• Alma mater Utrecht University

• Scientific career

• Institutions

• National Institute for Public Health and the Environment

• Erasmus MC

• Thesis : Diagnosis and epidemiology of torovirus infections in cattle (1990)

Maria Petronella Gerarda Koopmans^[1] (born 21 September 1956) is a Dutch virologist who is Head of the Erasmus MC Department of Viroscience. Her research considers emerging infectious diseases, noroviruses and veterinary medicine. In 2018 she was awarded the Netherlands Organisation for Scientific Research (NWO) Stevin Prize. She serves on the scientific advisory group of the World Health Organization.

Early life and education

Koopmans studied veterinary medicine at Utrecht University.^[2] She graduated from her Master's degree 1976, and remained there for her doctoral research. She earned two graduate degrees in veterinary medicine, and was officially registered as a veterinary microbiologist in 1977. She became increasingly interested in virology, and moved to the United States to specialise in viruses that can be transmitted between animals and humans.^[3] From 1991 to 1994 Koopmans completed a fellowship at the Centers for Disease Control and Prevention, where she studied enteric viruses.^[2] She joined the Virology Division, where she focussed on torovirus in cattle.

Research and career

Koopmans joined the National Institute for Public Health and the Environment (RIVM), where she was appointed Chief of Virology. She was involved with restructuring the department, and translating their research out of the laboratory and into practical applications for the control of infectious diseases. In 2006 she was appointed as Professor of Public Health at the Erasmus MC hospital in Rotterdam, which allowed her to strengthen the evidence-base of infectious disease research. Her laboratory makes use of basic scientific studies and epidemiology to understand the pathogenesis of infectious diseases, to establish their transmission routes and to translate this research base into diagnostic tools.

In 2003, when Influenza A virus subtype H7N7 spread around the Netherlands, Koopmans experienced her first infectious diseases outbreak. She was involved with the development of a coordinated public response, working with veterinarians and physicians to quickly develop public health policy. Her experiences in leading the response to the avian influenza outbreak prepared her for subsequent epidemics, including Middle East respiratory syndrome (MERS) and Zika virus. She was on the team that found, in 2013, that dromedary camels were an intermediate host for the virus that causes MERS.^[4] She has since worked with Elmoubasher Farag to test camels for antibodies against MERS.^[5]

During the Ebola outbreak in West Africa, Koopmans was responsible for the deployment of mobile laboratories in Sierra Leone and Liberia. Her Erasmus MC team trained volunteers to run testing and treatment programmes.^[6] Koopmans is a member of the scientific advisory group (SAG) of the World Health Organization's R&D Blueprint project.^[7] The project looks to understand what has gone wrong with epidemic and pandemic responses, and looks to build global disease preparedness.^[7] As part of this effort, Koopmans analysed the public health response to the Zika virus. She identified three significant bottlenecks to an efficient response; including delays in regulatory approvals, challenges in the logistics of laboratory support and the absence of a structured timeline for funding.^[8] Koopmans also leads the World Health Organization centre for Emerging Viral Diseases.^[9] She is the scientific coordinator of COMPARE, a Horizon 2020 project that looks to develop next generation sequencing techniques for outbreak identification and mapping.^[10] COMPARE look to contain and mitigate foodborne illnesses.^[10]

In 2018 Koopmans was honoured by the Netherlands Organisation for Scientific Research (NWO) for her work on the transfer of viruses from animals to humans.^[11] In 2019 she was awarded a $9 million NWO grant to establish a consortium, the Versatile Emerging infectious disease Observatory (VEO), that will study how changes in environment and travel will impact the risk of infectious diseases.^[12][13] The diseases considered by VEO include vector-borne and zoonotic diseases, as well as hidden pathogens.^[14] Koopmans wrote an article for Nature in which she called for a transformation in epidemic preparedness and response.^[15] In the article, she quoted the World Health Organization's leader on health emergencies, “We are entering a very new phase of high-impact epidemics… This is a new normal,”.^[16] In 2019 Koopmans was elected member of the Royal Netherlands Academy of Arts and Sciences.^[17]

From the start of 2020, Koopmans worked to understand SARS-CoV-2 and the spread of coronavirus disease.^[3][18][19] In the Netherlands, Koopmans made an effort to test healthcare workers, and identified that there were large numbers of asymptomatic carriers amongst the dutch population.^[20] With her team at the Erasmus MC, Koopmans looked to understand the efficacy of antibody tests.^[21][22] Alongside leading the scientific response, Koopmans was also involved with scientific communication about the virus, making use of social media and media interviews to share up-to-date research with the public.^[23][24] Koopmans said that as humans occupied more of planet earth, the number of dangerous diseases transmitted from animals to humans would increase.^[25] She was appointed to the coronavirus disease advisory panel of the European Commission.^[25] The panel served to develop public health recommendations to the member states during the pandemic.^[25]

