Skip to main content
  • Loading metrics

Henipaviruses—A constant threat to livestock and humans


In this review, we highlight the risk to livestock and humans from infections with henipaviruses, which belong to the virus family Paramyxoviridae. We provide a comprehensive overview of documented outbreaks of Nipah and Hendra virus infections affecting livestock and humans and assess the burden on the economy and health systems. In an increasingly globalized and interconnected world, attention must be paid to emerging viruses and infectious diseases, as transmission routes can be rapid and worldwide.

Emergence of infectious diseases

Infectious disease outbreaks have devastated the human population throughout history. The Black Death (1347 to 1351, 25 million deaths), smallpox (1520 to 1979, 56 million deaths), and/or Spanish flu (1918 to 1920, 50 to 100 million deaths) were serious and devastating pandemics in the past [1]. Nowadays, HIV/AIDS, cholera (latest outbreak 2018), or the ongoing Coronavirus Disease 2019 (COVID-19) pandemic are serious threats to human populations, causing significant economic and health burdens with high morbidity and mortality rates and bringing them into the focus of government authorities as a global concern [2].

Emerging diseases are per definition evoked by pathogens entering a new geographic area, expand their host range by transmission, for example, from wildlife to domesticated animals, and harbor a great potential to increase in number in the near future. The pandemic spread of emerging diseases is the result of a combination and interplay of manifold processes like the ongoing globalization (increased commercial air travel and trade), the change of lifestyles and urbanization leading to a massive deforestation and, thus, rerouting of wildlife migration patterns and closer contact of wildlife with domestic animals (farming), which accelerate the occurrence and circulation of newly appearing microbial agents [1]. Various factors influence the emergence of disease outbreaks, for example, environmental conditions or public health infrastructure. Among these factors, the genetic plasticity of the infectious agent plays an important role. Depending on the potential of the individual pathogen to evolve and adapt to ecological niches and new hosts, the likelihood increases that it can spread and facilitate its own transmission, which could lead to a global spread of the pathogen [2].

Although many established diseases, such as tuberculosis, cholera, and malaria, have bacterial or protozoal origin, the majority of relevant newly emerging and reemerging diseases in the past century have been caused by viruses (Fig 1) [2]. They are mainly based on zoonotic events, as it occurred for HIV-1 being transmitted from chimpanzees to humans in Central Africa [3], MERS-CoV, which was transmitted from camels to humans in Arabia [4], or the emergence of the arthropod-born Zika virus, which spread from mosquitos to humans [5].

Fig 1. Mapping emerging viral diseases.

Emerging diseases in new locations (orange) or caused by newly emerging viruses (yellow) are shown. Spread of emerging diseases are facilitated by urbanization and globalization, such as commercial air traffic and trade (with reprint permission taken from Marston and colleagues (; [6]).

Most of the zoonotic pathogens are not well adapted to humans and only emerge sporadically through spillover events that may lead to localized outbreaks, so called “viral chatters” [79]. However, these spillover events increase the pandemic risk by providing the opportunity for viruses to become better adapted to new hosts and potentially cause human-to-human transmissions [7,10]. Although surveillance and awareness of personal and sanitary hygiene nowadays enhances, the risk of local outbreaks that may become pandemic remains and is associated with poverty, population density, and inadequate healthcare systems [11]. Especially high-risk pathogens like bat-borne Henipaviruses or Ebola virus (EBOV) are a burden to developing countries and may lead to a public health crisis based on the lack of disease awareness, missing surveillance or adequate healthcare systems [12]. Recent outbreaks of EBOV in Democratic Republic of Congo (DRC) or Guinea in the End of 2020 and the beginning of this year, respectively, were declared as “public health emergency of international concern” due to spread into areas that had not been affected before [12]. Thus, effective emergency treatment is needed to respond faster for mitigation and to control disease outbreaks [13].

The discovery of Henipaviruses

The complexity of disease emergence can be highlighted by the emergence of the highly pathogenic Nipah virus (NiV) and Hendra virus (HeV). These zoonotic viruses cause fatal diseases in humans and animals and had been classified in the genus Henipavirus in the virus family Paramyxoviridae [14,15]. The genome of HeV and NiV consists of a single-stranded RNA molecule in negative-sense orientation surrounded by a lipid envelope [16]. Initially, HeV was recognized through a disease outbreak in 1994 in Australia, being named after the Brisbane suburb of Hendra where several horses and their trainer died from a pulmonary disease with hemorrhagic manifestations [1720]. A second outbreak in Queensland, Australia also occurred in 1994 and affected 2 horses and 1 person. However, this event was only recognized in 1995, after the infected person died from relapsing encephalitis [19,21].

