Nipah virus strain variation.

To the Editor: AbuBakar et al. described strain variation in Nipah virus during the 1998-1999 outbreak in Malaysia (1). They found an isolate from pigs in Perak, as well as from a flying fox, that differed markedly from pig and human isolates from the main epidemic in southern Malaysia. AbuBakar et al. proposed that this finding indicates 2 separate spillover events from bats to pigs occurred, the first in Perak in 1998 and the second in southern Malaysia in 1999. However, investigations at the time of the outbreak showed that many pigs were moved from Perak onto southern farms in early 1999. We suggest that successive spillovers of the pig population in the north can also explain the observed strain differences between northern and southern isolates.

A model from experimental studies and active farm data demonstrate that Nipah virus may have circulated repeatedly and become endemic within 1 or several large pig farms in Perak (J.R.C. Pulliam, unpub. data), which is consistent with the occurrence of human cases in Perak before the 1998-1999 outbreak. Evolution of the virus population in pigs, followed by the reintroduction in Perak of the original strain from bats and its subsequent southward movement in infected pigs, would explain observed strain differences. Models suggest that evolution of the virus within pig populations would result in lower death rates but prolonged illness. Although the pig-adapted virus strain may have circulated on both northern and southern farms, sampling biases in favor of the more virulent strain would be expected in areas of high death rates, which would explain the observed genetic relationships between sequenced isolates.

We suggest that pigs be experimentally infected with the Perak strain of Nipah virus to determine whether differences exist in illness and death caused by this virus. Further sequencing of virus from archived pig samples will clarify with greater confidence whether multiple strains circulated in both regions.

Acknowledgments

This work is published as part of a collaboration with the Australian Biosecurity Cooperative Research Center for Emerging Infectious Disease.

Funding for the Henipavirus Ecology Research Group is provided by a National Institutes of Health/National Science Foundation 'Ecology of infectious diseases award' (R01-TW05869) from the John E. Fogarty International Center.

Juliet R.C. Pulliam, * Hume E. Field, ([double dagger]) Kevin J. Olival, ([double dagger]) and the Henipavirus Ecology Research Group ([section]) (1)

* Princeton University, Princeton, New Jersey, USA; ([dagger]) Queensland Department of Primary Industries, Brisbane, Queensland, Australia; ([double dagger]) Columbia University, New York, New York, USA; and ([section]) Consortium for Conservative Medicine, New York, New York, USA

Reference

(1.) AbuBakar S, Chang LY, Ali AR, Sharifah SH, Yusoff K, Zamrod Z. Isolation and molecular identification of Nipah virus from pigs. Emerg Infect Dis. 2004;10:2228-30.

Address for correspondence: Juliet R.C. Pulliam, Department of Ecology and Evolutionary Biology, Princeton University, 102 Guyot Hall, Princeton, NJ 08544, USA; fax: [phone]; email: [e-mail]

(1) A full list of members of this group is available at www.henipavirus.org

In response: Pulliam et al. (1) presented a model to help explain the observed Nipah virus (NV) strain differences reported earlier by AbuBakar et al. (2). The model is built around an assumption that NV was endemic in several pig farms in the north of Malaysia and that a subsequent reintroduction of the original NV caused the fatal encephalitis outbreak in 1998.

While the model is plausible, that NV infection was endemic among pigs before the 1998 outbreak is difficult to imagine in the absence of verifiable evidence. As with any virus that crosses species, NV would likely have caused severe infection, and what happened in 1998 is a classic example. Before NV could have evolved, become less virulent, and subsequently become endemic, it would have been first introduced to pigs. This initial introduction would have caused an outbreak, but no such outbreaks were reported before 1998. Furthermore, the life span of pigs reared in farms is relatively short before they are sent to the markets, which limits the time in which NV evolution could take place. Slaughtering these pigs would also have caused infection among abattoir workers and pork handlers. At present, the finding of 2 different NV strains from 2 different outbreak foci favors the suggestion that 2 possibly overlapping NV outbreaks occurred in Malaysia in 1998. Further investigation of NV archived materials would shed further light into the possible origin of NV in the 1998 Malaysia outbreaks.

Sazaly AbuBakar *

* University Malaya, Kuala Lumpur, Malaysia

References

(1.) Pulliam JRC, Field HE, Olival KJ, and the Henipavirus Ecology Research Group. Nipah virus strain variation. Emerg Infect Dis. 2005;11:1978-9.

(2.) AbuBakar S, Chang L-Y, Mohd Ali AR, Sharifah SH, YusoffK, Zamrod Z. Isolation and molecular identification of Nipah virus from pigs. Emerg Infect Dis. 2004; 10:2228-30.

Address for correspondence: Sazaly AbuBakar, University Malaya, Department of Medical Microbiology, Faculty of Medicine, Kuala Lumpur 50603, Malaysia; fax: [phone]; email: [e-mail]