Managing limited resources such as testkits and antiviral drugs while trying to contain the spread of pandemic influenza is a major challenge faced by several countries. In the event where a fast and accurate testkit is not yet available, one has to rely on slower testkits, coupling their use with effective social distancing measures to minimize the wastage of antiviral drugs. In this work, we have developed a stochastic agent-based pandemic model to assess the necessity of a fast testkit. From our simulation results, we showed that intervention policies, and not testkits, are the key means to successfully contain an outbreak, and that casting a wider net for contact tracing is crucial for minimizing the total attack rate. However, although not yet included in our model, we can infer from the results that most of the drug wastage is due to prophylaxis being administered to the contacts. Considering the use of testkits on the contacts may be a better resource allocation strategy. Within each intervention policy, the use of slower testkits while holding the individual at the hospital can be an equally effective means of mitigating a pandemic outbreak as compared with a fast testkit. However, this is provided that proper infection controls, such as a hospital segregation policy, are in place. Otherwise, hospital transmission may limit the usefulness of other efforts such as contact tracing and quarantine orders. Rotavirus Structural Proteins and dsRNA Are Required for the Human Primary Plasmacytoid Dendritic Cell IFNα Response Rotaviruses are the leading cause of severe dehydrating diarrhea in children worldwide. Rotavirus-induced immune responses, especially the T and B cell responses, have been extensively characterized; however, little is known about innate immune mechanisms involved in the control of rotavirus infection. Although increased levels of systemic type I interferon (IFNα and β) correlate with accelerated resolution of rotavirus disease, multiple rotavirus strains, including rhesus rotavirus (RRV), have been demonstrated to antagonize type I IFN production in a variety of epithelial and fibroblast cell types through several mechanisms, including degradation of multiple interferon regulatory factors by a viral nonstructural protein. This report demonstrates that stimulation of highly purified primary human peripheral plasmacytoid dendritic cells (pDCs) with either live or inactivated RRV induces substantial IFNα production by a subset of pDCs in which RRV does not replicate. Characterization of pDC responses to viral stimulus by flow cytometry and Luminex revealed that RRV replicates in a small subset of human primary pDCs and, in this RRV-permissive small subset, IFNα production is diminished. pDC activation and maturation were observed independently of viral replication and were enhanced in cells in which virus replicates. Production of IFNα by pDCs following RRV exposure required viral dsRNA and surface proteins, but neither viral replication nor activation by trypsin cleavage of VP4. These results demonstrate that a minor subset of purified primary human peripheral pDCs are permissive to RRV infection, and that pDCs retain functionality following RRV stimulus. Additionally, this study demonstrates trypsin-independent infection of primary peripheral cells by rotavirus, which may allow for the establishment of extraintestinal viremia and antigenemia. Importantly, these data provide the first evidence of IFNα induction in primary human pDCs by a dsRNA virus, while simultaneously demonstrating impaired IFNα production in primary human cells in which RRV replicates. Rotavirus infection of primary human pDCs provides a powerful experimental system for the study of mechanisms underlying pDC-mediated innate immunity to viral infection and reveals a potentially novel dsRNA-dependent pathway of IFNα induction. Dendritic cells (DCs), a highly specialized subset of professional antigen-presenting cells, play a central role in the initiation of innate and adaptive immunity. There are two known major subsets of primary human and murine circulating DCs: myeloid DCs, which function principally in antigen presentation, and plasmacytoid DCs (pDCs), which secrete the type I interferons (IFN), IFNa and IFNb [1] , as well as a variety of other cytokines and chemokines. Viral induction of type I IFN expression has been well studied in recent years and has been shown to be mediated by multiple pattern recognition receptors (PRRs), including retinoic acid-inducible gene (RIG)-I, melanoma differentiation-associated gene (MDA)5, toll-like receptor (TLR)3, TLR7 and TLR9. PRR expression is restricted in pDCs, with only TLR7 and TLR9 implicated in viral-induced IFNa production through the recognition of single-stranded (ss)RNA or DNA, respectively [2, 3, 4, 5, 6, 7, 8, 9] . IFNa production by pDCs is also observed following TLR7/8 stimulus with synthetic resiquimods and imiquimods, or TLR9 antagonism by CpG oligodeoxynucleotides (ODN). pDCs are not generally thought to be able to respond to double-stranded (ds)RNA, as stimulation with poly I:C or long (500 base pairs) dsRNA molecules fail to elicit IFNa or upregulate activation or maturation markers, such as CD86 and CD83 [10, 11, 12] . However, low levels of IFNa production have been reported following pDC stimulation with poly A:U [13] or in vitro transcribed viral dsRNA [11] , and a recent report indicates a role for RIG-I-like helicases in recognizing replicating virus in murine pDCs lacking the IFN receptor [14] . Short interfering dsRNAs have also been demonstrated to elicit an IFNa response through TLR7, although this appears dependent on a specific sequence, and not on the dsRNA structure [12] .