Despite NiV causing multiple outbreaks since its first identification in Sungai Nipah, it affected over 265 patients during the outbreaks in Malaysia (1998) and Singapore (1999), with 105 confirmed deaths [22,23]. Due to immediate and effective actions from the government, no further cases were reported in Malaysia and Singapore since then [2225]. In 2001, an outbreak in Bangladesh occurred with 13 NiV-infected people; 9 of the patients died [24,26,27]. Since then, recurrent outbreaks have been detected almost every year in Bangladesh with a total of 17 outbreaks until 2015 [23]. These outbreaks were associated with a high mortality rate: From 261 identified cases, 199 individuals died [23,6,28]. Additional, locally restricted outbreaks took place in Siliguri, West Bengal, India, in 2001, with a case fatality rate of 68% [22,23,29,30] and a repeated outbreak in Nadia, West Bengal, India, in 2007, where all infected people died within 1 week after infection [22,24,27,30]. In 2014, the Philippines reported 17 confirmed NiV infections in humans; 9 patients died [31]. The latest outbreaks occurred 2018 in Kerala, India, with a case fatality rate of 91% (23 infected patients) and 2019; after 7 days of severe symptoms, the patient fully recovered [32].

Socioeconomic burden of Henipavirus outbreaks

Malaysia (43%), Bangladesh (42%), and India (15%) represent all incident cases of human NiV infections worldwide [27]. Apart from the human catastrophe of high morbidity and mortality rates during documented epidemic outbreaks, the economic impact is tremendous [33]. After the first NiV outbreak in 1999, Malaysian pig industry and related sectors suffered enormous damage, i.e., 1.1 million pigs were culled costing about US$66.8 million with a total decrease in the Malaysian economy of around 30% during that time [33,34]. In addition to direct losses in the livestock sector, the feed industry and oil and fat production were most affected [32]. Compared to the economic losses resulting from the EBOV outbreak in 2014, with GDP losses of US$2.2 billion in Guinea, Liberia, and Sierra Leone in 2015 [35], the burden on the Malaysian economy appears modest. Nevertheless, the economic situation in these countries is so different that a direct comparison of the overall figures does not allow for an accurate interpretation and assessment of the impact on the country. Due to the high socioeconomic burden that NiV and HeV outbreaks cause, intervention plans had been developed in several countries, including campaigns, staff costs, pretesting of materials, field visits, and transportations. In Bangladesh, these activities increased the economic damage to a total of US$255,000 [33] and led to a decline of the economic stability in affected countries [27]. Thus, there is an urgent need for information and awareness raising, including improved contact tracing, better knowledge of transmission routes to implement appropriate hygiene measures, early diagnostics, and effective therapies to reduce the socioeconomic burden.

Transmission of Henipaviruses

For both HeV and NiV, the Pteropus fruit bat, also known as flying fox, is considered as the natural animal reservoirs [15,36,37]. Transmission is supposed to occur from bats via saliva, urine, and excreta to humans with pigs (NiV) or horses (HeV and NiV) as intermediate hosts (Fig 2). Spillover events from bats to the intermediate hosts or humans are due to consumption of contaminated fruits or contact with contaminated secretions [29,38].

Fig 2. Schematic representation of pathogenic Henipavirus transmission from the natural host, fruit bats, to susceptible species.

Shown are supposed transmission routes: (1) from bats to bats via placental transmission, lactation, or matting; (2) fruit consumption; (3) excretion and partially eaten fruits; (4) from pig to farmer (NiV Malaysia); (5) date palm consumption (NiV Bangladesh); (6) excretion; (7) from horse to owner (HeV Australia, NiV Philippines); (8) bite, scratch, etc.; and (9) from human to human (NiV Philippines, NiV Bangladesh).

Since the first emerge of HeV in Australia, 55 events have been reported that caused fatal infections with 100 deaths in horses, mainly due to respiratory failure [36]. Seven human HeV infections are documented; 4 patients died [18,3942]. To prevent human HeV infections, horses diagnosed positive for HeV are subsequently killed [21]. Since 2015, an equine HeV vaccine has been fully registered in Australia, and no HeV-vaccinated horse has been tested positive for HeV infection since then [21]. Nevertheless, although vaccination against HeV exist, spillover events of HeV infection in horses still occur, since uptake of the vaccine is limited due to misperceptions of horse owner, such as the underestimation of severity of HeV infection, vaccine safety or impact on the performance of (racing) horses, costs or effectiveness of the vaccine [4345]. However, human interference into nature bears an increasing risk of expansion of flying fox populations into urban areas, resulting in direct transmissions from the viral reservoirs to humans [46].

NiV-infected pigs show symptoms that vary by age but include neurological and respiratory signs such as tremors and severe cough, also known as “barking cough” [47,48]. Spillover events from Henipavirus-infected pigs to slaughterhouse and farm workers possibly occur through contact with contaminated pigs and their meat during processing of infected pigs in slaughterhouses. In the NiV outbreaks of Malaysia and Singapore, infected pigs had been identified as the main source of infections [23,49]. However, in the Bangladesh outbreaks, no evidence could be found for transmission via pigs. In these cases, ingestion of date palm sap, contaminated by fruit bats secretion and excreta, are suggested to be the main source of infection [23,28,50,51].

Human encroachment into flying fox habitats, i.e., by deforestation, but also climate change increases the risk of outbreaks in new locations by changing habitats of the zoonotic reservoir hosts [14,5254]. In addition, globalization and international trade facilitate the spread of disease, as shown in the NiV outbreaks in Singapore and Malaysia. Importing infected pigs from a contaminated area in Malaysia infected 11 slaughterhouse workers and caused one death [15,23,25]. Based on these outbreaks, a study aimed to identify the potential threat of pig trading in the transmission of NiV and examined how long-distance transportations of living pigs may facilitate disease dissemination in Thailand [55]. Findings showed that, although the risk of NiV dissemination through pig trade is low, it is not negligible and may cause local outbreaks that requires preventive strategies concerning international trading [55].

