Vomiting is a common—perhaps the defining—feature of norovirus gastroenteritis. Indeed, the syndrome was once known as ‘‘winter vomiting disease.’’ Vomiting often occurs with no prodromic forewarning; thus, public vomiting appears to be the spark that starts the rapid spread of many outbreaks. Both classic outbreak investigations [1] and sophisticated modeling studies [2] have demonstrated the role of vomiting in direct transmission. This suggests a role for vomitus-oral transmission through droplets, more frequently associated with transmission of respiratory pathogens. Cases occurring through this mode of transmission occur within 1 incubation period (,48 hours for norovirus) from the time of the vomiting incident. In addition, after being aerosolized by vomiting, norovirus settles on surfaces and may persist and remain infectious, from which cases may occur days or even weeks later. After a public vomiting incident aboard a long haul flight on a Boeing 777-200, 27 flight attendants who worked on the aircraft on 8 flight sectors over 6 days suffered symptoms of gastroenteritis consistent with norovirus infection [3]. The evidence that these illnesses were a result of a common exposure to norovirus is circumstantial, but compelling nonetheless. Aside from the crew on the first flight sector on which the vomiting incident occurred, there was no apparent opportunity for direct transmission from symptomatic crew to each other. No flight attendants worked on the aircraft while ill or within 48 hours after they recovered. Although both preand postsymptomatic transmission of norovirus have been documented in other studies [4], this is not likely to have played a major role in this situation. Two flight attendants from different sectors had laboratory-confirmed infections with the rare genogroup 1 genotype 6 (G1.6) norovirus. The chances that both individuals were infected with this particular norovirus strain and were not part of the same chain of transmission are improbably small. The longstanding norovirus sequence database of the viruses causing outbreaks in New Zealand and worldwide [5] was crucial to making this molecular epidemiological inference. One particularly revealing observation was the dose-response relationship between norovirus exposure and the risk of developing disease. Attack rates among flight attendants decreased as exposure became more distant in time from the vomiting incident. This indeed may be a good proxy for the exposure dose. At the time of shedding, through vomitus in this case, most particles are likely to be infectious. In circumstances in which infectious particles still suspended in air can be inhaled and ingested, norovirus spreads very rapidly [6], which probably happened on the first flight sector, from which the attack rate among flight attendants was phenomenally high (90%). However, when the virus has to pass through the environment, transmission may not be as efficient. After landing on a surface, some of the infectious virus particles are lost for transmission, because they are on locations that cannot be touched or wiped off or because they are irreversibly attached. Surface-attached virus dies at a certain rate because of drying, exposure to sunlight, or other conditions adverse for the virus. Any virus particle that is picked up by humans touching contaminated surfaces can only cause infection when it is ingested [7]. This process likely explains why attack rates in the second 2-flight sector remained high (78%; 7 cases) and subsequently decreased over the next 6 sectors (#3 cases per sector). This complex process is what underlies Thornley et al’s Received 6 June 2011; accepted 10 June 2011. Correspondence: Ben Lopman, MSc, PhD, Centers for Disease Control and Prevention, 1600 Clifton Rd MS-G04, Atlanta, GA 30333 (blopman@cdc.gov). Clinical Infectious Diseases The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com. 1058-4838/2011/536-0004$14.00 DOI: 10.1093/cid/cir486