Coronavirus Disease 2019 (COVID-19): A Review of the Current Literature

ACHAIKI IATRIKI | 2020; 39(1): 36–44


Ioulia Sirokosta1, Mary Stathopoulou2

1Division of Infectious Diseases, Department of Internal Medicine, University Hospital of Patras, Patras, Greece
2Medical School, University of Patras, Patras, Greece

Received: 05 April 2020; Accepted: 12 April 2020

Corresponding author: Ioulia Sirokosta, Division of Infectious Diseases, Department of Internal Medicine, University Hospital of Patras, Patras, Greece Tel: 0030261999744, Fax: 00302610999740, E-mail:

Key words: SARS-CoV-2, COVID-19, coronaviruses, infection, acute respiratory disease



An acute respiratory disease caused by a novel coronavirus, the coronavirus disease -19 (COVID-19) has spread throughout China and to more than 200 countries worldwide and has received global attention. The World Health Organization (WHO) has characterized COVID-19 as a pandemic. Coronaviruses (CoV), named so due to their “crown-like” appearance, constitute a large family of viruses that spread from animals to humans. The new coronavirus is highly contagious with a reproduction number (R0) between 1.4-2.5 patients and recent epidemiological data indicate that it may affect up to 30-40% of the population. Its high transmissibility in combination with the presence of a large percentage of asymptomatic carriers and the current lack of an effective vaccine render the new virus a major threat for people’s health, especially for older age individuals and chronic disease patients. Although there is significant variation in case fatality rate for COVID-19, it is estimated to reach 2%.

Classification and historical perspective: from urbani-sars to mers and the covid-19 pandemic

Coronaviruses (CoV) are a group of large enveloped non-segmented positive-sense single-stranded RNA viruses belonging to the family of Coronaviridae [1]. All CoVs are pleomorphic RNA viruses containing crown-shape peplomers. They belong to a large family of viruses broadly affecting humans and other mammals [1-5]. They can be classified into four genera, namely alpha, beta, gamma and delta CoVs of thirty-eight unique species [6].

Previously identified human CoVs infections include the alpha CoV hCoV-NL63, hCoV-229E and the beta CoVs HCoV-OC43 and HKU1 that cause self-limiting common cold-like illnesses [1,4,5]. The two previous beta coronaviruses fatal infections [6], namely the severe acute respiratory syndrome coronavirus (SARS-CoV) [7] and the Middle East respiratory syndrome coronavirus (MERS-CoV), [8] had  pandemic potential and caused more than 10.000 cumulative cases during the past two decades, with mortality rates reaching 10% for SARS-CoV and 37% for MERS-CoV [6-8].

Several studies have shown that bats are the natural hosts of both SARS-CoV and MERS-CoV [9,10], while palm civets  (Pagumalarvata)  [11] and dromedary camels have served as intermediate hosts playing an important part in the transmission of these viruses from bats to humans [11-13]. During 2002-2003, SARS-CoV initially emerged in China and rapidly spread to a number of other countries, causing over 8,000 infections and approximately 800 deaths worldwide [7]. In 2012, MERS-CoV was first identified in the Middle East and then spread through the globe [8]. 2,494 MERS cases with 858 related deaths have been recorded in 27 countries [6,8]. Notably, new cases of MERS-CoV infections continue to be reported [13-15].

In December 2019, Wuhan State in Hubei Province, China became the center of global attention due to the outbreak of a pneumonia epidemic of unknown cause with characteristics similar to those of viral pneumonia [16]. Influenza viruses and all known coronaviruses were ruled out by laboratory testing which revealed the existence of a novel coronavirus [17]. This virus was named 2019-nCoV by WHO on January 12 (2019-nCoV) and was classified in the betacoronavirus 2b lineage [16,18]. It bares similarities to bat coronaviruses, and it has been postulated that bats constitute the primary source [17]. Although 2019-nCoV and SARS-CoV belong to the same beta coronavirus subgroup, genomic similarity is less than 79.5%, and the novel group has been found to show genetic differences from SARS-CoV [17,18]. The presence of high-risk animal contact in the medical histories of these patients suffering from a viral-like pneumonia has strengthened the likelihood of an infection transmitted from animals to humans [3,4].While the origin of the 2019-nCoV is still under investigation,  relevant studies have shown that the outbreak is likely to have started at Huanan, a large Seafood Market where live wild animals’ trade takes place [19]. Although the outbreak is likely to have started as a zoonotic transmission [3], it soon became clear that human-to-human transmission was also occurring [19].

