Irving AT, Rozario P, Kong PS, Luko K, Gorman JJ, Hastie ML, Chia WN, Mani S, Lee BP, Smith GJD, Mendenhall IH, Larman HB, Elledge SJ, Wang LF.

*Cellular and Molecular Life Sciences* &middot; April 2020 &middot; DOI: [10.1007/s00018-019-03242-x](https://doi.org/10.1007/s00018-019-03242-x)

 How to cite

### AMA

Irving AT, Rozario P, Kong PS, et al. Robust dengue virus infection in bat cells and limited innate immune responses coupled with positive serology from bats in IndoMalaya and Australasia. *Cell Mol Life Sci*. 2020;77(8):1607-1622. doi:10.1007/s00018-019-03242-x

### APA

```
Irving, A. T., Rozario, P., Kong, P. S., Luko, K., Gorman, J. J., Hastie, M. L., Chia, W. N., Mani, S., Lee, B. P., Smith, G. J. D., Mendenhall, I. H., Larman, H. B., Elledge, S. J., & Wang, L. F. (2020). Robust dengue virus infection in bat cells and limited innate immune responses coupled with positive serology from bats in IndoMalaya and Australasia. *Cellular and Molecular Life Sciences*, 77(8), 1607–1622. https://doi.org/10.1007/s00018-019-03242-x
```

### BibTeX

```
@article{Irving2020,
 title = {Robust dengue virus infection in bat cells and limited innate immune responses coupled with positive serology from bats in IndoMalaya and Australasia},
 author = {Irving, Aaron T. and Rozario, Phillip and Kong, Pui-San and Luko, Katja and Gorman, Jeffrey J. and Hastie, Marcus L. and Chia, Wan Ni and Mani, Shailendra and Lee, Benjamin P. and Smith, Gavin J. D. and Mendenhall, Ian H. and Larman, H. Benjamin and Elledge, Stephen J. and Wang, Lin-Fa},
 journal = {Cellular and Molecular Life Sciences},
 volume = {77},
 number = {8},
 pages = {1607--1622},
 year = {2020},
 doi = {10.1007/s00018-019-03242-x}
}
```

 Researchers from Duke-NUS Medical School, QIMR Berghofer, Johns Hopkins, and Harvard Medical School demonstrate that bat primary cells, immune cells, and cell lines support robust dengue virus replication with minimal interferon response — and pair the in-vitro work with new antibody serology evidence from wild bats sampled across IndoMalaya and Australasia. The combination raises the possibility that bats are at least transient hosts in the life cycle of dengue or other flaviviruses, with implications for spillover dynamics and surveillance design in dengue-endemic regions.

 [
 Read publication at Cellular and Molecular Life Sciences
 
 ](https://doi.org/10.1007/s00018-019-03242-x)

In this publication:

 - Old-world fruitbat primary cells, immune cells, and cell lines were productively infected with dengue virus, producing high titers of progeny virus.

 - At MOIs that drove substantial dengue production, bat cells mounted only a limited interferon response — an asymmetry between high viral output and minimal innate signaling that is the core mechanistic finding.

 - Antibody evidence collected from wild bat populations across IndoMalaya and Australasia documents prior dengue (or closely related flavivirus) exposure in the wild.

 - Combined cell-permissivity plus seropositive wild-bat serology raises the possibility that bats are at least transient hosts in the life cycle of dengue or other flaviviruses, with implications for spillover dynamics and surveillance design.

On the cell-line side, the authors show that old-world fruitbat cells can be productively infected with dengue virus, producing high titers of progeny virus while inducing only a limited interferon response at multiplicities of infection that drive substantial dengue production. The asymmetry between high viral output and limited innate response is the core mechanistic finding — consistent with bats being a permissive host capable of sustaining replication without disease.

On the serology side, antibody evidence collected from wild bat populations in Asia/Pacific regions documents prior dengue (or closely related flavivirus) exposure in the wild. The combination raises the possibility that bats are at least transient hosts in the life cycle of dengue or other flaviviruses, with implications for spillover dynamics and surveillance design in dengue-endemic regions.

Bats produce virus, not symptoms — and the cell-level mechanism for that asymmetry now has direct evidence. Combining the cell-replication data with positive serology from wild bats in IndoMalaya and Australasia adds bats to the set of plausible flavivirus carriers worth surveilling — important for outbreak preparedness in dengue-endemic regions where bat populations have historically been outside the surveillance focus. For arbovirology and One Health programs, bat cell lines become a tractable mechanistic model for studying flavivirus replication kinetics and innate-response uncoupling, useful for groups that have struggled with the limits of human or rodent cell models for reservoir-host biology.

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