The new coronavirus (SARS-CoV-2) and COVID-19: FACTS

Translated into plain English for non-specialists*

* The smaller-print sections in grey contain information that may be particularly useful for medical editors and translators

(Do not miss the abbreviation list in the end; also, check the new online virology training for translators and interpreters!)

Of note, some of the statements listed below concern facts that are still under investigation. They are true as of today but  as we learn more about the virus, this may change.  For those that are prone to change, the date of last update is indicated.

Make a good use of it!

You have questions, suggestions, you want another fact explained? Submit it here.

Important: mind that this is by no means meant to be any kind of medical advice; if you are unwell, seek medical advice with the designated healthcare institutions in your area.

FACT

What does it mean in practice?

SARS-CoV-2 is a virus

One of very important things that this implies is that using antibiotics does not work (viruses are not sensitive to antibiotics). You may have heard that some doctors prescribe antibiotics to patients with severe forms of COVID-19, the disease caused by the SARS-CoV-2 virus. This is not to fight the virus as such but to treat additional bacterial infections that develop at the same time.

Do not use antibiotics ‘just in case’, this will not help and may even be harmful by promoting the development of some bacteria resistant to antibiotics; it would also affect the ‘good’ bacteria that live in your body, which is not what you want.

SARS-CoV-2 is a Coronavirus

SARS-CoV-2 belongs to a large family of viruses called Coronaviruses (Coronaviridae in Latin); all viruses from the same family share some common characteristics.

Knowing where the virus belongs allows us to make some assumptions about how it may behave, which may accelerate characterising the virus (and so finding the ways to deal with it).

It is in this virus family that we find the SARS culprit: a virus called SARS-CoV (without the ‘-2’!) causing the disease called Severe Acute Respiratory Syndrome (SARS), which first appeared in 2002 and caused an epidemic in 2003.

A note for translators

You may come across the term ‘2019-nCoV’ (from ‘2019 novel Coronavirus’). This is one of the ways the SARS-CoV-2 virus was called before it was given its official name. It should not be called this way anymore.

SARS-CoV-2 is associated with COVID-19

The name of the virus is SARS-CoV-2 and it causes a disease which is called COVID-19 (from ‘Coronavirus Disease 2019’). Some sources tend to use these two terms somewhat interchangeably. Even though this is comprehensible, it is not correct (translators and editors, beware!)

A note for translators

We might still say ‘the COVID-19 virus’ knowing that it means ‘the virus causing the COVID-19 disease’ and not the virus whose name is COVID-19; to avoid confusion though, I recommend against using this phrasing;

If you ever have doubts about the correct name for any virus, check the website of the International Committee on Taxonomy of Viruses (ICTV).

SARS-CoV-2 is zoonotic

SARS-CoV-2 can be transmitted from infected animals to humans (which is probably what happened in Wuhan, China, in 2019).

This also implies that you should avoid close contact with animals as well eating raw or undercooked animal products in risk zones.

It does not mean that you get the virus from any animal. E.g. there is NO evidence that cats and dogs can spread COVID-19, so do not get rid of your pet.

It does not mean that infected people do not spread the infection, either – on the contrary, we know that SARS-CoV-2 has a capacity of ‘jumping’ (i.e. being transmitted) from person to person (there are some viruses which do not) just about like it ‘jumped’ from an animal to a person in Wuhan; in other words, you can get the virus from an infected person or an infected animal.

A note for translators

We also talk about ‘zoonotic diseases’ or ‘zoonoses’ (by the way, not all of them are caused by viruses).

SARS-CoV-2 infects people of various ethnicities

SARS-CoV-2 does not know human-imposed borders and does not seem to make a difference between hosts (organisms that it infects) of different ethnicities; a Caucasian American who had been in contact with an infected person is just as likely to be infected as a Han Chinese or a genuine Iranian with a similar history.

If even the virus is not racist, we should certainly not be either, let us be reasonable … and human.