The Coronavirus Study Group of the International Committee on Taxonomy of Viruses οn February 11, formally named the novel virus SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) and the relevant disease COVID-19 (Coronavirus Disease-2019) [20,21]. SARS-CoV-2 represents the seventh coronavirus known to cause human diseases. Population genetic analyses of SARS-CoV-2 genomes indicated that these viruses evolved into two major types, L and S. This probably explains why initial reports from Wuhan described a higher mortality than several more recent case series [22]. On March 11, 2020, COVID-19 was declared as global pandemic by WHO, based on reports of more than 118,000 cases in over 110 countries and the sustained risk of further spread worldwide [23].

Genomic structure and proteins

Coronaviruses’ genomic structure has been extensively studied. Two-thirds of the viral RNA encodes viral polymerase (RdRp), RNA synthesis materials, and two large nonstructural polyproteins not involved in modulating host-virus interaction (ORF1a-ORF1b). The remaining genome encodes four structural proteins [spike (S), envelope (E), membrane (M) nucleoprotein (N)], hematogglutinin-esterase (HE) and other helper proteins [6,18,24-27]. Viral infections initiate with the binding of viral particles to host surface cellular receptors. Receptor recognition constitutes an important determinant of the virus preference for specific cells and tissues (viral tropism). In addition, the gain-of-function of a virus to bind to the receptor-counterparts in other species is also a prerequisite for inter-species transmission [24]. Recently, the human angiotensin converting enzyme 2 (hACE2) has been reported as an entry receptor for SARS-CoV-2 [25].

Viral replication

The first step in viral infection is the interaction of human cells with viral spike protein (S). SARS-CoV-2 binds to the hACE2, located at the surface of type II alveolar cells and epithelium cells of the ileum and colon [16-18]. The S protein is subject to cleavage by host proteases into the S1 and S2 subunits that are responsible for receptor recognition and membrane fusion, respectively. S1 can be further divided into an N-terminal domain (NTD) and a C-terminal domain (CTD), which are called receptor binding domains (RBD) due to their receptor-binding properties [25]. SARS-CoV-2 uses the S1 CTD to bind to hACE2 in order to enter target cells and there is evidence of a specific region in ACE2 which is recognized by the virus’s spike (S) glycoprotein [25].

Following the virus’s entry into the cell through receptor binding and fusion of the viral envelope with the cell membrane, the incoming viral genome is translated to produce a polyprotein precursor. Subsequently, this large polyprotein is cleaved by proteases to release RNA-dependent RNA polymerase (RdRp). The RdRp is integrated into a membrane-associated viral enzyme complex which guides negative-strand RNA (−RNA) production resulting in intracellular viral replication. At the next step of this process, the newly-produced viral copies (virions) are released through exocytosis damaging the infected cell and potentially invading adjacent cells [28,29]. SARS-CoV-2 can infect kidney cells, liver cells, intestinal cells, T lymphocytes, and lung cells causing main symptoms and signs [25].


The entry of the virus into the host cell is accompanied by a rapid response of the innate and adaptive immune system characterized by the release of proinflammatory cytokines and the activation of CD4 and CD8+ T cells [12, 29]. Innate immune response is mediated by antigen presentation to dendritic cells, macrophage maturation and the subsequent activation of the type I IFN pathway. SARS-CoV-2 N (nucleocapsid) protein interferes with IFN signaling and synthesis [28]. In this way, the innate immune system plays a key part in controlling viral replication and promoting adaptive immune response, which is initiated by T cells proliferation and a further cascade of cytokine production including IL‐1, IL‐6, IL‐8, IL‐21 and tumor necrosis factor β (TNF‐β). CD4+ and CD8+ T cells play a significant antiviral role by balancing the fight against the virus and the risk of developing autoimmunity or overwhelming inflammation. CD4+ T cells promote the production of virus‐specific antibodies by activating T‐dependent B cells. CD8+ T cells eliminate virus-infected cells and secrete cytokines such as TNF-α and IFN-γ which induce protective immunity against intracellular micro-organisms. In addition, NK cells are recruited in in the host’s defense against the virus. They recognize infected cells in an antigen-independent manner, exert cytotoxic activities and rapidly produce large amounts of IFN-γ [28,29].