The threat of a potential global spread

Despite transmission and dissemination of Henipaviruses via infected livestock, a potential threat arises from human-to-human transmission. Whereas only a few cases of human HeV infections are reported, several NiV outbreaks have included person-to-person transmission with case fatality rates of up to 70% [29,56]. The capacity for NiV to spread in hospital settings between staff and patients was shown in an outbreak 2001 in Siliguri, India, which affected 66 people. The outbreak originated from an unidentified patient admitted to Siliguri District Hospital who infected 11 people [50]. Thus, the ability of NiV to spread from patients to nursing staff has raised concern that the virus might adapt to more efficient human-to-human transmission [15,29,37,50,5759]. In terms of the ability of human-to-human transmission, the different NiV strains differ. Therefore, it is quite conceivable that one of these strains acquires mutations during human infection that lead to more efficient and sustained human-to-human transmission. However, the virus is not dependent on replication in humans, so it can continue to spread through vectors even without adaptations to humans. In this regard, we should keep in mind the constant man-induced environmental changes, as these can lead to altered transmission patterns in emerging viruses with the chance for genetic variation. The lack of knowledge on the transmission route of the virus in the environment bears a high risk of a potential pandemic spread by facilitating viral transfer and disease transmission [29,57]. Together with considerable travel activities, including long-distance air traffic, but also increased international trading, might elevate the pandemic potential of Henipaviruses [29]. Thus, the perception of virus stability on surfaces under distinct environmental conditions as well as the successful inactivation of viral loads on these surfaces is a pressing need to improve safety practices for caretakers, researchers, and public health experts supporting an effective infection control [60,61].

Up to date, only few studies exist that examine Henipavirus stability on surfaces and objects and their role in viral disease transmission [62,63]. Fogarty and colleagues [57] analyzed the persistence of NiV and HeV under natural conditions relevant to bat transmission. The group tested viral loads of Henipavirus in bat urine and fruits under distinct conditions and revealed that survival of Henipaviruses in the environment varies between few hours and a couple of days is highly dependent on temperature and desiccation [57]. These results indicate that a short half-life of the virus requires close contact to the infected hosts or contaminated material for a successful transmission. However, under optimal conditions, Henipavirus is able to persist for days, which makes vehicle-borne transmission a potential source of danger [57].

Epidemiological studies of NiV outbreaks in several countries suggested that besides consumption of contaminated food, intermediate hosts and infected animals are the main source for human infections [23,28]. NiV-infected pigs are supposed to be an important factor for infections in humans. Transmission via pigs potentially occur through the respiratory route, but close contact with infected tissues of pigs might also result in NiV transmission [23,6466]. When examining the risk for transmission that might involve bodily fluids, Smither and colleagues [67] showed that the stability of NiV in blood or cell culture media under distinct conditions can last up to 1 week at room temperature, and, hence, providing the opportunity to cause fatal infections for a longer time period.

Despite transmission of Henipavirus via contaminated food [68], bats, or intermediate hosts, spread from infected persons to naïve individuals is a high-risk factor. Patients infected with Henipavirus shed viruses in body secretions, including blood, feces, urine, or saliva [50,51]. Studies have shown that the highest risk of being infected exists for family members who provide continuous care, and also for caregivers during hospitalization [59,6971]. Watanabe and colleagues demonstrated that NiV in human serum samples is able to survive for as long as 7 days at room temperature [72]. To analyze the risk potential of NiV-infected patients’ fomites contaminated surfaces in hospitals, samples collected in close proximity to diseased people from, i.e., the wall beside the patients’ bed, bed rail and sheets, clinical record files, and multipurpose towels were examined [70]. While no virus was detected on clinical files and wall surfaces nearby the patient, the most contaminated surfaces were bed sheets and towels [70]. However, these data did not show for how long infectious virus particles may persist on these surfaces.

Until now, limited data exist on the stability of Henipaviruses on surfaces. The ability to measure the persistence of NiV and HeV under different environmental conditions will therefore contribute to elucidating transmission routes, as in general studies on the survival of viruses in the environment and on surfaces and objects helps to intervene in and control viral outbreaks [73]. Based on this knowledge and the understanding on the role of surfaces on facilitating virus persistence, disinfectants can be adjusted to be more effective and drastically reduce viral titers in any spillage or contamination to limit or prevent the spread of viral infections and pathogen transmission [61,62]. After each Henipavirus outbreak, questions arise regarding adequate elimination and inactivation of medical waste and human remains [32]. So far, terminal decontamination at the end of outbreaks are an important challenge as no defined standards and guidelines are currently available [32]. After the Kerala outbreaks safety protocols came up that include using 2% to 5% Lysol/5% to 10% freshly prepared household bleach, followed by autoclaving or incineration. However, developing countries cannot afford expensive equipment and therefore need inactivation methods that are adapted to the possibilities without having to make any concessions in terms of security [27,32]. There are no studies performed to investigate the survival time of the pathogen on disinfected surfaces and objects or in human dead bodies [27].

