Informative as it may be, comparative sequence analysis will eventually not be sufficient to answer the FECV/FIPV question. What will be needed is a reverse genetics system to generate and manipulate the FCoV genome as well as a cell culture system to propagate the viruses, both of which have thus far not been achieved.  UNC93B1 Mediates Innate Inflammation and Antiviral Defense in the Liver during Acute Murine Cytomegalovirus Infection Antiviral defense in the liver during acute infection with the hepatotropic virus murine cytomegalovirus (MCMV) involves complex cytokine and cellular interactions. However, the mechanism of viral sensing in the liver that promotes these cytokine and cellular responses has remained unclear. Studies here were undertaken to investigate the role of nucleic acid-sensing Toll-like receptors (TLRs) in initiating antiviral immunity in the liver during infection with MCMV. We examined the host response of UNC93B1 mutant mice, which do not signal properly through TLR3, TLR7 and TLR9, to acute MCMV infection to determine whether liver antiviral defense depends on signaling through these molecules. Infection of UNC93B1 mutant mice revealed reduced production of systemic and liver proinflammatory cytokines including IFN-α, IFN-γ, IL-12 and TNF-α when compared to wild-type. UNC93B1 deficiency also contributed to a transient hepatitis later in acute infection, evidenced by augmented liver pathology and elevated systemic alanine aminotransferase levels. Moreover, viral clearance was impaired in UNC93B1 mutant mice, despite intact virus-specific CD8+ T cell responses in the liver. Altogether, these results suggest a combined role for nucleic acid-sensing TLRs in promoting early liver antiviral defense during MCMV infection. Initiation of inflammation following infection requires recognition of the invading microbe by innate immune pattern recognition receptors (PRRs) that signal in response to pathogen-associated molecular patterns (PAMPs). PRRs recognize selfand microbe-associated molecules [1] [2] [3] [4] . Members of the Toll-like receptor (TLR) family of PRRs are transmembrane receptors that are expressed either on the cell surface or within the endosomal compartment and respond to a variety of PAMPs [1] . Murine TLR3, TLR7 and TLR9 are expressed in the endolysosome and are implicated in recognition of viral dsRNA, ssRNA and dsDNA, respectively [1, [5] [6] [7] [8] [9] [10] [11] . Ligation of the nucleic acid-sensing TLRs results in transcription of antiviral genes including type I IFNs (IFN-a/b) and proinflammatory cytokines [1] . TLR3 responses require signaling through the adaptor molecule Toll/IL-1R domain-containing adapter-inducing interferon-b (TRIF), while TLR7 and TLR9 are dependent on the adaptor molecule myeloid differentiation primary response gene 88 (MyD88) to activate transcription factors and induce gene transcription [1, [12] [13] [14] .