human coronaviruses, remain infectious on surfaces after several days (6).

The persistence of dried viruses is affected by various environmental conditions and factors such as heat, moisture, pH, and the type of surface (1215).

Furthermore, the compositions of media may also influence the persistence of viruses.

The impact of drying on viral persistence has been evaluated in previous studies using viruses typically prepared in standardized media, including a cell culture medium supplemented or not with fetal calf serum (FCS) (419).

Temperature, ultraviolet radiation from sunlight, pH changes and salt can play a role in weakening a viral envelope. But one of the main factors is moisture.

“Viruses tend to be more stable in environments for which they’re known to reproduce,”.

 “If they live in warm, moist environments – for example, in your nostrils, in your throat, in your bronchial tree — they’re more stable. But when they’re exposed to a different material or to a non-moist environment, they can break down.”

This is why cold and flu viruses remain infectious on non-porous surfaces like light switches and countertops longer than porous surfaces like fabric and tissues.

Porous surfaces suck moisture away from the viruses, causing the structures to collapse.

Not all non-porous surfaces serve as ideal havens for these viruses.

Greatorex’s [1]  work found flu viruses could remain contagious for nine hours on stainless steel, and other research has suggested they can be infectious on the metal for up to seven days.

But on copper surfaces, the virus stops being infectious after six hours.

Mucus from a sneeze can protect a virus from the damaging influences of a dry environment and make the virus maintain infectiousness longer.

But on the plus side, Greatorex said, the more mucus a friend or co-worker sneezes, the shorter distance it will travel because of its increased weight and size.

Let’s take a short break and analyze what Coronavirus COVID-19 is and how it behaves with its host.

Coronaviruses (CoVs) (order Nidovirales, family Coronaviridae, subfamily Coronavirinae) are enveloped viruses with a positive sense, single-stranded RNA genome. With genome sizes ranging from 26 to 32 kilobases (kb) in length.

They infect humans and cause disease to varying degrees, from upper respiratory tract infections (URTIs) resembling the common cold, to lower respiratory tract infections (LRTIs) such as bronchitis, pneumonia, and even severe acute respiratory syndrome (SARS).

SARS-CoV and MERS-CoV cause severe infections that lead to high mortality rates (CDC, 2017; WHO, 2004).

The coronaviral genome encodes four major structural proteins:

  • the spike (S) protein,
  • nucleocapsid (N) protein,
  • membrane (M) protein,
  • the envelope (E) protein,

all of which are required to produce a structurally complete viral particle [29, 37, 38] .

More recently, however, it has become clear that some CoVs do not require the full ensemble of structural proteins to form a complete, infectious virion, suggesting that some structural proteins might be dispensable or that these CoVs might encode additional proteins with overlapping compensatory functions [35, 37, 39–42].

Individually, each protein primarily plays a role in the structure of the virus particle, but they are also involved in other aspects of the replication cycle.

 The S protein mediates attachment of the virus to the host cell surface receptors and subsequent fusion between the viral and host cell membranes to facilitate viral entry into the host cell [42–44].

In some CoVs, the expression of S at the cell membrane can also mediate cell-cell fusion between infected and adjacent, uninfected cells.

This formation of giant, multinucleated cells, or syncytia, has been proposed as a strategy to allow direct spreading of the virus between cells, subverting virus-neutralising antibodies [45–47].

The E protein is the smallest of the major structural proteins.

During the replication cycle, E is abundantly expressed inside the infected cell, but only a small portion is incorporated into the virion envelope. E participates in viral assembly, release of virions and pathogenesis of the virus.

The majority of the protein is localised at the site of intracellular trafficking, the ER, Golgi, and ERGIC, where it participates in CoV assembly and budding.

Recombinant CoVs lacking E exhibit significantly reduced viral titres, crippled viral maturation, or yield propagation incompetent progeny, demonstrating the importance of E in virus production and maturation (reviewed in Schoeman and Fielding (2019). Coronavirus envelope protein: current knowledge. Virol J. 16: 69. ).

What does that mean for airports?

Airports are one of the maximum ethnic aggregation points of a nation.

Millions of people from all over the world pass through the airport spaces.

The new infrastructures provide a series of points of maximum concentration of the influx of travelers.

  • Areas in front of the entrance for boarding aircraft
  • Baggage checkpoints
  • Bar
  • Check in
  • Checkpoints at boarding areas
  • Customs control points
  • Information points for travelers
  • Smoke areas
  • Toilet
  • VAT refound

How is it possible to contain contamination?

The international general provisions include the following actions:

1.            Temperature Screening

Airport staffs should be equipped with calibrated non-contact infrared thermometer to detect all passengers who has a fever, register the personal information of the febrile passengers, notify the airport emergency rescue department to quarantine, and report to the local health authority. Quarantine areas should be set up at terminal, and there are alcohol based hand rub available.

2.            Infection Control Measures for Airport Staffs

2.1          Routine Measures

Airport staffs should wear surgical mask and replace medical protective masks (or N95 masks) in the airport. The staff should perform hand hygiene and wear gloves if necessary.

2.2          Infection Control Measures for Handling Febrile Passengers

The staff should wear disposable medical caps, surgical masks, gloves, and disposable protective suits. If treating body fluids (such as respiratory secretions, vomit, blood, diarrhea) or contaminated objects and surfaces, the staff should wear medical protective masks, goggles and disposable shoe covers.

It is important to wear or remove PPE in the correct order, in which can help to reduce cross contamination. Removed PPE should be placed in medical waste bags as infectious waste.

 Reusable goggles should be disinfected and dried after use. Goggles with anti-fog film should not be wiped with disinfectant, but cleaned by water and then exposed to ultraviolet light for at least 30 minutes.

 3.           Airport Ventilation

The airport should enhance the management of air-conditioning systems and natural ventilation in public areas such as terminals. According to the terminal structure, layout and local climate conditions, air circulation should be strengthened by taking practical measures.

When the temperature is appropriate, open the door and window. Where air-conditioning system is used, start all fresh air operating and turn on the exhaust system to keep the air clean. The aircraft carrying ill passengers, should park at a special channel or a remote stand.

4.            Hygiene Requirements for Security Inspection

4.1          Infection Control Measures for Security Personnel

4.1.1      Primary Measures

Security personnel should wear surgical masks and unified labor suits, and be equipped with uniform caps (or disposable medical caps), goggles, protective suits, medical rubber gloves as required.

 The PPE should be worn in the sequence of the labor cap (or disposable medical cap), surgical mask, protective suits (or uniform suit), goggles, and medical rubber gloves.