Clinical features of Henipavirus infections

Once infected with Henipaviruses, the incubation period ranges from a few days to about 2 months depending on the route of transmission [17,74,75]. While the median incubation period in case of raw date palm sap consumption was 10 days, exposure to infected pigs can result in incubation periods of up to several weeks, whereby the majority of patients show symptoms after 2 weeks or less [24,75,76]. In humans, HeV infections result in most cases in influenza-like symptoms such as fever, myalgia, headaches, cough, and pharyngitis, before patients develop a fatal encephalitis [15,27]. Individuals infected with NiV typically present with clinical symptoms often associated with neurological disorders and acute encephalitis, while in addition, respiratory symptoms are found in approximately 25% of all patients [77]. Person-to-person transmission of viral particles is thought to occur at late stages of disease progression in NiV- and HeV-infected patients when the respiratory tract is involved in pathogenicity [50,78,79]. In fact, during the 2018 outbreak in Kerala, India, all nosocomial transmissions potentially occurred through droplet infection while the index patient was near end-stage disease and had a persistent cough [27,79,80]. This outbreak stresses the awareness among public and health caretakers for effective containment measures to prevent future outbreaks [32]. Precautions by safety measures such as personal protective equipment and proper hygiene after handling infected patients are important as rapid isolation and minimizing patient-to-caretaker exposure via bodily fluids [27,32]. Hence, the urgent need for a substantiated knowledge exists about the persistence of viruses outside their vectors or infected hosts to reduce the risk of further spread of the disease [62,63].

Currently, there is no vaccine available and treatment of patients infected with Henipaviruses is primarily based on supportive care [81,82]. Thereby, raising the awareness of risk factors, prevention of transmission, and controlling outbreaks by trained healthcare workers is the only effective principal measure, so far.

Closing remarks

The recent SARS-CoV-2 pandemic has shown limitation of disease containments in a globalized world. Within months, we went from the first case of COVID-19 to thousands of deaths reported worldwide [83]. This pandemic has raised concerns about effective measurements and strategies to prevent the global spread of diseases. International air traffic, traveling, and international trading induce higher risks during disease outbreaks and hamper real-time monitoring and identification of infected people by health authorities [83]. Disease outbreaks, including the NiV outbreak in India in 2018, the Lassa virus outbreak in Nigeria in 2018, or the reemergence of Ebola in Guinea and the DRC in 2021, raised the question how to predict outbreaks and develop response plans to be able to manage and control spread of diseases [84]. In addition, there is a continuing risk from newly discovered Henipaviruses and Henipa-like viruses of endemic and epidemic potential in the human population. In 2009, a study contacted in Kumasi/Ghana found putative Henipaviruses via RNA analysis of fecal material from African straw-colored fruit bats and discussed the probability of a fecal–oral transmission in comparison to more likely transmission routes like the consumption of bat meat [85]. In 2012, the isolation of a novel paramyxovirus, named Cedar virus (CedPV), from pooled urine samples of fruit bats in Cedar Grove, South East Queensland, Australia, was reported [86]. Though initial studies revealed CedPV being nonpathogenic in Henipavirus infection models, an elevated IFN-b induction by CedPV compared to HeV in human cells [86].

Effective precaution and containment measures presuppose a knowledge at all levels of disease emergence, i.e., understanding the route of transmission, stability outside vectors and hosts on objects and surfaces, rapid diagnosis, and an effective treatment. Therefore, gaining a deeper understanding of the molecular mechanisms of replication in host cells and the persistence of pathogens in the environment are fundamental to protect against infectious diseases with epidemic and pandemic potential. Due to the drastic impact of zoonotic diseases and often high mortality rates, it is recommended that scientists, public health authorities, and policy makers pay attention to the pandemic risk of Henipaviruses.

Key Learning Points

  1. > Henipaviruses transmit via distinct infection routes including contact to contaminated food or meat or direct contact to infected animals or persons.
  2. > Personal protective equipment and proper hygiene are highly recommended for farm and slaughterhouse workers as well as healthcare workers and medical personnel.
  3. > To date, there is no vaccine available leaving the treatment of patients infected with Henipaviruses primarily to the application of supportive care.

Top Five Papers

  1. Pillai VS, Krishna G, Veettil MV. Nipah Virus: Past Outbreaks and Future Containment. Viruses. 2020;12(4).
  2. Daszak P, Zambrana-Torrelio C, Bogich TL, Fernandez M, Epstein JH, Murray KA, et al. Interdisciplinary approaches to understanding disease emergence: the past, present, and future drivers of Nipah virus emergence. Proc Natl Acad Sci U S A. 2013;110(Suppl 1):3681–8.
  3. Yuen KY, Fraser NS, Henning J, Halpin K, Gibson JS, Betzien L, et al. Hendra virus: Epidemiology dynamics in relation to climate change, diagnostic tests and control measures. One Health. 2021;12:100207.
  4. Hassan MZ, Sazzad HMS, Luby SP, Sturm-Ramirez K, Bhuiyan MU, Rahman MZ, et al. Nipah Virus Contamination of Hospital Surfaces during Outbreaks, Bangladesh, 2013–2014. Emerg Infect Dis. 2018;24(1):15–21.
  5. Epstein JH, Field HE, Luby S, Pulliam JRC, Daszak P. Nipah virus: impact, origins, and causes of emergence. Curr Infect Dis Rep. 2006;8(1):59–65.