SARS-CoV-2 is a serious public health concern

We have to take the SARS-CoV-2 virus seriously as it is new to humans (it had not been known to infect humans before December 2019), it is capable of spreading between people (not just from animals to humans), and it causes severe disease (which may lead to death in extreme cases) in some people. So the relevant authorities do their best to limit the spread of the virus and to keep healthcare institutions prepared to act accordingly when suspected or confirmed cases appear.

A note for translators

WHO has declared the outbreak to be a ‘public health emergency of international concern’ (PHEIC; January 2020) – mind the wording

COVID-19 mean incubation period is between 5 and 6 days;

the incubation period does not exceed 11.5 days for nearly 98% of infected individuals

(last fact update:

September 10, 2020)

The average* time lapse between the infection with SARS-CoV-2 (i.e. the moment when the virus enters the body) and the first signs and symptoms of the COVID-19 disease which is caused by this virus is between 5 and 6 days;

(* yes, the mean and the average are not exactly the same but I guess we can use them as synonyms for the sake of this explanation)

almost 98% of people infected with SARS-CoV-2 (i.e. a vast majority) will develop the disease symptoms within 11.5 days

It is important to determine the exact length of the incubation period because this is the time when the person may be infected without knowing it, so may unintentionally spread the infection. It also allows to determine the appropriate quarantine duration to limit – if not prevent – the spread of the disease.

A note for translators

The relevant specialist terms / expressions are:

incubation period, disease onset, the onset of symptoms, symptomatic, asymptomatic, or presymptomatic patient

Infectious SARS-CoV-2 particles persist on cardboard for up to 24 hours, and on plastic surfaces and on stainless steel for up to three days, if not more

(last fact update:

September 10, 2020)

This implies that we can get the virus for example from a plastic table we put our hands on two days (or even later, this depends on several factors) after someone has spread the virus on it. Like from any other plastic surface that got contaminated by someone infected. For cardboard, this time is shorter (up to 24 hours) but we still need to be cautious. As many factors influence the time for which the virus can persist on surfaces, mind that it may even be longer under some conditions. As we are going through the pandemic, do not touch anything you do not need to touch e.g. when shopping. Do not touch your face (mouse, nose, eyes). Discard all unnecessary plastic and cardboard packages and the like as soon as you get home. Wash your hands properly in any case.

Check our linked article of March 18, 2020 for more interpretation.

Older age is associated with a higher COVID-19 fatality.

This means that older people are at a higher risk to develop severe disease when infected with SARS-CoV-2 and die of it than those at younger ages. In simple words, older COVID-19 patients end up in intensive care units more often than younger patients. However, this does not mean that younger people are ‘safe’. Even though older people die of COVID-19 more often, there are also younger and healthy people who die and we still do not know why. So being older definitely means that you should be extremely cautious not to catch the virus, but being younger does not mean you do not need to care.

COVID-19 case fatality is much higher than that of seasonal influenza (flu)

That means that there are - proportionally - more deaths among COVID-19 patients than among patients suffering from seasonal influenza (commonly called flu). The word ‘proportionally’ is important here. You can hear many people comparing crude numbers with rates, or death rates from the two diseases in different periods of time etc. We need to compare what is comparable. Higher case fatality due to COVID-19 means that if we take hundred COVID-19 patients and hundred patients with seasonal flu, the death number will be higher among those with COVID-19.  How much higher, depends on the country, on the access to healthcare, the local epidemic dynamics and other factors, but right now, the difference may be as high as 40-fold in some cases. This may change, e.g. if we find an efficacious treatment  but as of now, COVID-19 is much more fatal than seasonal flu.