After duty, the protective equipment should be removed in the sequence of gloves, hand disinfection, goggles, protective suits (or labor suit), hand disinfection, masks, and caps. Please be aware of the following points:

  • Disinfect hand before wearing protective equipment;
  • Replace surgical masks every 4 hours;
  • Fully cover all hair and hairline shreds by wearing a cap. Hair up before wearing a cap when the hair is long, and make the edge of the cap close to both sides of ears;
  • Replace protective equipment immediately when it contacts the passenger’s blood, vomit and other pollutants with infection risk;      Disinfect and dry reusable goggles in time after each use;
  • Be careful not to touch the face with both hands when taking off protective equipment;
  • Put the removed disposable protective equipment into the medical waste bag.

4.1.2      Advanced Measures

Travel document checkers should be equipped with labor caps (or disposable medical caps), medical rubber gloves, surgical masks (or N95 masks) and goggles or medical protective screens. It is recommended to install isolation barrier at the document check counter.

Passenger searchers should be equipped with labor caps (or disposable medical caps), medical rubber gloves, surgical masks (or N95 masks which are preferable), goggles (or medical protective screens), and wear protective suits or uniforms as required.

The labor uniforms should be disinfected by the high-temperature steam for 20~40mins or the ultraviolet lamp irradiation for 1~2 hours off duty every day. The soles should be disinfected by foot pads with disinfectant.

4.2          Hygiene Requirements for Security Inspection Area

The airport should enhance the management of the air-conditioning system and natural ventilation in security inspection area, to keep the air clean. The key areas (e.g., document check counters, baggage inspection desk, baggage baskets) should be cleaned and disinfected regularly.

There are alcohol-based hand rub available on security inspection channels.

After daily operations, the inspection area and facilities (i.e., waste bins) should be wet-cleaned and disinfected thoroughly to keep in a sanitary condition.

5.            Waste Disposal

The airport should take measures to classify waste, collect used masks and remove in time. Garbage containers should be cleaned and disinfected with chlorine-containing disinfectant by spraying or wiping regularly.

6.            Airport Public Area Disinfection

Airport public area disinfection should be performed in accordance with the Guidelines for Hygiene Protection against Novel Coronavirus Infection in Public Places and the Technical Specifications for Public Place Disinfection issued by NHC.

6.1          Daily Routine Cleaning and Preventive Disinfection

The airport should take routine cleaning and disinfection in the public areas every day, publicize the disinfection status on the prominent place, and keep the record of disinfection.

 6.1.1     Air Disinfection

Use natural ventilation when appropriate, and strengthen air conditioning ventilation. Clean and disinfect the exhaust fan once a month.

Disinfect by spraying with 250 ~500mg/L chlorine-containing disinfectant or 250mg/L chlorine dioxide for more than 30 minutes, or the ultra-low volume spraying with hydrogen peroxide in key areas.

Take ventilation after disinfection is completed.

6.1.2      Object Surface Disinfection

Disinfect the frequently contacted object surfaces in general population areas (self- service check-in/ check-in counters, credential verification counters, elevator buttons, handrails, etc.), by spraying and wiping with250~500mg/L chlorine-containing disinfectant or 250mg/L chlorine dioxide.

6.2          Terminal Disinfection

In case of any suspected patients, confirmed patients or ill passengers, terminal disinfection should be performed by professionals. One of the following methods may be used:

6.2.1      Disinfect the air and environment integratedly by using the vaporization (gasification) hydrogen peroxide disinfection device. Operate the equipment according to its Instruction Manual.

6.2.2      Disinfect the air with an aerosol spray in an amount of 20ml/m3with the use of 0.5% peroxyacetic acid or 3% hydrogen peroxide or 500mg/L chlorine dioxide. Close the doors and windows before disinfection, spray the surface and space evenly from up to down and from left to right, and open the windows for ventilation after 60 minutes. After spray disinfection, wipe (drag) the surface of all objects by using the preventive disinfection method.

6.2.3      For the contaminated key areas, spray or wipe with 1000~2000mg/L chlorine- containing disinfectant for more than 30 minutes.

The standardization of the procedures listed above helps …. but does not limit the diffusion substantially!

What can we add to the above?

First of all, containment means PREVENTION.

From countless studies it is clear that COVID-19 has a great ability to survive on surfaces, therefore contact with people or other surfaces can amplify the possibility of contagion.

  • The installation of sanitation ” foggy air tunnel ” in front of the entrance to the airport where all travelers must pass before accessing the Check in.
  • All personal effects contained inside the hand baggage and inside the bags must be treated by the airport control staff as potentially contagious material.
  • The containers for X-Ray control equipment must be sanitized at regular intervals, to avoid the accumulation of viral load.
  • Specialized personnel who monitor passengers must be equipped with all Coronavirus prevention equipment, replacing the prevention equipment every 2 hours at the latest.
  • Passport control points must be sanitized at short and regular intervals, in order to limit the passage of COVID-19 from surfaces in contact with customs operators.
  • All equipment for passengers with special needs must be sanitized through “foggy air tunnel” at close intervals.
  • The toilets must have sanitizing vaporizers.
  • All contact surfaces for mechanical activation (dryers, taps, toilet drains, … must be replaced with automatic mechanisms (photocells, etc.)
  • New passenger control protocols must be introduced in boarding procedures. Airport operators must give precise provisions for the aircraft access procedures (call the numbers of seats that will access the aircraft afterwards) in order to reduce the aggregation of passengers to a minimum.
  • Eliminate any administration of food inside the restaurant that is not protected by a hermetically sealed envelope.
  • Hot drinks must be provided by personnel equipped with all the necessary equipment for the prevention of viral contaminants (working staff are also a constant source of contamination)

What does that mean for airplanes?

The World Health Organization defines contact with an infected person as being seated within two rows of one another.

But people don’t just sit during flights, particularly ones lasting longer than a few hours.

They visit the bathroom, stretch their legs, and grab items from the overhead bins. In fact, during the 2003 coronavirus outbreak of the severe acute respiratory syndrome (SARS), a passenger aboard a flight from Hong Kong to Beijing infected people well outside the WHO’s two-row boundary.

The New England Journal of Medicine noted that the WHO criteria “would have missed 45 percent of the patients with SARS.”

Inspired in part by that case, a team of public health researchers set out to study how random movements about the airplane cabin might change passengers’ probability of infection.

The “FlyHealthy Research Team” observed the behaviors of passengers and crew on 10 transcontinental U.S. flights of about three and a half to five hours.

 Led by Emory University’s Vicki Stover Hertzberg and Howard Weiss, they not only looked at how people moved about the cabin, but also at how that affected the number and duration of their contacts with others.

The team wanted to estimate how many close encounters might allow for transmission during transcontinental flights.

“Suppose you’re seated in an aisle seat or a middle seat and I walk by to go to the lavatory,” says Weiss, professor of biology and mathematics at Penn State University.