  1. 1. Akin L, Gozel MG. Understanding dynamics of pandemics. Turk J Med Sci. 2020;50(SI-1):515–9. pmid:32299204
  2. 2. Morens DM, Fauci AS. Emerging Pandemic Diseases: How We Got to COVID-19. Cell. 2020;183(3):837. pmid:33125895
  3. 3. Sharp PM, Hahn BH. Origins of HIV and the AIDS pandemic. Cold Spring Harb Perspect Med. 2011;1(1):a006841. pmid:22229120
  4. 4. Han HJ, Yu H, Yu XJ. Evidence for zoonotic origins of Middle East respiratory syndrome coronavirus. J Gen Virol. 2016;97(2):274–80. pmid:26572912
  5. 5. Centeno-Tablante E, Medina-Rivera M, Finkelstein JL, Herman HS, Rayco-Solon P, Garcia-Casal MN, et al. Update on the Transmission of Zika Virus Through Breast Milk and Breastfeeding: A Systematic Review of the Evidence. Viruses. 2021;13(1).
  6. 6. Marston HD, Folkers GK, Morens DM, Fauci AS. Emerging viral diseases: confronting threats with new technologies. Sci Transl Med. 2014;6(253):p. 253ps10. pmid:25210060
  7. 7. Madhav N, Oppenheim B, Gallivan M, Mulembakani P, Rubin E, Wolfe N, et al. Pandemics: Risks, Impacts, and Mitigation. Disease Control Priorities: Improving Health and Reducing Poverty. Washington (DC); 2017.
  8. 8. Pike BL, Saylors KE, Fair JN, LeBreton M, Tamoufe U, Djoko CF, et al. The origin and prevention of pandemics. Clin Infect Dis. 2010;50(12):1636–40. pmid:20450416
  9. 9. Wolfe ND, Daszak P, Kilpatrick AM, Burke DS. Bushmeat hunting, deforestation, and prediction of zoonoses emergence. Emerg Infect Dis. 2005;11(12):1822–7. pmid:16485465
  10. 10. Walsh MG, Haseeb M. The landscape configuration of zoonotic transmission of Ebola virus disease in West and Central Africa: interaction between population density and vegetation cover. PeerJ. 2015;3:e735. pmid:25648654
  11. 11. Fernandez-Montero JV, Soriano V, Barreiro P, de Mendoza C, Artacho MÁ. Coronavirus and other airborne agents with pandemic potential. Curr Opin Environ Sci Health. 2020;17:41–8. pmid:32995685
  12. 12. Gupta S, Gupta N, Yadav P, Patil D. Ebola virus outbreak preparedness plan for developing Nations: Lessons learnt from affected countries. J Infect Public Health. 2021;14(3):293–305. pmid:33610938
  13. 13. Duan J, Jiao F. Novel Case-Based Reasoning System for Public Health Emergencies. Risk Manag Healthc Policy. 2021;14:541–53. pmid:33603520
  14. 14. Daszak P, Zambrana-Torrelio C, Bogich TL, Fernandez M, Epstein JH, Murray KA, et al. Interdisciplinary approaches to understanding disease emergence: the past, present, and future drivers of Nipah virus emergence. Proc Natl Acad Sci U S A. 2013;110(Suppl 1):3681–8.
  15. 15. Chua KB, Bellini WJ, Rota PA, Harcourt BH, Tamin A, Lam SK, et al. Nipah virus: a recently emergent deadly paramyxovirus. Science. 2000;288(5470):1432–5. pmid:10827955
  16. 16. Broder CC. Henipavirus outbreaks to antivirals: the current status of potential therapeutics. Curr Opin Virol. 2012;2(2):176–87. pmid:22482714
  17. 17. Broder CC, Weir DL, Reid PA. Hendra virus and Nipah virus animal vaccines. Vaccine. 2016;34(30):3525–34. pmid:27154393
  18. 18. Murray K, Rogers R, Selvey L, Selleck P, Hyatt A, Gould A, et al. A novel morbillivirus pneumonia of horses and its transmission to humans. Emerg Infect Dis. 1995;1(1):31–3. pmid:8903153
  19. 19. Rogers RJ, Douglas IC, Baldock FC, Glanville RJ, Seppanen KT, Gleeson LJ, et al. Investigation of a second focus of equine morbillivirus infection in coastal Queensland. Aust Vet J. 1996;74(3):243–4. pmid:8894043
  20. 20. Hooper PT, Gould AR, Russell GM, Kattenbelt JA, Mitchell G. The retrospective diagnosis of a second outbreak of equine morbillivirus infection. Aust Vet J. 1996;74(3):244–5. pmid:8894044
  21. 21. Yuen KY, Fraser NS, Henning J, Halpin K, Gibson JS, Betzien L, et al. Hendra virus: Epidemiology dynamics in relation to climate change, diagnostic tests and control measures. One Health. 2021;12:100207. pmid:33363250