Clinical manifestations

Spectrum of illness

Incubation time ranges between 2-14 days and is divided into two stages. The first stage is characterized by non-specific symptoms, fever, headache, myalgia and to a lesser extent diarrhea. The second stage includes the respiratory phase of the disease and occurs after the seventh day with productive cough, dyspnea and chest pain [30-33]. It may progress into acute respiratory distress that requires intubation and mechanical ventilation [34,35]. In this phase, jaundice is high and there may be multi-organ involvement [35]. There is an increase in inflammatory markers, including CRP and ferritin. Procalcitonin is usually not elevated, unless there is a bacterial co-infection. CRP levels have prognostic value [34,36,37]. In severely ill patients, particularly those with strong inflammatory reactions, cytokine storm may contribute to multiorgan failure and eventually death [32].

It is emphasized that due to the unpredictability of the disease’s clinical course, treatment is needed in the early stages [33].  Corticosteroids were used both in SARS and MERS cases [14,15] but initial results regarding corticosteroid treatment of COVID-19 were rather disappointing and other solutions are being investigated, such as IL-6 inhibitors or anti-TNF agents. Colchicine is presently used in patients with a history of heart disease [28]. It has been noted that the virus shows tropism for the myocardium, causing myocarditis. Initial troponin measurement is mandatory and increased levels also constitute an adverse prognostic factor [36].

Symptoms and signs

SARS-CoV-2 causes mild influenza-like symptomatology with nasal congestion, sore throat, cough and fever, but it may progress into severe pneumonia, ARDS, sepsis or septic shock, requiring hospitalization in intensive care units (ICUs), with a fatal outcome in 2.9 % of laboratory confirmed cases [33].  Huang et al (2020) reported that the most common clinical finding was fever (98%), followed by cough (76%) and myalgia / fatigue (44%) [33]. Headache, sputum production, and diarrhea were less common. In many cases in Europe, acutely emerged anosmia and taste disturbance were reported as early symptoms [38]. Leukopenia and lymphopenia were common in the early stages affecting almost 66% of patients [31,32,36,37]. According to WHO situation report on February 12th 2020, among 44,730 confirmed cases in Chine, 8,204 (18%) cases were recorded as severe infections [39]. People with chronic illnesses, including cardiovascular disorders, diabetes, liver disorders, respiratory diseases, cancer and the elderly appear more prone to serious illness [31,34,36]. Children are usually asymptomatic or have mild symptoms but co-infection with bacterial pneumonia is common. Children with comorbidities are more vulnerable [40].

Risk Factors

Mortality risk factors have not been well described. In-hospital death risk can be predicted by older age, higher Sequential Organ Failure Assessment (SOFA) score, higher breathing rate, elevated lymphocyte count, creatinine, lactate dehydrogenase, creatine kinase, elevated d-dimer, high-sensitive cardiac troponin I, serum ferritin and interleukin-6 (IL-6) [34,36]. Sepsis was a common complication, which might be causally related to COVID19, but further research is needed to clarify its pathogenesis [34]. Cardiac complications, including arrhythmia, myocardial infarction or heart failure are frequently encountered in patients suffering from pneumonia [34]. 28-day mortality in septic patients is strongly associated with high d-dimer levels through systemic pro-inflammatory cytokine responses which mediate local inflammation and plaque rupture, induction of procoagulant factors, and haemodynamic alterations further contributing to ischemia and thrombosis [37].

Infections with the pre-existing coronaviruses have been shown to be linked to severe complications during pregnancy. Given that SARS-CoV2 has the potential for similar behavior, systemic screening for any suspected infection during pregnancy is recommended [33,34]. At present, there are no conclusive findings regarding the risk of vertical mother-baby transmission. Limited data suggest that there is not an increased risk of intrauterine infection in women who were infected during late pregnancy. In addition, there are no sufficient data on the perinatal outcome when women are infected during the first or second trimester, however these pregnancies should be closely monitored [41].

Diagnostic tools

Diagnostic tests are powerful tools to combat COVID-19 and include molecular methods, serology and viral culture. There are two types of SARS-CoV-2 tests: those that detect the virus and those that detect the host’s response to the virus. Molecular methods including RT-PCR (reverse transcription) or real-time PCR, which use RNA from respiratory samples such as oropharyngeal swabs, sputum, nasopharyngeal aspirate, deep tracheal aspirate, or bronchoalveolar lavage, constitute the most common diagnostic methods [42]. Serological assays can also be useful, but they do not address the same questions [43,44]. The sensitivity of antibody detection is generally lower compared to that of molecular methods and is mostly used in retrospective diagnosis. Serological testing may help identify patients who are asymptomatic or immunized to SARS-CoV-2.