“We’re going to be in close contact, meaning we’ll be within a meter. So if I’m infected, I could transmit to you…Ours was the first study to quantify this.”

As the study revealed in 2018, most passengers left their seat at some point – generally to use the restroom or check the overhead bins – during these medium-haul flights.

Overall, 38 percent of passengers left their seats once and 24 percent more than once.

Another 38 percent of people stayed in their seats throughout the entire flight.

This activity helps pinpoint the safest places to sit.

The passengers who were least likely to get up were in window seats: only 43 percent moved around as opposed to 80 percent of people seated on the aisle.

Accordingly, window seat passengers had far fewer close encounters than people in other seats, averaging 12 contacts compared to the 58 and 64 respective contacts for passengers in middle and aisle seats.

Choosing a window seat and staying put clearly lowers your likelihood of coming into contact with an infectious disease.

But, as you can see in the accompanying graphic, the team’s model shows that passengers in middle and aisle seats – even those that are within the WHO’s two-seat range – have a fairly low probability of getting infected.

Weiss says that’s because most contact people have on airplanes is relatively short.

“If you’re seated in an aisle seat, certainly there will be quite a few people moving past you, but they’ll be moving quickly,” Weiss says. “In aggregate, what we show is there’s quite a low probability of transmission to any particular passenger.”

The story changes if the ill person is a crew member.

Because flight attendants spend much more time walking down the aisle and interacting with passengers, they are more likely to have additional – and longer – close encounters.

As the study stated, a sick crew member has a probability of infecting 4.6 passengers, “thus, it is imperative that flight attendants not fly when they are ill.”

But what if we are considering long-haul flights or airplanes with more than one aisle ?

We simulated 100 2019-nCoV infected travellers planning to board a flight who would pose a risk for seeding transmission in a new region.

The duration of travel was considered as the flight time plus a small amount of additional travel time (ca 1 hour) for airport procedures.

We assumed that infected individuals will develop symptoms, including fever, at the end of their incubation period (mean 5.2 days (Table)) [8] and progress to more severe symptoms after a few days, resulting in hospitalisation and isolation.

We also took into account that individuals may have asymptomatic (subclinical) infection that would not be detected by thermal scanning or cause them to seek medical care, although these individuals may be infectious, and that infected travellers may exhibit severe symptoms during their travel and be hospitalised upon arrival without undergoing entry screening.

We then estimated the proportion of infected travellers who would be detected by exit and entry screening, develop severe symptoms during travel, or go undetected, under varying assumptions of:

  • the duration of travel;
  • (ii) the sensitivity of exit and entry screening;
  • (iii) the proportion of asymptomatic infections;
  • (iv) the incubation period and
  • (v) the time from symptom onset to hospitalisation (Table).

Table. Parameter values and assumptions for the baseline scenario estimating effectiveness of exit and entry screening at airports for detecting passengers infected with novel coronavirus (2019-nCoV)

Duration of travel 12 hours Beijing – London [18]
Sensitivity of exit screening 86% Sensitivity of infrared thermal image scanners [19]
Sensitivity of entry screening 86% Sensitivity of infrared thermal image scanners [19]
Proportion of asymptomatic infections undetectable by typical screening procedures 17% 1 of 6 reported asymptomatic in a 2019-nCoV family cluster [2]
Incubation period Mean 5.2 days, variance 4.1 days Reported Gamma distributed mean, variance estimated from uncertainty interval of mean [8]
Time from symptom onset to hospitalisation Mean 9.1 days, variance 14.7 days Reported Gamma distributed mean, variance estimated from uncertainty interval of mean [8]

We assume that the time of starting travel is randomly and uniformly distributed between the time of infection and twice the expected time to severe disease, ensuring that simulated travellers are travelling during their incubation period.

However, we only consider those travellers who depart before their symptoms progress to being so severe that they would require hospital care [8].

We simulate travellers with individual incubation period, time from onset to severe disease, flight start times and detection success at exit and entry screening according to the screening sensitivities (Figure 1).

An individual will be detected at exit screening if their infection is symptomatic i.e. has detectable fever, their departure time exceeds their incubation period, and their stochastic exit screening success indicates detection.

An individual will be detected at entry screening if their infection is symptomatic, their incubation period ends after their departure but before their arrival, they have not been detected at exit screening, and their entry screening result is positive despite imperfect sensitivity.

Entry screening detections are further divided into detection due to severe symptoms and detection of mild symptoms via equipment such as thermal scanners.

We used 10,000 bootstrap samples to calculate 95% confidence intervals (CI).

Figure 1. Simulated infection histories of travellers infected with novel coronavirus (2019-nCoV)

The incubation period begins on infection and travellers then progress to being symptomatic and having severe symptoms. Travellers may fly at any point within the incubation or symptomatic phases; any would-be travellers who show (severe) symptoms and are hospitalised before exit.

Vertical lines represent the exit screening at start of travel (solid) and entry screening at end of travel (dashed) 12 hours later.

The model code is available via GitHub [9] and the results can be further explored in a Shiny app [3] at (Figure 2).

Figure 2. Screenshot of Shiny appa displaying the number of travellers infected with novel coronavirus (2019-nCoV) detected at airport exit and entry screening with baseline assumptionsb, 95% bootstrap confidence intervals, time distributions for incubation period and time to severe disease*

  1. Source [9].
  2. Baseline assumptions according to the Table.

Results are from stochastic simulation, and so there may be small variations in the number of travellers in each group when the same parameters are used twice.

Sliders are provided to modify the duration of travel, the sensitivity of both exit and entry screening, the proportion symptomatic, and the natural history parameters for the infection.

Effect of screening on detection

For the baseline scenario we estimated that 44 (95% CI: 33–56) of 100 infected travellers would be detected by exit screening, no case (95% CI: 0–3) would develop severe symptoms during travel, nine (95% CI: 2–16) additional cases would be detected by entry screening, and the remaining 46 (95% CI: 36–58) would not be detected.

The effectiveness of entry screening is largely dependent on the effectiveness of the exit screening in place. Under baseline assumptions, entry screening could detect 53 (95% CI: 35–72) instead of nine infected travellers if no exit screening was in place.

However, the probability of developing symptoms during the flight increases with flight time and hence exit screening is more effective for longer flights (Figure 3).

Figure 3. Probability of detecting travellers infected with novel coronavirus (2019-nCoV) at airport entry screening by travel duration and sensitivity of exit screening

Each cell is a mean of 10,000 model simulations. Other parameters (incubation period, symptom onset to hospitalisation period, and proportion of asymptomatic infections) were fixed at baseline assumptions (Table). Intervals are probabilities of detection, binned at increments of 10% (0–10%, 10–20%, etc.).