On 02 December 2020, Koopmans was appointed to the 13 member team of the World Health Organization's investigation into the origins of COVID-19.^[26]

Awards and honours

• 2004 Dutch Association for Infectious Diseases WRO Goslings Prize ^[27]

• 2017 Technical University of Denmark Honorary Doctorate Honorary Doctor ^[28]

• 2018 Netherlands Organisation for Scientific Research Stevin Prize^[11]

Selected publications

• Fouchier, R.A.M. (Ron) Schneeberger, P.M. (Peter) Rozendaal, F.W. (Frans) Broekman, J.M. (Jan) Kemink, S.A. (Stiena) Munster, V.J. (Vincent) Rimmelzwaan, G.F. (Guus) Schutten, M. (Martin) Doornum, G.J.J. (Gerard) van Koch, G. (Guus) Bosman, A. (Arnold) Koopmans D.V.M., M.P.G. (Marion) Osterhaus, A.D.M.E. (Albert) Kuiken, T. (Thijs) (3 February 2004). "Avian influenza A virus (H7N7) associated with human conjunctivitis and a fatal case of acute respiratory distress syndrome". Proceedings of the National Academy of Sciences of the United States of America. 101 (5): 1356–61. doi:10.1073/pnas.0308352100. OCLC 929966166. PMC 337057. PMID 14745020.

• Newell, Diane G.; Koopmans, Marion; Verhoef, Linda; Duizer, Erwin; Aidara-Kane, Awa; Sprong, Hein; Opsteegh, Marieke; Langelaar, Merel; Threfall, John; Scheutz, Flemming; der Giessen, Joke van (30 May 2010). "Food-borne diseases — The challenges of 20years ago still persist while new ones continue to emerge". International Journal of Food Microbiology. Future Challenges to Microbial Food Safety. 139: S3–S15. doi:10.1016/j.ijfoodmicro.2010.01.021. ISSN 0168-1605. PMC 7132498. PMID 20153070.

• Koopmans, Marion; Duizer, Erwin (1 January 2004). "Foodborne viruses: an emerging problem". International Journal of Food Microbiology. 90 (1): 23–41. doi:10.1016/s0168-1605(03)00169-7. ISSN 0168-1605. PMC 7127053. PMID 14672828.

• "The Novel Coronavirus Outbreak: What We Know and What We Don't". Cell. 180 (6): 1034–1036. 19 March 2020. doi:10.1016/j.cell.2020.02.027. ISSN 0092-8674. PMC 7154513. PMID 32078801.

A novel coronavirus, desygnated as 2019-nCoV, emerged in Wuhan, China, at the end of 2019. As of January 24, 2020, at least 830 cases had been diagnosed in nine countries: China, Thailand, Japan, South Korea, Singapore, Vietnam, Taiwan, Nepal, and the United States. Twentysix fatalities occurred, mainly in patients who had serious underlying illness.1 Although many details of the emergence of this virus — such as its origin and its ability to spread among humans — remain unknown, an increasing number of cases appear to have resulted from human-to-human transmission. Given the severe acute respiratory syndrome coronavirus (SARS-CoV) outbreak in 2002 and the Middle East respiratory syndrome coronavirus (MERS-CoV) outbreak in 2012,2 2019-nCoV is the third coronavirus to emerge in the human population in the past two decades — an emergence that has put global public health institutions on high alert.

China responded quickly by informing the World Health Organization (WHO) of the outbreak and sharing sequence information with the international community after discovery of the causative agent. The WHO responded rapidly by coordinating diagnostics development; issuing guidance on patient monitoring, specimen collection, and treatment; and providing up-to-date information on the outbreak.3 Several countries in the region as well as the United States are screening travelers from Wuhan for fever, aiming to detect 2019-nCoV cases before the virus spreads further. Updates from China, Thailand, Korea, and Japan indicate that the disease associated with 2019-nCoV appears to be relatively mild as compared with SARS and MERS.

After initial reports of a SARS-like virus emerging in Wuhan, it appears that 2019-nCoV may be less pathogenic than MERS-CoV and SARS-CoV (see table). However, the virus’s emergence raises an important question: What is the role of overall pathogenicity in our ability to contain emerging viruses, prevent large-scale spread, and prevent them from causing a pandemic or becoming endemic in the human population? Important questions regarding any emerging virus are, What is the shape of the disease pyramid? What proportion of infected people develop disease? And what proportion of those seek health care? These three questions inform the classic surveillance pyramid (see diagram).4 Emerging coronaviruses es raise an additional question: How widespread is the virus in its reservoir? Currently, epidemiologic data that would allow us to draw this pyramid are largely unavailable (see diagram).