PCR seems to have a sensitivity of ~75% [45]. Sensitivity is even lower if the sample is derived from the upper respiratory tract, or it is obtained relatively early in the course of the disease and a negative result does not preclude infection. When there is strong clinical suspicion of serious illness, repetition of diagnostic testing using samples from the lower respiratory tract is strongly recommended. In addition, in cases of high clinical suspicion, the detection of another pathogenic microorganism does not exclude the presence of the new virus, as data on the role of coinfection have so far been limited [43]. If RT-PCR is negative but there is a high clinical suspicion of COVID-19, it is recommended that the individual remains isolated testing should be repeated at a later time. Specificity seems to be high (although contamination can cause false-positive results) [45].

One question that arises in the case of patients with positive CT scan and negative RT-PCR, is which of these diagnostic tools is more sensitive for early diagnosis. PCR sensitivity is around 75% [45] due to difficulties in sampling and other technical issues. CT scan appears to show earlier lesions specific to COVID-19, namely bilateral ground glass lung opacities [43,45]. It is preferable, in order to have patients detected and quarantined as early as possible, to perform CT scan to confirm cases of COVID-19, in spite of a negative PCR [45].

Treatment and  protection

There is currently no specific treatment or effective preventive measure for COVID-19. Numerous antiviral agents, immunotherapies and vaccines are being researched and developed as potential therapies. Finding effective treatments for COVID-19 infection is a complex process


There is currently no vaccine to prevent COVID-19 infection. Vaccines studies are conducted worldwide but it is estimated that a clinically useful product will not be available before 2021 [46]. Wide-range collaboration between scientists from multiple disciplines and policy makers will enhance and even accelerate vaccine development and testing. Furthermore, social and ethical issues associated with COVID-19 vaccine distribution should be carefully addressed in order to implement a global and successful disease prevention strategy.

Development of a COVID-19 vaccine will not only have protective implications in the present day, but also advance preparedness for future coronavirus outbreaks.


No specific antiviral treatment is recommended for the 2019-nCoV infection [47]. Patients should receive supportive care to help relieve symptoms. Vital organs’ function should be supported in severe cases. [47]. A large number of researchers and clinicians worldwide are currently focusing on finding a treatment for COVID-19 [48]. There are almost 60 clinical trials around the world regarding effective treatment. Most of them focus on existing drugs which are known to be safe for human use and need to be tested for effectiveness against the SARS-CoV-2 virus [48].

Antiviral Agents

Favipiravir has been approved in Japan and China for influenza and is currently under testing for potential use in COVID-19. Preliminary results of antiviral effect on COVID-19 are satisfactory [47]. Remdesivir (GS-5734) is another broad-spectrum antiviral agent. This drug, which appeared rather ineffective in Ebola infection, appears to be effective in treating COVID-19 [47,48]. To this end, 5 clinical trials are currently underway in China and the US. Remdesivir is a nucleotide analog pre-drug which interrupts the replication of the SARS-CoV-2 virus without damaging the human cell, so it has a targeted effect. Positive results have been reported. Prophylactic and therapeutic remdesivir treatment improved pulmonary function and reduced viral loads and lung histopathological lesions in experimental models. Clinical trials with remdesivir are ongoing, but so far it is the only antiviral agent that according to WHO may display real efficacy. Other antivirals being tested against COVID-19 are arbidol, darunavir and various protease-inhibitor combinations in trials in China and Thailand [47,48]. The WHO has just launched the SOLIDARITY trial, a randomized, multicenter trial of antiviral medications, currently involving 45 countries [49].

