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Human Respiratory Viruses: 'New Kids on the Block' Human Respiratory Viruses: ‘new kids on the block’ Ab Osterhaus DVM PhD Director Research Center for Emerging Infections and Zoonoses (RIZ) University of Veterinary Medicine Hannover Chair One Health Platform Chair ESWI 10th GVN network meeting Fondation Merieux, les Pensieres November 2018 03.12.2018 1 1980 1990 2000 2010 Past decades: zoonoses at the origin of major human disease outbreaks Reperant LA, Cornaglia G, Osterhaus AD Curr Top Microbiol Immunol.2013 The importance of understanding the human-animal interface: from early hominins to global citizens <100% Identification of viral pathogens based on surveillance activities: ErasmusMC / RIZ TiHo 1995 CDV as the cause of mass mortality in Serengeti lions 1996 -herpesvirus in seals (phocid herpesvirus-2) novel molecular techniques 1997 monk seal morbilliviruses (MSMV-WA/G) 1997 influenza A (H5N1) virus in humans 1998 lentivirus from Talapoin monkeys (SIVtal) 1999 influenza B virus in seals 2000 human metapneumovirus (hMPV) 2002 re-emerging PDV in Europe Funding: 2003 SARS CoV cause of SARS in humans (Koch`s postulates) EU: EMPERIE; ANTIGONE; 2003 influenza A (H7N7) virus in humans PREPARE; COMPARE… 2004 fourth human coronavirus (CoV NL63) NL: VIRGO-FES… 2005 H16 influenza A viruses (new HA!) in black headed gulls 2008 dolphin herpesvirus DFG: N-RENNT; VIPER 2009 deer astrovirus 2010 human astrovirus, human picobirnavirus 2011 ferret coronavirus, ferret HEV, porcine picobirnavirus, stone marten anellovirus. influenza A (H1N1) virus in dogs 2012 human calicivirus, MERS CoV, boa arenaviruses 2013 seal parvovirus, seal anelloviruses, deer papillomavirus, fox hepevirus, fox parvovirus, turtle herpesvirus 2014 canine bocavirus, porcine bocavirus, python nidovirus, camel circovirus, phocid herpes virus-7 2015 influenza A (H10N7) virus seals 2017… morbillivirus fin whale, hepadnavirus Tinamou, rec.canine circovirus, rec.canine bocavirus, herpesvirus sperm whale, Batai virus seal, avian metapneumovirus, novel pestivirus… XXX human respiratory 03.12.2018 4 Parvoviruses: wide spectrum of disease in humans and animals alike Asymptomatic Brain involvement Erythema infectiosum (Human B19) Anemia Immune disorders (Human B19, (Aleutian mink disease, Human B19) non-human primate erythroviruses) Hepatitis, myocarditis Respiratory disease (Canine parvovirus, Goose (Human bocavirus, parvovirus, B19) Canine bocavirus) Fetal hydrops Gastro-enteritis (Human B19, Porcine parvoviruses) (Canine parvovirus, Human bocavirus, Bufavirus) Virus discovery in pigs, dogs and seals with ENCEPHALITIS (comparative virology) Novel (recombinant) canine bocaviruses Novel porcine bocavirus novel seal parvovirus Bodewes et al., PLoS One 2013 / 2014; Vet Microbiol.2014 Piewbang et al., Vet Pathol. 2018 Moesker F. et al., Clin Microbiol Infect 2016 Rinderpest eradication: lessons for measles eradication? de Swart RL, Duprex WP, Osterhaus AD. Curr Opin Virol. 2012 Morbillivirus PDV RPV TuV CDV Henipahvirus MV hPIV3 HeV bPIV3 Respirovirus Paramyxovirinae NiV SeV hPIV1 Pneumovirinae hRSV NDV Avulavirus bRSV LPMV Metapneumovirinae MuV Rubulavirus APV hPIV2 SV5 SV41 HMPV Jo Lei W. et al., Thesis & Curr.Opin.Virol. 2018 Morbilliviruses crossing species barriers a pandemic risk after measles eradication? PDV: European Harbour seals CDV: Baikal seals CDV: Caspian seals Nature 1988 / Science 2002 Nature 1988 EID 2000 DMV: CDV: Serengeti lions Med. monk seals Vaccine 1994 DMV: Nature 1997 CDV: Fin Whale Denmark Should we continue Rhesus macaques JWD 2016 measles vaccination for ever? China, EID 2011 CD150 is the primary morbillivirus MV is predominately lymphotropicentry in vivoreceptor de Vries RD, et al., PLoS Pathog. 2012 spleen 03.12.2018 11 PVRL4 is the morbillivirus receptor infection with rMVonKSEGFP(3): epithelial buccal cells mucosa and tongue de Vries RD, et al., PLoS Pathog. 2012 Inner cheek DAPI/CYK/EGFP Koplik spot EGFP 03.12.2018 12 RESEARCH ◥ We propose that, if loss of acquired immuno- REPORT logical memoryafter measlesexists,theresulting impaired host resistance should be detectable in theepidemiological datacollected during periods VACCINES when measles wascommon and [in contrast to previousinvestigationsthat focuson low-resource settings(5–12)] shouldbeapparent in high-resource Long-term measles-induced settings where mortality from opportunistic in- fections during acute measles immune suppres- sion waslow. Relatively few countries report the immunomodulation increases overall necessar y parallel measl es and mortality timese- ries to test this hypothesis. National-level data childhood infectious diseasemortality from England, Wales, the United States, and Denmark [Fig. 1, A to C; see supplementary F1 M ichael J. M ina,1,2* C. Jessica E. M etcalf,1,3 Rik L. de Swart,4 