  22. 22. Banerjee S, Gupta N, Kodan P, Mittal A, Ray Y, Nischal N, et al. Nipah virus disease: A rare and intractable disease. Intractable Rare Dis Res. 2019;8(1):1–8. pmid:30881850
  23. 23. Sharma V, Kaushik S, Kumar R, Yadav JP, Kaushik S. Emerging trends of Nipah virus: A review. Rev Med Virol. 2019;29(1):e2010. pmid:30251294
  24. 24. Kulkarni DD, Tosh C, Venkatesh G, Kumar DS. Nipah virus infection: current scenario. Indian J Virol. 2013;24(3):398–408. pmid:24426305
  25. 25. Looi LM, Chua KB. Lessons from the Nipah virus outbreak in Malaysia. Malays J Pathol. 2007;29(2):63–7. pmid:19108397
  26. 26. Hsu VP, Hossain MJ, Parashar UD, Ali MM, Ksiazek TG, Kuzmin I, et al. Nipah virus encephalitis reemergence, Bangladesh. Emerg Infect Dis. 2004;10(12):2082–7. pmid:15663842
  27. 27. Pillai VS, Krishna G, Veettil MV. Nipah Virus: Past Outbreaks and Future Containment. Viruses. 2020;12(4).
  28. 28. Islam MS, Sazzad HMS, Satter SM, Sultana S, Hossain MJ, Hasan M, et al. Nipah Virus Transmission from Bats to Humans Associated with Drinking Traditional Liquor Made from Date Palm Sap, Bangladesh, 2011–2014. Emerg Infect Dis. 2016;22(4):664–70. pmid:26981928
  29. 29. Luby SP. The pandemic potential of Nipah virus. Antivir Res. 2013;100(1):38–43. pmid:23911335
  30. 30. Luby SP, Rahman M, Hossain MJ, Blum LS, Husain MM, Gurley E, et al. Foodborne transmission of Nipah virus, Bangladesh. Emerg Infect Dis. 2006;12(12):1888–94. pmid:17326940
  31. 31. Ching PK, de los Reyes VC, Sucaldito MN, Tayag E, Columna-Vingno AB, Malbas FF Jr, et al. Outbreak of henipavirus infection, Philippines, 2014. Emerg Infect Dis. 2015;21(2):328–31. pmid:25626011
  32. 32. Sahay RR, Yadav PD, Gupta N, Shete AM, Radhakrishnan C, Mohan G, et al. Experiential learnings from the Nipah virus outbreaks in Kerala towards containment of infectious public health emergencies in India. Epidemiol Infect. 2020;148:e90. pmid:32321607
  33. 33. Ochani RK, Batra S, Shaikh Asim, Asad A. Nipah virus—the rising epidemic: a review. Infez Med. 2019;27(2):117–27. pmid:31205033
  34. 34. Hosono H. Economic Impact of Nipah Virus infection Outbreak in Malaysia; 2006.
  35. 35. The World Bank. GDP growth (annual %); 2014.
  36. 36. Reynes JM, Counor D, Ong S, Faure C, Seng V, Molia S, et al. Nipah virus in Lyle’s flying foxes, Cambodia. Emerg Infect Dis. 2005;11(7):1042–7. pmid:16022778
  37. 37. Field H, Young P, Yob JM, Mills J, Hall L, Mackenzie J. The natural history of Hendra and Nipah viruses. Microbes Infect. 2001;3(4):307–14. pmid:11334748
  38. 38. Montgomery JM, Hossain MJ, Gurley E, Carroll GDS, Croisier A, Bertherat E, et al. Risk factors for Nipah virus encephalitis in Bangladesh. Emerg Infect Dis. 2008;14(10):1526–32. pmid:18826814
  39. 39. Kohl C, Tachedjian M, Todd S, Monaghan P, Boyd V, Marsh GA, et al. Hervey virus: Study on co-circulation with Henipaviruses in Pteropid bats within their distribution range from Australia to Africa. PLoS ONE. 2018;13(2):e0191933. pmid:29390028
  40. 40. Mbu’u CM, Mbacham WF, Gontao P, Kamdem SLS, Nlôga AMN, Groschup MH, et al. Henipaviruses at the Interface Between Bats, Livestock and Human Population in Africa. Vector Borne Zoonotic Dis. 2019;19(7):455–65. pmid:30985268
  41. 41. Ball MC, Dewberry TD, Freeman PG, Kemsley PD, Poe I. Clinical review of Hendra virus infection in 11 horses in New South Wales, Australia. Aust Vet J. 2014;92(6):213–8. pmid:24730376
  42. 42. Marsh GA, Todd S, Foord A, Hansson E, Davies K, Wright L, et al. Genome sequence conservation of Hendra virus isolates during spillover to horses, Australia. Emerg Infect Dis. 2010;16(11):1767–9. pmid:21029540
  43. 43. Goyen KA, Wright JD, Cunneen A, Henning J. Playing with fire—What is influencing horse owners’ decisions to not vaccinate their horses against deadly Hendra virus infection? PLoS ONE. 2017;12(6):e0180062. pmid:28636633
  44. 44. Gilkerson JR. Hendra virus: to vaccinate or not to vaccinate? What is the alternative? Aust Vet J. 2020;98 (12):575–7. pmid:33258486