 Syndromic screening designed to prevent infected and potentially infectious cases entering a country undetected is highly vulnerable to the proportion of asymptomatic infections and long incubation periods.

If our baseline scenario is modified to have 0% asymptomatic 2019-nCoV infections and 100% sensitivity of entry screening, the incubation period will need to be around 10-fold shorter than the period from symptom onset to severe disease (e.g. hospitalisation) in order to detect more than 90% of infected travellers that would not otherwise report illness at either exit or entry screening.

Once the possibility of contagion inside an aircraft has been analyzed, it is important to determine the real effectiveness of the HEPA filters used inside the aircraft.

Bacterial and Virus Removal Efficiency of Pall HEPA Cabin Air Filters

What is a HEPA cabin air filter?

The current aerospace industry accepted definition of HEPA cabin air filters is a minimum removal efficiency of 99.97% when tested using a DOP challenge or 99.99% when tested with a sodium flame challenge.

How effective are Pall HEPA filters at removing bacteria & viruses?

Engineers from Pall’s Aerospace group teamed up with scientists from Pall’s Medical group to develop and validate the microbial removal efficiency of aircraft cabin air filters, following standard practices used in the healthcare and pharmaceutical industries.

Viruses can typically range from about 0.01 to 0.2 micron in size, although they may cluster or attach to larger particles.

Description Virus, approximate size
SARS corona virus, 0.08 to 0.16 microns
MERS-CoV corona virus, 0.08 to 0.16 microns
Swine Flu A(H1N1) virus, 0.08 to 0.12 microns
Avian Flu A(H5N1) and A(H7N9) virus, 0.1 microns


The DOP test specified by Boeing consists of challenging the filter with an aerosol mist of DOP (dioctyl phthalate) droplets having a mean size of 0.3 microns. The sodium flame test specified by Airbus consists of challenging the filter with an aerosol mist of sodium chloride particles having a mean size of 0.58 microns. The removal efficiency is calculated by measuring the particle concentrations upstream and downstream of the filter element being tested.

Centre for Applied Microbiology & Research (CAMR), now known as Public Health England.

Why cabin air filters do not need an anti-microbial treatment

In free air, most microbes die within a few minutes. Once captured by the filter media, the survival rate of microorganisms in the aircraft environment is very low. Most bacteria require high humidity and a source of nutrition to survive. The conditions typically found in the aircraft recirculation system are 10-15% relative humidity and lack of a source of nutrition.

Is there a danger to maintenance personnel by removing used cabin air filters?

There is no more risk involved in replacing a cabin air filter than carrying out general maintenance on any aircraft part that has been in service for a number of years.

 Maintenance staff should wear the same personal protective equipment as for other aircraft maintenance tasks which require protection against dust, and per the local regulations.

The used HEPA filter should be placed and sealed in a plastic bag. A specific biohazard bag is not required for disposal of the HEPA filter in most juristictions.

The air in-flight is recirculated and filtered regularly by High-Efficiency Particulate Air (HEPA) filters.

The HEPA filters and frequent air circulation, the air you breathe is likely to be cleaner than most office buildings and it is on par with the air quality in most hospitals.

As shown below, the cabin air is changed 20-30 times per hour.

Based on statements from Airbus, we can analyze the impact of COVID-19 on specific aircraft models.

Reference: 21.00.00119                                  Issue date: 23-JAN-2020                              Last check date: 23-JAN-2020                                          Status: Open A/C type/serie: A300, A300-600, A310, A318, A319, …                                                  ATA: 21-00

Engine manufacturer:


Purpose / Reason for revision: To expand the scope of the ISI to include Wuhan Corona Virus

Applicability : All Aircraft

References : OIT 999.0032/09

We would like to provide you with the following information in relation to questions on the MERS Corona virus, the currently-named “Wuhan Corona” virus, and Corona viruses in general.

Based on the currently available information, we consider that the OIT 999.0032 (swine flu, attached) is equally applicable to the MERS and Wuhan Corona virus.

To Airbus current knowledge, there are no “special products” being suggested as necessary for MERS Corona virus or Wuhan Corona Virus disinfection. Therefore, we assume that the existing cleaning and disinfection procedures detailed in the relevant sections of each aircraft AMM remain sufficient.

Background (Air Quality)

All of the air in Airbus cabins is, on average, completely changed every 3 minutes – even after taking account of filtered and recirculated air. This is a much higher rate of flow than people experience in other indoor environments, and means that passengers are provided with about 80 times as much air as they need to breathe.

The air in Airbus aircraft cabins is a mix of fresh air drawn from outside, and air that has been passed through extremely efficient filters, which remove particles in the air down to the size of microscopic bacteria and virus clusters (with an efficiency of better than 99.99 per cent).

These filters – called High- Efficiency-Particulate Arrestors (HEPA) – have been shown in tests to provide air that meets the standards set for hospital operating theatres.

With reference to the below efficiency chart, we can see that particles  within the size range of typical Viruses are captured by the HEPA filters with in excess of 99.99% efficiency.

You can also refer to the attached information from filter manufacturers PALL and Donaldson-Le Bozec.

As stated in the attached OIT we consider that the HEPA air recirculation filters capture viruses such as the MERS (Corona virus) and Wuhan Corona virus with extremely high efficiency.

In normal operation, less than a half of the air is filtered and recirculated – the rest is fresh air drawn in from outside.

None of the air that is supplied to aircraft toilets, galleys and cargo-holds is filtered and re-circulated – instead it is dumped directly overboard.

The air supply to the cabin comes in at the level of the overhead stowage compartments – from above or underneath them, depending on the Airbus aircraft type – and is extracted at floor level, which means that it is drawn down rather than going up. Most importantly, there is no flow forward or rearward along the cabin.

 In order to understand how the airflow patterns within the cabin in relation to the possibility of spreading viruses, please see the following;

Fresh/Recirculation Airflow

In general, the fresh air (from outside) is mixed with recirculated air in a mixer unit and then this air is supplied to the cabin, and all occupied areas within the fuselage. This means that there is no specific recirculation airflow entering the cabin that is separate from the fresh air flow.

There is only 1 airflow which is comprised of mixed fresh and recirculated air.

See the diagram for A320 family below. The A330/A340/A350 family aircraft are similar.

On A380, the airflow follows the same general principle, but is slightly more complicated, see below. In this case there is some additional local recirculation of air in the upper deck, but this is still mixed with air from the central mixer unit.

Even though the diagram below does not show it, all recirculated air is passed through a HEPA filter before re-entering the cabin or being mixed with fresh air.

A320 Family

The ventilation system of the Airbus Single Aisle Aircraft (A318/ 319/ 320/ 321) have got two air outlets per side.

