subjected to many of the same variables (Box 1.12).
Perspectives
A fundamental principle of virology is that for a virus to be maintained in a host population, sufficient quantities of infectious virus particles must be released from one infected host to infect another. This process of serial infection, while simple in principle, is difficult to study in natural systems given the mind-boggling number of host, viral, and environmental variables. Nevertheless, epidemiology, the study of this process, is evolving rapidly as new ways to track and identify infectious agents are developed. To thwart a potential epidemic, viral epidemiologists must master diverse skills. In tracking the origins of infection, epidemiologists must consider simultaneously multiple variables and clues, some of which are false leads. They must understand the dynamics of the animal or human populations at risk and how aspects of behavior, social structure, and environment might influence the potential for infection. Epidemiologists must then integrate these diverse pieces of information. Furthermore, as investigation often begins only after an epidemic is under way and victims have been identified, they must be able to work under great pressure, within a constrained time frame, and often under intense media scrutiny and dangerous work conditions. We are witnessing these pressures and challenges in real time, as epidemiologists struggle to contain the worldwide pandemic caused by the SARS-Coronavirus-2 (Box 1.13). Individuals working in computer science, bioinformatics, frontline health care delivery, public policy, and international medicine also are crucial for successful control of a viral outbreak. Containing an epidemic under diverse, often unknown, pressures is a monumental challenge, especially when no certain therapy exists that can be offered to patients, and when, as Zinsser first surmised in the 1930s, the “enemy” may lurk in a ubiquitous and minuscule organism, such as the mosquito.
DISCUSSION
This moment in time: the SARS-CoV-2 pandemic
It is 5:31 AM on Sunday, March 1, 2020, and 12 hours ago the first death in the United States was confirmed due to the pandemic coronavirus, SARS-CoV-2. Worldwide, tens of thousands are infected and thousands have died, and most believe that we’ve yet to see the peak impact of this pandemic. Beyond the impact of the virus on these lives, the worldwide outbreak is on the front page of every newspaper, facemasks are flying off the shelves, the stock market has plunged (and may continue to do so), a Vice President with no scientific background was appointed head of the United States Task Force, tourist destinations are at record low attendance, schools in China and Japan are closed, and there is even some discussion about cancelling the Olympics, which do not begin until the end of July. Adding to a sense of global anxiety, some individuals are being diagnosed as coronavirus-positive with no recent history of travel to countries severely affected by the outbreak, and no known contact with infected individuals. (Of course, this is to be expected, as asymptomatic individuals can be efficient vectors for transmission). Many professionals are reminding the public that this is a lower respiratory tract infection much like influenza A virus, and underscore that many of the same people who are worried about COVID-19 (the name for the disease caused by SARS-CoV-2) are among those who, paradoxically, do not routinely get their flu shot. Despite such comparisons to influenza A virus, however, there are many things we do not know about this virus and the disease it can cause. For example, there are suggestions that the case fatality ratio is similar to influenza, but data collection varies in reliability, and appears to differ based on region and time of the outbreak (the case fatality rate appears to have been higher earlier in the outbreak than now). Also, although most deaths occur in the elderly or severely immunocompromised (as with flu), some otherwise young and immunocompetent individuals, including the Chinese physician who was among the first to sound the alarm about this virus, are also succumbing. Moreover, while initially it was presumed that infections of humans originated in a fish market in Wuhan, China, there are now doubts that this is true, and while bats are presumed to be the vector for spread to humans, until recently some purported that pangolins—animals resembling scaly anteaters—may be a source of zoonotic transmission. A silver lining is that at least we now know what pangolins are.
At this moment, of course, no one knows what comes next. Like every pandemic that has come before, the number of cases of SARS-CoV-2 infection will eventually abate as individuals develop immunity, prophylactic measures (such as preventative quarantining of people who recently traveled to high risk countries) begin to take effect, and eventually, antivirals and vaccines are developed. But surely the fear, confusion, uncertainty, and conspiracy theories of today must echo what occurred in Philadelphia in the summer of 1793, when people were inexplicably dying on the streets of what we would later learn was yellow fever.
REFERENCES
Books
Crosby AW. 2003. America’s Forgotten Pandemic: the Influenza of 1918, 2nd ed. Cambridge University Press, Cambridge, United Kingdom.
Crosby M 2006. The American Plague: the Untold Story of Yellow Fever, the Epidemic That Shaped Our History. Berkley Books, New York, NY.
Diamond J. 1997. Guns, Germs and Steel: the Fates of Human Societies. W. W. Norton, New York, NY.
Katze MG, Korth MJ, Law GL, Nathanson N. 2016. Viral Pathogenesis, 3rd ed. Academic Press, London, United Kingdom.
Krauss H, Weber A, Appel M, Enders B, Isenberg HD, Schiefer HG, Slenczka W, von Graevenitz A, Zahner H. 2003. Zoonoses: Infectious Diseases Transmissible from Animals to Humans, 3rd ed. ASM Press, Washington, DC.
McNeill WH. 1977. Plagues and Peoples. Anchor Press, Garden City, NY.
Murphy K, Travers P, Walport M. 2008. Janeway’s Immunobiology, 7th ed. Garland Science, New York, NY.
Nash AA, Dalziel RG, Fitzgerald JR. 2015. Mims’ Pathogenesis of Infectious Disease, 6th ed. Academic Press, Orlando, FL.
Notkins AL, Oldstone MBA (ed). 1984. Concepts in Viral Pathogenesis. Springer-Verlag, New York, NY.
Oldstone MBA. 1998. Viruses, Plagues and History. Oxford University Press, New York, NY.
Parham P. 2009. The Immune System, 3rd ed. Garland Science, New York, NY.
Richman DD, Whitley RJ, Hayden FG (ed). 2009. Clinical Virology, 3rd ed. ASM Press, Washington, DC.
Sompayrac L. 2002. How Pathogenic Viruses Work. Jones and Bartlett, Sudbury, MA.
Zinsser H. 1935. Rats, Lice and History. Transaction Publishers, Piscataway, NJ.
Review Articles
Ahmed R, Oldstone MBA, Palese P. 2007. Protective immunity and susceptibility to infectious diseases: lessons from the 1918 influenza pandemic. Nat Immunol 8:1188–1193.
Keesing F, Belden LK, Daszak P, Dobson A, Harvell CD, Holt RD, Hudson P, Jolles A, Jones KE, Mitchell CE, Myers SS, Bogich T, Ostfeld RS. 2010. Impacts of biodiversity on the emergence