  45. 45. Manyweathers J, Field H, Longnecker N, Agho K, Smith C, Taylor M. "Why won’t they just vaccinate?" Horse owner risk perception and uptake of the Hendra virus vaccine. BMC Vet Res. 2017;13(1):103. pmid:28407738
  46. 46. Middleton D. Hendra virus. Vet Clin North Am Equine Pract. 2014;30(3):579–89. pmid:25281398
  47. 47. Weingartl H, Czub S, Copps J, Berhane Y, Middleton D, Marszal P, et al. Invasion of the central nervous system in a porcine host by nipah virus. J Virol. 2005;79(12):7528–34. pmid:15919907
  48. 48. Epstein JH, Field HE, Luby S, Pulliam JRC, Daszak P. Nipah virus: impact, origins, and causes of emergence. Curr Infect Dis Rep. 2006;8(1):59–65. pmid:16448602
  49. 49. Parashar UD, Sunn LM, Ong F, Mounts AW, Arif MT, Ksiazek TG, et al. Case-control study of risk factors for human infection with a new zoonotic paramyxovirus, Nipah virus, during a 1998–1999 outbreak of severe encephalitis in Malaysia. J Infect Dis. 2000;181(5):1755–9. pmid:10823779
  50. 50. Luby SP, Gurley ES, Hossain MJ. Transmission of human infection with Nipah virus. Clin Infect Dis. 2009;49(11):1743–8. pmid:19886791
  51. 51. Pernet O, Schneider BS, Beaty SM, LeBreton M, Yun TE, Park A, et al. Evidence for henipavirus spillover into human populations in Africa. Nat Commun. 2014;5:5342. pmid:25405640
  52. 52. Araujo MB, New M. Ensemble forecasting of species distributions. Trends Ecol Evol. 2007;22(1):42–7. pmid:17011070
  53. 53. Satterfield BA, Cross RW, Fenton KA, Agans KN, Basler CF, Geisbert TW, et al. The immunomodulating V and W proteins of Nipah virus determine disease course. Nat Commun. 2015;6:7483. pmid:26105519
  54. 54. Singh RK, Dhama K, Chakraborty S, Tiwari R, Natesan S, Khandia R, et al. Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies—a comprehensive review. Vet Q. 2019;39(1):26–55. pmid:31006350
  55. 55. Wongnak P, Thanapongtharm W, Kusakunniran W, Karnjanapreechakorn S, Sutassananon K, Kalpravidh W, et al. A ’what-if’ scenario: Nipah virus attacks pig trade chains in Thailand. BMC Vet Res. 2020;16(1):300. pmid:32838786
  56. 56. Gomez Roman R, Wang L-F, Lee B, Halpin K, de Wit E, Broder CC, et al. Nipah@20: Lessons Learned from Another Virus with Pandemic Potential. mSphere. 2020;5(4). pmid:32641430
  57. 57. Fogarty R, Halpin K, Hyatt AD, Daszak P, Mungall BA. Henipavirus susceptibility to environmental variables. Virus Res. 2008;132(1–2):140–4. pmid:18166242
  58. 58. Nipah virus outbreak(s) in Bangladesh, January-April 2004. Wkly Epidemiol Rec. 2004;79(17):168–71. pmid:15132054
  59. 59. Homaira N, Rahman M, Hossain MJ, Epstein JH, Sultana R, Khan MSU, et al. Nipah virus outbreak with person-to-person transmission in a district of Bangladesh, 2007. Epidemiol Infect. 2010;138(11):1630–6. pmid:20380769
  60. 60. Wigginton KR, Kohn T. Virus disinfection mechanisms: the role of virus composition, structure, and function. Curr Opin Virol. 2012;2(1):84–9. pmid:22440970
  61. 61. Smither S, Phelps A, Eastaugh L, Ngugi S, O’Brien L, Dutch A, et al. Effectiveness of Four Disinfectants against Ebola Virus on Different Materials. Viruses. 2016;8(7).
  62. 62. Boone SA, Gerba CP. Significance of fomites in the spread of respiratory and enteric viral disease. Appl Environ Microbiol. 2007;73(6):1687–96. pmid:17220247
  63. 63. Sagripanti JL, Rom AM, Holland LE. Persistence in darkness of virulent alphaviruses, Ebola virus, and Lassa virus deposited on solid surfaces. Arch Virol. 2010;155(12):2035–9. pmid:20842393
  64. 64. Mohd Nor MN, Gan CH, Ong BL. Nipah virus infection of pigs in peninsular Malaysia. Rev Sci Tech. 2000;19(1):160–5. pmid:11189713
  65. 65. Hooper PT, Williamson MM. Hendra and Nipah virus infections. Vet Clin North Am Equine Pract. 2000;16(3):597–603, xi. pmid:11219352
  66. 66. Paton NI, Leo YS, Zaki SR, Auchus AP, Lee KE, Ling AE, et al. Outbreak of Nipah-virus infection among abattoir workers in Singapore. Lancet. 1999;354(9186):1253–6. pmid:10520634