Recently, anti-malaria drugs have received attention as potential COVID-19 treatments. Chloroquine and hydroxychloroquine are substances that have been officially approved for the treatment of malaria, systemic lupus erythematosus and rheumatoid arthritis. It appears, from the results of clinical trials, that they may be effective in COVID-19 [47,48]. In France and other countries, an experimental protocol of a hydroxychloroquine and azithromycin combination has been used for potential prophylaxis or treatment for COVID-19 [50,51]. At 6 days, among patients given combination therapy, the percentage of cases still carrying SARS-CoV-2 was no more than 5%. Azithromycin was added due to its effectiveness against bacterial pneumonia but also because it has been shown to be effective in vitro against a large number of viruses. Chloroquine and hydroxychloroquine help to neutralize acids, making the environment less friendly for the virus. Another possibility is that these drugs have subtle effects on a wide variety of immune cells. Hydroxychloroquine was found to be more potent than chloroquine in vitro. Hydroxychloroquine’s therapeutic effect is evident in relatively low doses and the authors recommend a loading dose of 400 mg PO BID, followed by 200 mg BID for 4 days. In this dosage, hydroxychloroquine reduced viral load, symptoms duration and severe cardiac or psychiatric side effects, pain or fever were less common [50]. The main complication (retinal toxicity) is rare and is evident after at least 5 years of continuous use. Both hydroxychloroquine and azithromycin are listed as definite causes of torsade de pointes (TdP) and for this reason there are specific recommendations regarding their use. These include monitoring cardiac rhythm and QT interval, sustaining potassium levels above 4 mEq/L and magnesium levels above 2 mg/dL and avoiding other QTc-prolonging agents when possible. In addition, these drugs are contraindicated in patients with baseline QT prolongation (e.g., QTc of at least 500 msec) or with congenital long QT syndrome [47,50,51].


Immunomodulators and other investigational drugs

Researchers are investigating treatment agents that boost the immune system to fight the virus [47-49]. Drugs like interferons have already been used to treat COVID-19 cases in China, but their effectiveness as monotherapy has not been established. Interferons combined with other drugs could be more effective [49]. Therapeutic antibodies can be administered to patients and help their immune system counteract right away. A set of premade antibodies can be used prophylactically to prevent infection as well as therapeutically to treat the disease [47,48]. Recently scientists have worked to develop a convalescent serum therapy to treat COVID-19 using blood plasma from recovered patients. Convalescent plasma antibody-rich products are collected from recovered COVID-19 patients. Cellular therapy, using mesenchymal stem cells, has been shown to reduce inflammation and trigger tissue regeneration and is being evaluated in patients with acute respiratory distress syndrome (ARDS). There are ongoing clinical trials is to determine the safety and efficacy of mesenchymal stem cells (MSCs) therapy for severe COVID-19 [52]. As COVID-19 can lead to overreaction of the immune system and activation of the inflammation cascade known as cytokine storm leading to detrimental effects, immunosuppressive agents are tested [28,47]. By reducing the excessive inflammatory reaction, it is hoped that the body’s immune system will be able to fight the coronavirus, and prevent the complications of pneumonia, organ failure and death.

IL-6 inhibitors

IL-6 inhibitors may prevent severe pulmonary damage caused by cytokine release in COVID-19 patients. Several studies have indicated that clinical worsening is attributed to a “cytokine storm” with release of IL-6, IL-1, IL-12, and IL-18, along with TNF-α and other inflammatory mediators. The increased pulmonary inflammatory response may result to increased alveolar-capillary gas exchange, making oxygenation difficult for patients with severe illness [28,29].

Tocilizumab, an IL-6 inhibitor, is currently used in the treatment of rheumatoid arthritis. Patients with severe COVID-19 received a single intravenous dose of 400mg tocilizumab with satisfying results. In general, patients improved with lower oxygen requirements, lymphocyte counts returned to normal, and they were discharged with a mean hospitalization duration of 15.5 days [47,53].

On March 16, 2020, the initiation of a phase 2/3 trial of the IL-6 inhibitor sarilumab was announced [53]. The ODYSSEY study is another clinical trial focusing on the efficacy and safety of tradipitant (85 mg PO BID) in cases of lung injury associated with severe COVID-19 infection. Tradipitant is a neurokinin-1 (NK-1) receptor antagonist. Substance P binds to the NK-1 receptor and triggers neuroinflammatory processes which lead to severe lung injury [54].

Rintatolimod is a toll-like receptor 3 (TLR-3) agonist which has been used in chronic fatigue syndrome, HIV and influenza. It is currently evaluated as a potential treatment for COVID-19 by the National Institute of Infectious Diseases (NIID) in Japan and the University of Tokyo [55]. Recently, colchicine has been authorized to enter clinical trials to determine whether short-term treatment reduces mortality and lung complications related to COVID-19 in heart disease patients. Colchicine is an anti-inflammatory agent used to treat gout, Behcet’s syndrome and Familial Mediterranean Fever. In addition, it is regularly prescribed as a short-term treatment of pericarditis. It is supported that colchicine may moderate the overproduction of immune cells and their activating compounds thus reducing the likelihood of heart complications such as myocardial injury observed in COVID-19 patients [24].