The lower one ensures a sufficient flow to the passenger seats, the other one to the upper cabin space, which is the head space for working flight attendants or walking passengers:

•          Flow from upper part of the cabin downwards

•          Two air outlets per cabin side

•          Lower outlets ensure good ventilation to seat area

•          Upper outlets ensure good ventilation for persons standing/ working in the aisle

A330/A340 Family

The ventilation system of the Airbus Wide Body and Long Range Aircraft (A300, A310, A330, A340) have got one air outlet per side, which was proven to be appropriate to get an equal distribution of the air within the cabin.


On A350 there are Aisle ceiling outlets and also outlets between the baggage bins and the sidewall.


On A380 there are 2 air outlets per side, making the airflow pattern similar to that of the A320 family.

Can Recirculated Air Spread the Corona Virus ?

This is unlikely. As mentioned above, the airflow induced by the recirculation system is mixed with fresh air in the mixer unit, and the combined air enters the cabin through the air outlets.

This airflow passes over the occupants as it passes towards the floor level where it is extracted. This air will then go overboard via the pressurization outflow valves(s), or will pass through a HEPA filter for injection back into the mixer unit.

Therefore, because the HEPA filters have an extremely high efficiency in capturing the Corona virus, the recirculation airflow does not spread the Corona virus throughout the cabin.

What happens when we are seated?

While viruses associated with the common cold and upper respiratory track infections tend to be larger in size and heavier (consequently falling to the floor rather quickly), these particles linger. Which is where your vent comes in.

By using the vent and turning it on medium or low, you can create an invisible air barrier around you that creates turbulence — simultaneously blocking these particles and forcing them to the ground faster.

Planes also have low humidity, which means your mucous membrane can dry out on during a flight. When this happens, you’re more susceptible to contracting a virus, which is why keeping them away becomes all the more important.

And because those heavy common cold particles can still travel up to six feet every time you cough, sneeze, or speak, it’s equally important to wipe down and avoid touching surfaces (like that tray table you were probably resting your head on).

Detection of respiratory viruses on air filters from aircraft

To evaluate the feasibility of identifying viruses from aircraft  cabin air,  we evaluated whether respiratory viruses trapped by commercial aircraft air fil- ters can be extracted and detected using a multiplex PCR, bead-based assay.

Methods and Results: The ResPlex II assay was first tested for its ability to  detect inactivated viruses applied to new filter material; all 18 applications of virus at a high concentration were detected.

The ResPlex II assay was then used to test for 18 respiratory viruses on 48 used air filter samples from commercial aircraft.

Three samples tested positive for viruses, and three viruses were detected: rhinovirus, influenza A and influenza B. For 33 of 48 samples, internal PCR controls performed suboptimally, suggesting sample matrix effect.

Conclusion: In some cases, influenza and rhinovirus RNA can be detected on aircraft air filters, even more than 10 days after the filters were removed from aircraft.

Commercial air travel has a potentially important role in disseminating infectious diseases among cities and conti- nents. Aircraft travel has hastened the spread of influenza strains (Laurel et al. 2001; Brownstein et al. 2006; Khan   et al. 2009) and led to the  intercontinental  spread  of  severe acute respiratory syndrome (SARS) in 2002 (World

Health Organization 2003). In addition, close public quarters in aircraft cabins are a concern for disease trans- mission (Mangili and Gendreau 2005), although docu- mented cases of disease transmission onboard  airplanes are limited (Moser et al. 1979; Kenyon et al. 1996; Olsenet al. 2003; Mangili and Gendreau 2005; Byrne 2007; Hanet al. 2009; Baker et al. 2010). To make appropriate, cost- effective public health decisions, information about infectious viruses in aircraft is needed. Two recent studies have determined   that   a   variety   of   respiratory   viruses   are present in symptomatic air travellers (Luna et al. 2007; Follin et al. 2009).

However, at present, it is not known which viruses are typically present in aircraft cabin air, whether viruses are often present in infectious amounts (Fabian et al. 2008; Stelzer-Braid et al. 2009; Wagner et al. 2009; Hwang et al. 2011) and whether viruses survive degradation in cabin air to remain viable or detectable (Weber and Stilianakis 2008; Tang 2009). To our knowledge, only two studies have detected viruses in aircraft cabin air to date (La Duc et al. 2006; Yang et al. 2011).

One possible way to evaluate  airborne  viruses  in aircraft is to sample aircraft  ventilation filters. In a typi-  cal commercial aircraft, about half  of  the  aircraft  cabin air is recirculated after being filtered through fibreglass High Efficiency Particulate Air (HEPA) filters.

These HEPA filters are expected to capture virus-sized particles with   >99Æ9%   efficiency   (Bull   2008).   Ventilation   filters have been used to sample micro-organisms in other environments (Echavarria et al. 2000; Farnsworth et al. 2006; Stanley et al. 2008).

Aircraft filter material is not expected to be as efficient as other methods for collecting intact, infectious viruses because filter material may dam- age virus structure or damage viruses via desiccation (Mahony 2008; Verreault et al. 2008). Nevertheless, viral nucleic acids may remain detectable via PCR and RT-PCR.

Used air filters offer a potential advantage  over  other sampling methods for characterizing viral diversity  in aircraft because they sample air over a long period, up  to 15 000 h of flight time.

To evaluate multiple viruses simultaneously (multiplex analysis), rapidly, with high sensitivity (measured as the percentage of true-positive samples that actually test positive), high specificity (measured as the percentage of true-negative samples that actually test negative) and at relatively low cost, new multiplex molecular  techniques are being developed (Mahony 2008).

The ResPlex II assay (QIAGEN) uses multiplex PCR and RT-PCR, coupled to bead-based flow cytometry to detect 18 different viral genetic sequences. Versions of this assay have been used  to detect respiratory viruses in human samples with high sensitivity and specificity (Brunstein and Thomas 2006; Li et al. 2007; Wang et al. 2009); Li et al. reported sensitivity of 72–90%  and specificity  of 99Æ7–100% for six viruses in 360 clinical specimens.

In this study, we evaluate the ability of the ResPlex II assay to detect inactivated viruses applied to new HEPA filters and viruses extracted from used HEPA filters from commercial aircraft.


Detection of inactivated viruses applied to new high efficiency particulate air filters

For all 18 new filter samples treated with inactivated INFA, RSVA or PIV2 viruses, the ResPlex II assay yielded positive detections, with mean fluorescence intensities that ranged from 589 to 5448, all above the positive cut-off value of 250.

Applied viruses were detected at all three time-points (0, 4 or 16 h) after application and drying, indicating that detectable viral RNA can persist on filter material for at least 16 h.