materials (SM) 1 for details], spanning the dec- A. D. M. E. Osterhaus,4 Bryan T. Grenfell 1,3 ades surrounding theintroduction of massmea- sl esvaccination campaigns,meet our datacriteria. Immunosuppression after measles is known to predispose people to opportunistic Toassesstheunderlyingimmunological hypo- infections for a period of several weeks to months. Using population-level data, we show thesis (Fig. 1D) using population-level data, we that measles has a more prolonged effect on host resistance, extending over 2 to 3 years. required that first, nonmeasles mortality should We find that nonmeasles infectious disease mortality in high-income countries is tightly be correlated with measles incidence data, espe- coupled to measles incidence at this lag, in both the pre- and post-vaccine eras. We cially because the onset of vaccination reduces conclude that long-term immunologic sequelae of measles drive interannual fluctuations in thelat ter.Second,an immunememorylossmecha- nonmeasles deaths. This is consistent with recent experimental work that attributes the nism should present as a strengthening of this immunosuppressive effects of measles to depletion of B and T lymphocytes. Our data association when measlesincidencedataaretrans- provide an explanation for the long-term benefits of measles vaccination in preventing formed to reflect an accumulation of previous all-cause infectious disease. By preventing measles-associated immune memory loss, measlescases(a measles“shadow”). For example, vaccination protects polymicrobial herd immunity. if immunememory loss(or morebroadly, immu- nomodulation) lasts 3 years, the total number easlesvaccines wereintroduced 50 years Pr oposed mechanisms for a nonspecific bene- of immunomodulated individuals (S)inthe nth agoand werefollowed by strikingreduc- fici al effect of measles vaccination range from quarter can becalculated asthesum of themea- tions in child morbidity and mortal ity suggestionsthat livevaccinesmaydirectlystimu- sles cases (M) over the previous (and current) (1,2). Measlescontrol isnow recognized late cross-reactive T cell responses or that they 12 quar ters: Sn = Mn–11 + Mn–10 + …+ Mn–1+ Mn. as oneof themost successful publichealth may train innate immunity to take on memory- In practice, we weighted the quarters using a Minterventions ever undertaken (3). Despite this, likephenotypes (13,18 –21). Although well described gamma function. Dividing Sby the total popula- in many countries vaccination targets remain by Aaby (11, 12)and others (22) in observational tion of interest thus provides the prevalence of unmet, and measles continues to take hundreds studies, primarily in low-resource settings, these immunomodulation (seeSM 2,fig. S1,and movie of thousands of lives each year (3). Even where effects may not fully explain the long-term ben- S1 for detailed methods). Third, the strength of control has been successful, vaccine hesitancy efitsobserved with measlesvaccination and can- thisassociation should begreatest when themean threatens the gains that have been made (1, 4). not explain the pre-vaccination associ ations of duration over which the cases are accumulated The introduction of mass measles vaccination measles and mortality we describe below. The matches the mean duration required to restore has reduced childhood mortality by 30 to 50% World Health Organization (WHO) recently ad- immunological memoryafter MVinfection.Fourth, in resource-poor countries (5–8) and by up to dressed this issue (22)and concluded that mea- theestimated duration should be consistent both 90%in themost impoverished populations(9,10 ). slesvaccination isassociated with lar gereduct ions with the available evidence of increased risk of Theobserved benefitscannot be explained by the in all-causechildhood mortality but that thereis mortality after MV, compared with uninfected prevention of primary measles virus (MV) infec- no firm evidence to explain an immunological children, and with the time required to build a tionsalone(11,12), and they remain acentral mys- mechanism for the nonspecific vaccine benefits. protectiveimmunerepertoirein earlylife(Fig.1D, tery (13 ). Recent work (17, 23)invoked a different hypo- fig. S2, and SM). MV infection is typified by a profound, but thesisthat alossof immunememorycellsafter MV To explicitly address whether the observed generally assumed to be transient, immunosup- infection resets previously acquired immunity, nonspecific benefits of vaccination can be attri- pression that renders hosts more susceptible to and vaccination preventsthiseffect .deVrieset al. buted to the prevention of MV immunomodula- other pathogens(14 –17). Thus, contemporaneous (17)reproduced transient measles immune sup- tion, evidence for the four hypotheses must be reductions in nonmeasl
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