WHO has proposed a therapeutic algorithm for COVID-19 in February 2020, however, due to the constantly growing research on this new infection, WHO’s guidelines are frequently updated [48].

Transmission routes  

The virus is transmitted mainly through respiratory droplets produced during coughing or sneezing or by direct contact with infected hands, surfaces or objects. Airborne spread is not considered a major transmission route except during certain aerosol-generating procedures which are exclusively conducted in health-care facilities. Fecal shedding has been demonstrated from some patients, and viable virus has been detected in feces in a few case reports. Nevertheless, the fecal-oral route does not appear to be a major cause of COVID-19 transmission; its role and significance for COVID-19 spread remains to be determined [56,57].

Incubation time is usually 5-6 days, although it can range from 2 to 14 days [30-33]. For this reason, people who may have contacted a confirmed case are asked to limit themselves for a period of 14 days [32]. Most cases of COVID-19 appear to be spread by people with symptoms. A small number of people may be infected before their symptoms have been developed [57,58]. The virus can remain in the air for 30’ to 3 hours. It can survive for 24 hours on cardboard, for 2 days on metals, and has a longer survival time on plastic (at least 3 days) [59]. According to recent research, the novel coronavirus was most stable on plastic and stainless steel, with some virus remaining viable up to 72 hours [59].  Coronaviruses have the potential to contaminate cutlery, plates or other surfaces, through sneezing or coughing, and can survive on these surfaces for some time. An epidermal infection could theoretically be possible if the virus is transmitted by cutlery or hands to the mucosa of the mouth, throat or eyes. However, no contamination with SARS-CoV-2 has been proven through this transmission pathway [56,57].

Are there any measures to prevent its transmission?

Like all encapsulated viruses in which the genetic material is coated with a layer of fat, coronaviruses are susceptible to fat-soluble substances, [59] such as alcohol or surfactants, contained in soaps and dish detergents [2]. These substances are thought to damage the surface of the virus thus rendering it inactive. This is especially true if dishes are washed and dried in a dishwasher at 60oC or higher. Antiseptic alcoholic solutions neutralize the new coronavirus. Personal hygiene measures are therefore very important: good hand washing, with soap and water, for at least 20 seconds, according to the WHO guidelines. Good hygiene practice and social distancing remain the best means to prevent viral spread. [59].

Instructions for health professionals

Prior to patients’ arrival [59]

Screen all patients for new respiratory infection symptoms before non-urgent care or elective visits. Ask about cough, shortness of breath, and fever. Explore alternatives to face-to-face triage and visits to reduce risk of transmission and spare personal protective equipment (PPE) supplies. Consider limiting facility points of entry and establishing triage stations outside the facility to screen patients before entering. Ensure rapid and safe triage of patients with symptoms of suspected COVID-19. Display signs on all entrances about COVID-19 symptoms. Ask symptomatic patients to inform triage personnel of symptoms upon arrival. Provide them with respiratory hygiene supplies, including masks, hand sanitizers, and tissues. Consider installing a barrier, such as a glass or plastic window, to limit contact between triage personnel and patients. Isolate symptomatic patients in an examination room as soon as possible. If not available, identify a separate, well-ventilated place where patients can be separated by 6 feet. Provide easy access to hygiene supplies.

During patients visit

Reserve airborne infection isolation rooms (AIIR) for aerosol-generating procedures. Healthcare facilities should provide healthcare workers with respirators during aerosol-generating procedures performed on suspected or confirmed COVID-19 patients [59]. Use PPE, according to guidance from your facility. This includes clean, non-sterile gloves, gowns and eye protection, like goggles or eye shields. If there are shortages, the existing equipment should be reserved for aerosol-generating procedures and close-contact care or anticipated splashes or sprays. Recruit specific staff to care exclusively for patients with suspected or confirmed COVID-19. Limit personnel in patient rooms to essential staff, and limit aimless patients’ wandering. Basic precautions must be applied systematically and in all cases. Additional precautions for contact and droplets should be applied as long as the patient is symptomatic [59].

Conflict of Interest disclosure

None to declare

Declaration of funding sources

None to declare

Author contributions: Mary Stathopoulou was responsible for literature search and collection of data; Mary Stathopoulou and Ioulia Sirokosta were responsible for drafting the manuscript and interpreting the data; Mary Stathopoulou and Ioulia Sirokosta approved the submitted version of the manuscript.


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