To evaluate whether there was RNA loss owing to extraction, MFIs from the 18 test samples were com- pared to MFIs from positive controls, which consisted of virus directly applied to the assay without filter application and extraction.

All but one of the test samples had MFI values lower than the positive control for the correspond- ing virus; this suggests that there was viral RNA loss dur- ing filter application and extraction.

Because  the ResPlex II is a semi-quantitative assay, it is not possible to derive  an exact percentage for extraction loss.

Among the 18 samples, there were no false-positive results for viruses not applied.

However,  in three  of  the six samples treated with inactivated RSVA, there were elevated background signals (MFI values between 150 and 250) for a virus that was not applied, parainfluenza virus type (PIV1.)

No cross-reactivity between the PIV1 and RSVA probes was previously observed in testing hundreds of clinical samples. Overall, these results show that the extraction procedure and ResPlex II assay can recover and accurately detect viruses from HEPA filter material.

Detection of viruses on used aircraft high efficiency particulate air filters

Among the 48 samples from used aircraft filters, three samples tested positive for viruses (Table 1).

One was positive for INFA, one was positive for rhinovirus (RhV; most common cause of the common cold) and one was positive for both RhV and influenza B  (INFB.)  There  were also borderline positive results for coronavirus (OC43; causes common cold), INFB and RhV (Table 1). All samples tested negative for the 14 other viruses  assayed by ResPlex II.

Controls revealed no sign of virus contamination in PCR.

For 15 negative controls (water), there were no positive or borderline virus results. In addition, the positive virus control (inactivated RSVA, INFA and PIV2 applied to a single new filter sample) yielded positive results for the three tested viruses (MFI values 2116, 4429 and 1461, respectively) with no positive or borderline positive results for other viruses.

To assess whether amplification and detection per- formed properly, each sample contained an internal control consisting of an artificial transcript that can be amplified and detected by the assay. The internal control yielded MFI ranging from 371 to 842 in used filter samples that had positive or borderline positive results for viruses; these values are consistent with the assay per- forming as expected.

 Internal control values in this range (MFI ‡ 370) were seen in only seven of the 40 used filter samples that were negative for all viruses. Among the 33 samples with internal control MFI below 370, 19 had internal control MFI below the recommended 250 positive cut-off value.

 These weak internal control results cou- pled with negative virus results indicate that the assay performed suboptimally for these samples, potentially owing to the presence of PCR inhibitors. Consequently, if viruses were present, they may not have been detected.

To examine whether there was a relationship between internal control amplification and the amount of time filters were in aircraft operation, hours in service were compared for samples with MFIs above and below 370 using  an anova test; 370 was chosen because there  were  no virus detections in samples with internal control MFI  below this number.

 The test revealed the absence of a significant    association    at    the    P = 0Æ05    level    (F = 2Æ59 df = 1.46  P = 0Æ11;  hours  in  service  were  square  root-transformed). In fact, samples with control MFI above or equal to 370 and below 370 had identical median operating times (4800 h in service) and similar ranges (‡370 range: 2100–15 190 h; <370 range: 500–10 800 h in ser- vice). In addition, there was a large range in hours in service among samples with positive and borderline detections (2730–15 190 h.)Furthermore, there was no apparent association between detection and the amount of time before sample preservation in RNA later (range for samples with positive and borderline detections: 11–22 days, identical to the whole sample set.)

Overall, 15 of 48 samples had internal control MFI above 370, and eight  of  these 15 samples had positive and borderline  positive  virus detections.


Alvarez, A.J., Buttner, M.P. and Stetzenbach, L.D. (1995) PCR for bioaerosol monitoring: sensitivity and environmental interference. Appl Environ Microbiol 61, 3639–3644.

Baker, M.G., Thornley, C.N., Mills, C., Roberts, S., Perera, S., Peters, J., Kelso, A., Barr, I. et al. (2010) Transmission of pandemic A ⁄ H1N1 2009 influenza on passenger aircraft: retrospective cohort study. BMJ 340, c2424.

Blachere, F.M., Lindsley, W.G., Pearce, T.A., Anderson, S.E., Fisher, M., Khakoo, R., Meade, B.J., Lander, O. et  al. (2009) Measurement of airborne influenza virus in a hos- pital emergency department. Clin Infect Dis 48, 438–440.

Brankston, G., Gitterman, L., Hirji, Z.,  Lemieux,  C.  and Gardam, M. (2007) Transmission of influenza A in human beings. Lancet Infect Dis 7, 257–265.

 Broemeling, D., Pel, J., Gunn, D.,  Mai,  L.,  Thompson,  J., Poon, H. and Marziali, A. (2008) An instrument for auto- mated purification of nucleic acids from contaminated forensic samples. JALA Charlottesv Va 13, 40–48.

Brownstein, J.S., Wolfe, C.J. and Mandl, K.D. (2006) Empirical

evidence for the effect of airline travel on inter-regional influenza spread in the United States. PLoS Med 3, 1826– 1835.

Brunstein, J. and Thomas, E. (2006) Direct screening of clini-   cal specimens for multiple respiratory pathogens using the Genaco respiratory panels 1 and 2. Diagn Mol Pathol 15, 169–173.

Bull, K. (2008) Cabin air filtration: helping to protect occu- pants from infectious diseases. Travel Med Infect Dis 6, 142–144.

Byrne, N. (2007) Low prevalence of TB on long-haul aircraft.

Travel Med Infect Dis 5, 18–23.

Chen, P.S., Lin, C.K., Tsai, F.T., Yang, C.Y., Lee, C.H., Liao, Y.S., Yeh, C.Y., King, C.C. et al. (2009) Quantification of airborne influenza and avian influenza virus in a wet poultry market using a filter ⁄ real-time qPCR method. Aerosol Sci Technol 43, 290–297.

Echavarria, M., Kolavic, S.A., Cersovsky, S., Mitchell, F., Sanchez, J.L., Polyak, C., Innis, B.L. and Binn, L.N. (2000) Detection of adenoviruses (AdV) in culture-negative environmental samples by PCR during an AdV-associated respiratory disease outbreak. J Clin Microbiol 38, 2982– 2984.

Fabian, P., McDevitt, J.J., DeHaan, W.H., Fung, R.O.P., Cowl-

ing, B.J., Chan, K.H., Leung, G.M.  and  Milton,  D.K. (2008) Influenza virus in human exhaled breath: an obser- vational study. PLoS ONE 3, e2691.

Fabian, P., McDevitt, J.J., Lee, W.-M., Houseman, E.A. and Milton, D.K. (2009) An optimized method to detect influ- enza virus and human rhinovirus from exhaled breath and the airborne environment. J Environ Monit 11, 314–317.