There is currently no universally  approved treatment for the SARS-CoV-2 infection

(last fact update:

November 20, 2020)

So far, there are no treatments that can directly ‘kill’ (destroy) SARS-CoV-2 in the patient’s body approved for widespread use. However, several therapeutic options are being tested in clinical trials (see also the note on chloroquine, just the next fact below) and some have been granted ‘exceptional’ use authorisations. Besides, doctors can prescribe some drugs to alleviate symptoms of the associated disease (which are mild in most – but not all – people). Do not take antibiotics or available anti-viral drugs on your own, this is not going to help. Do not buy new ‘drugs’ claimed to treat the infection on the internet – these are fake and may be dangerous to your health. Seek real medical advice and follow it closely.

You may have heard about dexamethasone, a long-known corticosteroid used for example in rheumatic patients, for treating critically ill COVID-19 patients. Indeed, we have some preliminary results from a big clinical trial suggesting that dexamethasone may help patients with severe symptoms (to be precise, it reduces the risk of death due to COVID-19). Dexamethasone does not directly target the virus but modulates the patient’s immune response so as to reduce the infection-related damage and increase the chances to survive.

Antiviral drug remdesivir has been the first drug to be approved by the American Food and Drug Administration (FDA; full approval issued on the 22nd of October, 2020) for treatment of some hospitalised COVID-19 patients. Remdesivir is also the first drug recommended for conditional marketing authorisation in the European Union by The European Medicines Agency (EMA). However, the most recent results of big clinical trials do not confirm that this drug is effective in treating COVID-19 patients. Therefore, on the 20th of November, 2020, the World Health Organisation (WHO) issued a conditional recommendation against the use of remdesivir in COVID-19 patients. As studies continue, we gain more and more knowledge about the virus, the disease, and possibilities to fight it. Therefore, this recommendation may change. Follow WHO to stay up to date.

Finally, plasma obtained from COVID-19 patients who have recovered, called convalescent plasma, may also help some critically ill patients and have been granted an Emergency Use Authorisation by FDA on the 23rd of August 2020. However, obtaining convalescent plasma which actually works against the virus causing COVID-19 is not easy, which makes it impossible to use on a larger scale.

A note for translators

As research on potential therapeutic agents is ongoing, you may come across such terms as antivirals, candidate drugs, experimental drugs, preclinical testing … and more

Chloroquine and hydroxychloroquine, even though shown to have anti-viral activity in vitro, have not been shown to be effective in the treatment of COVID-19 and are not approved for this indication.

(last fact update:

September 17, 2020)

This means that we do not know yet whether these medications work against SARS-CoV-2 and – if they do – how they should be used in order to work properly. They have been shown to prevent the SARS-CoV-2 virus from replicating in vitro (i.e. in cells grown in research labs; this is promising but there are many compounds that were shown to work in cells cultured in a lab which do not work in people). There were also some reports hinting that chloroquine and/or hydroxychloroquine might work in patients suffering from COVID-19 but this must be verified in rigorously designed and evaluated clinical trials. Some are ongoing now. It is noteworthy that early data from clinical trials and some other reports do not support a hypothesis that these compounds are of any good to COVID-19 patients (‘no clinical benefit’). To make absolutely sure that this is true, it is being further investigated.

Physicians and all other specialists involved in conducting clinical trials are really doing their best to get the results as quickly as possible but they need to take some time to obtain and analyse the data in order to provide reliable results. It is not just about finding a simple ‘yes’ or ‘no’ reply to a question whether these drugs work. They may work only at some stages of the disease. They may work very well for some people but be harmful to others – we must know when and why, not to put anybody in danger. They may be safe to use at some doses but be toxic at others (they will surely be toxic at some doses in fact, so we must be sure of the thresholds). There may be some particular ‘forms’ of the compounds that may work (mind that chloroquine and hydroxychloroquine are not exactly the same), we must know which ones for sure. We really have to know answers to these and many other questions before any treatment can be safely used. And in any case, such treatments should only be taken when prescribed by a doctor. Do not take any treatment said to work against COVID-19 on your own, this may be very dangerous to you.