Clearly, efficient human-to-human transmission is a requirement for large-scale spread of this emerging virus. However, the severity of disease is an important indirect factor in a virus’s ability to spread, as well as in our ability to identify those infected and to contain it — a relationship that holds true whether an outbreak results from a single spillover event (SARS-CoV) or from repeated crossing of the species barrier (MERS-CoV).

If infection does not cause serious disease, infected people probably will not end up in health care centers. Instead, they will go to work and travel, thereby potentially spreading the virus to their contacts, possibly even internationally. Whether subclinical or mild disease from 2019-nCoV is also associated with a reduced risk of virus spread remains to be determined.

Much of our thinking regarding the relationship between transmissibility and pathogenicity of respiratory viruses has been influenced by our understanding of influenza A virus: the change in receptor specificity necessary for efficient human-to-human transmission of avian influenza viruses leads to a tropism shift from the lower to the upper respiratory tract, resulting in a lower disease burden. Two primary — and recent — examples are the pandemic H1N1 virus and the avian influenza H7N9 virus. Whereas the pandemic H1N1 virus — binding to receptors in the upper respiratory tract — caused relatively mild disease and became endemic in the population, the H7N9 virus — binding to receptors in the lower respiratory tract — has a case-fatality rate of approximately 40% and has so far resulted in only a few small clusters of human-to-human transmission.

It is tempting to assume that this association would apply to other viruses as well, but such a similarity is not a given: two coronaviruses that use the same receptor (ACE2) — NL63 and SARS-CoV — cause disease of different severity. Whereas NL63 usually causes mild upper respiratory tract disease and is endemic in the human population, SARS-CoV induced severe lower respiratory tract disease with a case-fatality rate of about 11% (see table). SARS-CoV was eventually contained by means of syndromic surveillance, isolation of patients, and quarantine of their contacts. Thus, disease severity is not necessarily linked to transmission efficiency.

Even if a virus causes subclinical or mild disease in general, some people may be more susceptible and end up seeking care. The majority of SARS-CoV and MERSCoV cases were associated with nosocomial transmission in hospitals, 5 resulting at least in part from the use of aerosol-generating procedures in patients with respiratory disease. In particular, nosocomial super-spreader events appear to have driven large outbreaks within and between health care settings. For example, travel from Hong Kong to Toronto by one person with SARS-CoV resulted in 128 SARS cases in a local hospital. Similarly, the introduction of a single patient with MERSCoV from Saudi Arabia into the South Korean health care system resulted in 186 MERS cases.

The substantial involvement of nosocomial transmission in both SARS-CoV and MERS-CoV outbreaks suggests that such transmission is a serious risk with other newly emerging respiratory coronaviruses. In addition to the vulnerability of health care settings to outbreaks of emerging coronaviruses, hospital populations are at significantly increased risk for complications from infection. Age and coexisting conditions (such as diabetes or heart disease) are independent predictors of adverse outcome in SARS-CoV and MERS-CoV. Thus, emergingviruses that may go undetected because of a lack of severe disease in healthy people can pose significant risk to vulnerable populations with underlying medical conditions.

A lack of severe disease manifestations affects our ability to contain the spread of the virus. Identification of chains of transmission and subsequent contact tracing are much more complicated if many infected people remain asymptomatic or mildly symptomatic (assuming that these people are able to transmit the virus). More pathogenic viruses that transmit well between humans can generally be contained effectively through syndromic (fever) surveillance and contact tracing, as exemplified by SARS-CoV and, more recently, Ebola virus. Although containment of the ongoing Ebola virus outbreak in the Democratic Republic of Congo is complicated by violent conflict, all previous outbreaks were contained through identification of cases and tracing of contacts, despite the virus’s efficient person-to-person transmission.

We currently do not know where 2019-nCoV falls on the scale of human-to-human transmissibility. But it is safe to assume that if this virus transmits efficiently, its seemingly lower pathogenicity as compared with SARS, possibly combined with super-spreader events in specific cases, could allow large-scale spread. In this manner, a virus that poses a low health threat on the individual level can pose a high risk on the population level, with the potential to cause disruptions of global public health systems and economic losses. This possibility warrants the current aggressive response aimed at tracing and diagnosing every infected patient and thereby breaking the transmission chain of 2019-nCoV.

Epidemiologic information on the pathogenicity and transmissibility of this virus obtained by means of molecular detection and serosurveillance is needed to fill in the details in the surveillance pyramid and guide the response to this outbreak. Moreover, the propensity of novel coronaviruses to spread in health care centers indicates a need for peripheral health care facilities to be on standby to identify potential cases as well. In addition, increased preparedness is needed at animal markets and other animal facilities, while the possible source of this emerging virus is being investigated. If we are proactive in these ways, perhaps we will never have to discover the true epidemic or pandemic potential of 2019-nCoV.