  67. 67. Smither SJ, Eastaugh LS, Findlay JS, O’Brien LM, Thom R, Lever MS. Survival and persistence of Nipah virus in blood and tissue culture media. Emerg Microbes Infect. 2019;8(1):1760–2. pmid:31823683
  68. 68. Epstein JH, Anthony SJ, Islam A, Kilpatrick AM, Khan SA, Balkey MD, et al. Nipah virus dynamics in bats and implications for spillover to humans. Proc Natl Acad Sci U S A. 2020;117(46):29190–201. pmid:33139552
  69. 69. Gurley ES, Montgomery JM, Hossain MJ, Bell M, Azad AK, Islam MR, et al. Person-to-person transmission of Nipah virus in a Bangladeshi community. Emerg Infect Dis. 2007;13(7):1031–7. pmid:18214175
  70. 70. Hassan MZ, Sazzad HMS, Luby SP, Sturm-Ramirez K, Bhuiyan MU, Rahman MZ, et al. Nipah Virus Contamination of Hospital Surfaces during Outbreaks, Bangladesh, 2013–2014. Emerg Infect Dis. 2018;24(1):15–21. pmid:29260663
  71. 71. Homaira N, Rahman M, Hossain MJ, Nahar N, Khan R, Rahman M, et al. Cluster of Nipah virus infection, Kushtia District, Bangladesh, 2007. PLoS ONE. 2010;5(10):e13570. pmid:21042407
  72. 72. Watanabe S, Fukushi S, Harada T, Shimojima M, Yoshikawa T, Kurosu T, et al. Effective inactivation of Nipah virus in serum samples for safe processing in low-containment laboratories. Virol J. 2020;17(1):151. pmid:33036623
  73. 73. de Wit E, Bushmaker T, Scott D, Feldmann H, Munster VJ. Nipah virus transmission in a hamster model. PLoS Negl Trop Dis. 2011;5(12):e1432. pmid:22180802
  74. 74. Mahalingam S, Herrero LJ, Playford EG, Spann K, Herring B, Rolph MS, et al. Hendra virus: an emerging paramyxovirus in Australia. Lancet Infect Dis. 2012;12(10):799–807. pmid:22921953
  75. 75. Ambat AS, Zubair SM, Prasad N, Pundir P, Rajwar E, Patil DS, et al. Nipah virus: A review on epidemiological characteristics and outbreaks to inform public health decision making. J Infect Public Health. 2019;12(5):634–9. pmid:30808593
  76. 76. Rahman MA, Hossain MJ, Sultana S, Homaira N, Khan SU, Rahman M, et al. Date palm sap linked to Nipah virus outbreak in Bangladesh, 2008. Vector Borne Zoonotic Dis. 2012;12(1):65–72. pmid:21923274
  77. 77. Chua KB. Nipah virus outbreak in Malaysia. J Clin Virol. 2003;26(3):265–75. pmid:12637075
  78. 78. Thomas B, Chandran P, Lilabi MP, George B, Sivakumar CP, Jayadev VK, et al. Nipah Virus Infection in Kozhikode, Kerala, South India, in 2018: Epidemiology of an Outbreak of an Emerging Disease.?. 2019;44(4):383–7. pmid:31802805
  79. 79. Arunkumar G, Chandni R, Mourya DT, Singh SK, Sadanandan R, Sudan P, et al. Outbreak Investigation of Nipah Virus Disease in Kerala, India, 2018. J Infect Dis. 2019;219(12):1867–78. pmid:30364984
  80. 80. Clayton BA, Middleton D, Bergfeld J, Haining J, Arkinstall R, Wang L, et al. Transmission routes for nipah virus from Malaysia and Bangladesh. Emerg Infect Dis. 2012;18(12):1983–93. pmid:23171621
  81. 81. Ramphul K, Mejias SG, Agumadu VC, Sombans S, Sonaye R, Lohana P. The Killer Virus Called Nipah: A Review. Cureus. 2018;10(8):e3168. pmid:30416895
  82. 82. Aditi , Shariff M. Nipah virus infection: A review. Epidemiol Infect. 2019;147:e95. pmid:30869046
  83. 83. Senatore V, Zarra T, Buonerba A, Choo K-H, Hasan SW, Korshin G, et al. Indoor versus outdoor transmission of SARS-COV-2: environmental factors in virus spread and underestimated sources of risk. EuroMediterr J Environ Integr. 2021;6(1):30. pmid:33585671
  84. 84. Jaca A. Insights from the fifth International One Health Congress, 2018, Saskatoon, Canada. Pan Afr Med J. 2019;32:168. pmid:31303937
  85. 85. Drexler JF, Corman VM, Gloza-Rausch F, Seebens A, Annan A, Ipsen A, et al. Henipavirus RNA in African bats. PLoS ONE. 2009;4(7):e6367. pmid:19636378
  86. 86. Marsh GA, de Jong C, Barr JA, Tachedjian M, Smith C, Middleton D, et al. Cedar virus: a novel Henipavirus isolated from Australian bats. PLoS Pathog. 2012;8(8):e1002836. pmid:22879820