You may have heard that some ‘forms’ of chloroquine (namely hydroxychloroquine sulphate and chloroquine phosphate) had received the Emergency Use Authorisation from the US Food and Drug Administration (FDA; granted on March 28, 2020). Mind that this authorisation has recently been revoked due to safety concerns, possible interactions with other treatments and low probability that it actually works against SARS-CoV-2 infection (decision announced by FDA on June 15, 2020).

The debate over the use of hydroxychloroquine seems to have gone political and has risen lots of unnecessary emotions and preliminary hopes. However, from a scientific point of view, we still have no data that would support the hypothesis that using it to treat COVID-19 patients can actually help these patients get better. We do, however, have data which call for caution in using it due to serious safety concerns. There is also emerging evidence indicating that these compounds are in fact rather unlikely to be efficient in treating COVID-19.

SARS-CoV-2 is an RNA virus

The genome of SARS-CoV-2 is made of RNA, i.e. RNA is the genetic material of this virus (unlike in humans and other living organisms whose genome is made of DNA).

It is important to know as RNA viruses tend to mutate (in other words: evolve, change) quicker than DNA viruses, which makes their diagnosis and treatment more difficult.

COVID-19 cases can be confirmed by RT-PCR

RT-PCR is a kind of a molecular biology test which can be used to detect specific RNA bits in a sample; as SARS-CoV-2 has a genome made of RNA, we can design the test in such a way so that it detects some fragment (or fragments) of this RNA which is (are) characteristic for this virus only.

You may have heard about a new test by Roche which received the Emergency Use Authorisation of the US Food and Drug Administration (FDA) on March 12, or a new test by Biomerieux which obtained the same on March 23 - both are kits based on an RT-PCR analysis.

RT-PCR is very sensitive and can be designed to be very specific (in this case meaning detecting only SARS-CoV-2 RNA and not any other RNA), so this is the recognised reference method for confirming COVID-19 cases. However, other detection methods are also being developed, in particular rapid tests which could be run outside a specialised diagnostic lab and which would produce results quicker. Many of them will not use RT-PCR, looking for a compromise between advantages (e.g. the ease of use or shorter analysis time) and disadvantages of this fact (e.g. some may not be able to confirm infection until some time elapses). Some of these rapid tests have already been granted the Emergency Use Authorisation by FDA.

In any case, the timing of the testing is of utmost importance to obtain a reliable result (see also the fact below).  

A note for translators

Some of you may have followed our Molecular diagnostics for translators training - here we have the practical application!

RT-PCR tests may give false-negative results in a proportion of infected individuals

(last fact update:

September 17, 2020)

A false-negative result means that a person who is positive for the virus (here: SARS-CoV-2) has a negative test result, i.e. the test does not detect the virus.

Diagnosing SARS-CoV-2 by RT-PCR is based on detecting some parts of the virus in the body of the infected person. These viral ‘parts’ are not produced at any time at any part of the body, and not in the same way in persons who are severely ill and those who have no symptoms. All that means that it is very important what specimens are taken for analysis (e.g. will it be a swab from the nose or from lower parts of the respiratory tract) and when they are collected with regard to the suspected exposure to the virus and to the occurrence of symptoms. Therefore, negative RT-PCR results must be interpreted with caution, and that is why you may be prescribed two subsequent tests: to make sure that you are really negative.

Check also WHO’s COVID-19 Questions and Answers as well as Myth busters websites

A note for translators

Abbreviations and acronyms can be a nightmare (isn’t that right?)

That implies that you may like a list of those related to COVID-19 et al, will you?