Farnsworth, J.E., Goyal, S.M., Kim, S.W., Kuehn, T.H.,

Raynor, P.C., Ramakrishnan, M.A.,  Anantharaman,  S. and Tang, W. (2006) Development of a method for bac- teria and virus recovery  from  heating,  ventilation,  and air conditioning (HVAC) filters. J Environ Monit 8, 1006–1013.

Follin, P., Lindqvist, A., Nystro¨m, K. and Lindh, M. (2009) A variety of respiratory viruses found in symptomatic travel- lers returning from countries with ongoing spread of the new influenza A(H1N1)v virus strain. Euro Surveill 14, 19242.

Han, K., Zhu, X., He, F., Liu, L., Zhang, L., Ma, H., Tang, X., Huang, T. et al. (2009) Lack of airborne transmission dur- ing outbreak of pandemic (H1N1) 2009 among tour group members, China, June 2009. Emerg Infect Dis 15, 1578–


Hwang, G.M., DiCarlo, A.A. and Lin, G.C. (2011) An analysis on the detection of biological contaminants aboard air- craft. PLoS ONE 6, e14520.

 Kenyon, T.A., Valway, S.E., Ihle, W.W., Onorato, I.M. and Castro, K.G. (1996) Transmission of multidrug-resistant Mycobacterium tuberculosis during a long airplane flight. N Engl J Med 334, 933–938.

Khan, K., Arino, J., Hu, W., Raposo, P., Sears, J., Calderon, F., Heidebrecht, C., Macdonald, M. et al. (2009) Spread of a novel influenza A (H1N1) virus via global airline transportation. N Engl J Med 361, 212–214.

La Duc, M., Osman, S., Dekas,  A.,  Stuecker,  T.,  Newcombe, D., Piceno, Y., Furhman, J., Andersen, G. et al. (2006) A Comprehensive Assessment of Biologicals Contained Within Commercial Airliner Cabin Air. Pasadena, CA: Jet Propul-

sion Laboratory, National Aeronautics and Space Adminis- tration.

Laurel, V.L., De Witt, C.C., Geddie, Y.A., Yip, M.C., Dolan,

D.M., Canas, L.C., Dolan, M.J. and Walter, E.A. (2001) An outbreak of influenza A caused by imported virus in the United States, July 1999. Clin Infect Dis 32, 1639–1642.

Li, H., McCormac, M.A., Estes, R.W., Sefers, S.E., Dare, R.K., Chappell, J.D., Erdman, D.D., Wright, P.F. et al. (2007) Simultaneous detection and high-throughput identification of a panel of RNA viruses causing respiratory tract infec- tions. J Clin Microbiol 45, 2105–2109.

Lindsley, W.G., Blachere, F., Davis, K.A., Pearce, T.A., Fisher, M.A., Khakoo, R., Davis, S.M., Rogers, M.E. et al. (2010) Distribution of airborne influenza virus and respiratory syncytial virus in an urgent care medical clinic. Clin Infect Dis 50, 693–698.

Luna, L., Kleberde, S., Panning, M., Grywna, K., Pfefferle, S. and Drosten, C. (2007) Spectrum of viruses and atypical bacteria in intercontinental air travelers with symptoms of acute respiratory infection. J Infect Dis 195, 675–679.

Mahony, J.B. (2008) Detection of respiratory viruses by molecular methods. Clin Microbiol Rev 21, 716–747.

Mangili, A. and Gendreau, M.A. (2005) Transmission of infectious diseases during commercial air travel. Lancet 365, 989–996.

Miller, D.N., Bryant, J.E., Madsen, E.L. and Ghiorse, W.C. (1999) Evaluation and optimization of DNA extraction  and purification procedures for soil and sediment samples. Appl Environ Microbiol 65, 4715–4724.

Moser, M.R., Bender, T.R., Margolis, H.S., Noble, G.R., Ken-

dal, A.P. and Ritter, D.G. (1979) An outbreak of influenza aboard a commercial airliner. Am J Epidemiol 110, 1–6.

Myatt, T.A., Johnston, S.L., Zuo, Z.F., Wand, M., Kebadze, T., Rudnick, S. and Milton, D.K. (2004) Detection of airborne rhinovirus and its relation to outdoor air supply in office environments. Am J Respir Crit Care Med 169, 1187–1190.

Olsen, S.J., Chang, H.-L., Cheung, T.Y.-Y., Tang, A.F.-Y., Fisk,

T.L., Ooi, S.P.-L., Kuo, H.-W., Jiang, D.D.-S. et al. (2003)

Transmission of the severe acute respiratory syndrome on aircraft. N Engl J Med 349, 2416–2422.

R Development Core Team (2009) R: A language and environment for statistical computing. Vienna, Austria: R Foundation for Statistical Computing.

 Stanley, N.J., Kuehn, T.H., Kim, S.W., Raynor, P.C., Ananthar- aman, S., Ramakrishnan, M.A. and Goyal, S.M. (2008) Background culturable bacteria aerosol in two large public buildings using HVAC filters as long term, passive, high- volume air samplers. J Environ Monit 10, 474–481.

Stelzer-Braid, S., Oliver, B.G., Blazey, A.J., Argent, E., New-

some, T.P., Rawlinson, W.D. and Tovey, E.R. (2009) Exhalation of respiratory viruses by breathing, coughing, and talking. J Med Virol 81, 1674–1679.

Tang, J.W. (2009) The effect of environmental parameters on the survival of airborne infectious agents. Interface Focus 6, S737–S746.

Tellier, R. (2009) Aerosol transmission of influenza A virus: a review of new studies. Interface Focus 6, S783–S790.

Thomas, Y., Vogel, G., Wunderli, W., Suter, P., Witschi, M., Koch, D., Tapparel, C. and Kaiser, L. (2008) Survival of influenza virus on banknotes. Appl Environ Microbiol 74, 3002–3007.

Verreault, D., Moineau, S. and Duchaine, C. (2008) Methods  for sampling of airborne viruses. Microbiol Mol Biol Rev 72, 413–444.

 Wagner, B., Coburn, B. and Blower, S. (2009) Calculating the potential for within-flight transmission of influenza A (H1N1). BMC Med 7, 81.

Wang, W., Ren, P., Sheng, J., Mardy, S., Yan, H., Zhang, J., Hou, L., Vabret, A. et al. (2009) Simultaneous detection of respiratory viruses in children with acute respiratory infection using two different multiplex reverse transcription- PCR assays. J Virol Methods 162, 40–45.

Weber, T.P. and Stilianakis, N.I. (2008) Inactivation of influenza A viruses in the environment and modes of transmis- sion: a critical review. J Infect 57, 361–373.

World Health Organization (2003) Consensus document on the epidemiology of severe acute respiratory syndrome (SARS).

Yang, W., Elankumaran, S. and Marr, L.C. (2011) Concentrations and size distributions of airborne influenza A viruses measured indoors at a health centre, a day-care centre and on aeroplanes. Interface Focus 8, 1176–1184.


1.  Greatorex JS, Digard P, Curran MD, Moynihan R, Wensley H, Wreghitt T, et al. (2011) Survival of Influenza A(H1N1) on Materials Found in Households: Implications for Infection Control. PLoS ONE 6(11):e27932.

2. Chan JF-W, Yuan S, Kok K-H, To KK-W, Chu H, Yang J, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet. 2020;0(0):S0140-6736(20)30154-9.  PMID: 31986261 

3. Chang W, Cheng J, Allaire JJ, Xie Y, McPherson J. shiny: Web Application Framework for R. R package version 1.4.0. 2019. [Accessed 27 Jan 2020]. Available from:

4. Brady MT, Evans J, Cuartas J. Survival and disinfection of parainfluenza viruses on environmental surfaces. Am J Infect Control. 1990;18:18–23. [PubMed] [Google Scholar]

6. Geller C, Varbanov M, Duval RE. Human coronaviruses: insights into environmental resistance and its influence on the development of new antiseptic strategies. Viruses. 2012;4:3044–3068. [PMC free article] [PubMed] [Google Scholar]

8. Li Q, Guan X, Wu P, Wang X, Zhou L, Tong Y, et al. Early Transmission Dynamics in Wuhan, China, of Novel Coronavirus-Infected Pneumonia. N Engl J Med. 2020;NEJMoa2001316.  PMID: 31995857 

9. Kramer A, Schwebke I, Kampf G. How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infect Dis. 2006;6:130. [PMC free article] [PubMed] [Google Scholar]

10. Mahl MC, Sadler C. Virus survival on inanimate surfaces. Can J Microbiol. 1975;21:819–823. [PubMed] [Google Scholar]

11. Rajtar B, Majek M, Polański Ł, Polz-Dacewicz M. Enteroviruses in water environment—a potential threat to public health. Ann Agric Environ Med. 2008;15:199–203. [PubMed] [Google Scholar]

12. Rzezutka A, Cook N. Survival of human enteric viruses in the environment and food. FEMS Microbiol Rev. 2004;28:441–453. [PubMed] [Google Scholar]

13. Sane F, Caloone D, Gmyr V, Engelmann I, Belaich S, Kerr-Conte J, Pattou F, Desailloud R, Hober D. Coxsackievirus b4 can infect human pancreas ductal cells and persist in ductal-like cell cultures which results in inhibition of Pdx1 expression and disturbed formation of islet-like cell aggregates. Cell Mol Life Sci. 2013;70:4169–4180. [PubMed] [Google Scholar]

14. Scheuplein RJ, Morgan LJ. “Bound water” in keratin membranes measured by a microbalance technique. Nature. 1967;214:456–458. [PubMed] [Google Scholar]

15. Thevenin T, Lobert PE, Hober D. Inactivation of coxsackievirus b4, feline calicivirus and herpes simplex virus type 1: unexpected virucidal effect of a disinfectant on a non-enveloped virus applied onto a surface. Intervirology. 2013;56:224–230. [PubMed] [Google Scholar]

17. Van Bueren J, Simpson RA, Jacobs P, Cookson BD. Survival of human immunodeficiency virus in suspension and dried onto surfaces. J Clin Microbiol. 1994;32:571–574. [PMC free article] [PubMed] [Google Scholar]

18.       British Airways. Timetables. British Airways. [Accessed 27 Jan 2020]. Available from:

19.       Priest PC, Duncan AR, Jennings LC, Baker MG. Thermal image scanning for influenza border screening: results of an airport screening study. PLoS One. 2011;6(1):e14490.  PMID: 21245928 

29. Masters PS. The molecular biology of coronaviruses. Adv Virus Res. 2006;66:193–292. doi: 10.1016/S0065-3527(06)66005-3. [PubMed] [CrossRef] [Google Scholar]

35. DeDiego ML, Álvarez E, Almazán F, Rejas MT, Lamirande E, Roberts A, et al. A severe acute respiratory syndrome coronavirus that lacks the E gene is attenuated in vitro and in vivo. J Virol. 2007;81(4):1701–1713. doi: 10.1128/JVI.01467-06. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

37. Mortola E, Roy P. Efficient assembly and release of SARS coronavirus-like particles by a heterologous expression system. FEBS Lett. 2004;576(1–2):174–178. doi: 10.1016/j.febslet.2004.09.009. [PubMed] [CrossRef] [Google Scholar]

38. Wang C, Zheng X, Gai W, Zhao Y, Wang H, Wang H, et al. MERS-CoV virus-like particles produced in insect cells induce specific humoural and cellular immunity in rhesus macaques. Oncotarget. 2017;8(8):12686–12694. [PMC free article] [PubMed] [Google Scholar]

39. Kuo L, Masters PS. The small envelope protein E is not essential for murine coronavirus replication. J Virol. 2003;77(8):4597–4608. doi: 10.1128/JVI.77.8.4597-4608.2003. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

42. Siu Y, Teoh K, Lo J, Chan C, Kien F, Escriou N, et al. The M, E, and N structural proteins of the severe acute respiratory syndrome coronavirus are required for efficient assembly, trafficking, and release of virus-like particles. J Virol. 2008;82(22):11318–11330. doi: 10.1128/JVI.01052-08. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

44. Song HC, Seo M-Y, Stadler K, Yoo BJ, Choo Q-L, Coates SR, et al. Synthesis and characterization of a native, oligomeric form of recombinant severe acute respiratory syndrome coronavirus spike glycoprotein. J Virol. 2004;78(19):10328–10335. doi: 10.1128/JVI.78.19.10328-10335.2004. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

45. Fehr AR, Perlman S. Coronaviruses: An overview of their replication and pathogenesis. Coronaviruses: Springer; 2015. pp. 1–23. [PMC free article] [PubMed] [Google Scholar]

46. Glowacka I, Bertram S, Müller MA, Allen P, Soilleux E, Pfefferle S, et al. Evidence that TMPRSS2 activates the severe acute respiratory syndrome coronavirus spike protein for membrane fusion and reduces viral control by the humoral immune response. J Virol. 2011;85(9):4122–4134. doi: 10.1128/JVI.02232-10. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

47. Qian Z, Dominguez SR, Holmes KV. Role of the spike glycoprotein of human Middle East respiratory syndrome coronavirus (MERS-CoV) in virus entry and syncytia formation. PLoS One. 2013;8(10):e76469. doi: 10.1371/journal.pone.0076469. [PMC free article] [PubMed] [CrossRef] [Google Scholar]



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