(of course, all acronyms / abbreviations must be interpreted in their context; below we provide the most common meanings in the context of COVID-19 and coronaviruses)

ABHR: alcohol-based hand rub

ACE2: angiotensin-converting enzyme 2

ACH: air changes per hour

AGPs: aerosol-generating procedures

AH: absolute humidity

AIIR: airborne infection isolation room

ARDS: acute respiratory distress syndrome

BNP: B-type natriuretic peptide

BSL: biosafety level (e.g. when referring to a lab)

CAP: community-acquired pneumonia

CBC: complete blood count

CC50: the 50% cytotoxic concentration

CDC: Centers for Disease Control and Prevention (US)

CFR: case fatality rate

CIA: chemiluminescent immunoassay

CoVs: coronaviruses

CP: convalescent plasma

CPAP: continuous positive airway pressure [device]

CPE: cytopathic effect

CPP: Clinical Characterisation Protocol

CRF: Case Record Form CRF

CRS: cytokine release syndrome

CWB: convalescent whole blood

CT: computed tomography

CXR: chest X-ray

EC50: half maximal effective concentration

ECDC: European Centre for Disease Prevention and Control

ECMO: extracorporeal membrane oxygenation

EID(s): emerging infectious disease(s)

ELISA: enzyme-linked immunosorbent assay

EM: electron microscopy

EPA: Environmental Protection Agency (US)

EUA: Emergency Use Authorisation

FDA: US Food and Drug Administration

FFP: filtering face piece

FFR: filtering facepiece respirator

GGO: ground-glass opacity (radiological term; e.g. pulmonary GGO on a CT scan)

HAN: Health Alert Network

HCWs: healthcare workers

HCoV: human coronavirus

HCP: healthcare personel / professional

HCQ: hydroxychloroquine

HTO: high-touch objects

ICT: immunochromatographic test

ICU: intensive care unit

IDSA: Infectious Diseases Society of America

IFA: (indirect) immunofluorescence assay

IFN: interferon

Ig: immunoglobulin

ILI: influenza-like-illness

IND: investigational new drug (when referring to drug approval)

IPC: infection prevention and control

ISG: interferon-stimulated gene

IVIg (also: IVIG): intravenous immunoglobulins

LAN: lymphadenopathy

LF: lateral flow

LFA: Lateral flow assay

LFD: Lateral flow device

LFIA: lateral flow immunoassay

LFT: Lateral flow test

LFTs: liver function tests

LOD: limit of detection

LRTI(s): lower respiratory tract infection(s)

MCC: mucociliary clearance

MIS-C: multisystem inflammatory syndrome in children

MMWR: Morbidity and Mortality Weekly Report (by CDC)

NAbs or nAbs: neutralising antibodies

NAT: nucleic acid test / testing

NID: neglected infectious diseases

NIOSH: The National Institute for Occupational Safety and Health (US)

NPA: nasopharyngeal aspirate

NPIs: non-pharmaceutical interventions

NPS: nasopharyngeal swab

nt: nucleotide

ORF: open reading frame

PAPR: powered air purifying respirator

PBNA: pseudovirion-based neutralisation assay

PCR: polymerase chain reaction

PFU: plaque forming unit(s)

PM: particulate matter

POC: point-of-care 

PPE: personal protective equipment

RPP: respiratory pathogen panel  (careful, this acronym is not widely used;  I’d recommend spelling it out when translating to avoid ambiguity)

PRTs: pathogen inactivation/reduction technologies

PUI: patient / person under investigation

RAD: rapid antigen detection

RDT: rapid diagnostic test

RH: relative humidity

RT-PCR: real-time reverse-transcriptase PCR (beware, RT may also stand for reverse transcription or room temperature)

RUO: research use only

SARS: Severe Acute Respiratory Syndrome

S/D: solvent/detergent (a mixture)

SI: selectivity index (in pharmacology)

SS: superspreader

SSEs: superspreading events

SoC or SOC: standard of care

TCID: tissue culture infectious dose

UHPLC-UV: ultra-high performance liquid chromatography coupled with ultraviolet detection

URTI(s): upper respiratory tract infection(s) (sometimes this is abbreviated to URI but the latter is also used for urinary tract, so I would stick to URTI for clarity)

WBC: white blood cells

… to be continued…

We have also written about abbreviations and acronyms in medical translation on LinkedIn.