Human metapneumovirus (HMPV) is a major causative agent of severe bronchiolitis and pneumonia. Its fusion (F) protein must be cleaved by host proteases to cause membrane fusion, a critical step for virus infection. By generating Vero cells constitutively expressing the transmembrane serine protease TMPRSS2 and green fluorescent protein-expressing recombinant HMPV, we show that TMPRSS2, which is expressed in the human lung epithelium, cleaves the HMPV F protein efficiently and supports HMPV multiplication. The results indicate that TMPRSS2 is a possible candidate protease involved in the development of lower respiratory tract illness in HMPV-infected patients.

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Measles is an acute febrile infectious disease with high morbidity and mortality. The genome of measles virus (MV), the causative agent, encodes two accessory products, V and C proteins, that play important roles in MV virulence. The V but not the C protein of the IC-B strain (a well-characterized virulent strain of MV) has been shown to block the Jak/Stat signaling pathway and counteract the cellular interferon (IFN) response. We have recently shown that a recombinant IC-B strain that lacks C protein expression replicates poorly in certain cell lines, and its growth defect is related to translational inhibition and strong IFN induction. Here, we show that the V protein of the MV IC-B strain also blocks the IFN induction pathway mediated by the melanoma differentiation-associated gene 5 product, thus actively interfering with the host IFN response at two different steps. On the other hand, the C protein per se possesses no activity to block the IFN induction pathway. Our data indicate that the C protein acts as a regulator of viral RNA synthesis, thereby acting indirectly to suppress IFN induction. Since recombinant MVs with C protein defective in modulating viral RNA synthesis or lacking C protein expression strongly stimulate IFN production, in spite of V protein production, both the C and V proteins must be required for MV to fully circumvent the host IFN response.Measles is an acute febrile infectious disease with high morbidity and mortality and accounts for ϳ4% of deaths in children aged Ͻ5 years worldwide (5). Measles virus (MV), the causative agent, belongs to the genus Morbillivirus of the family Paramyxoviridae and has a nonsegmented negative-strand RNA genome of ϳ16 kb in length. The genome has six genes that encode the phosphoprotein (P) and the nucleocapsid (N), matrix (M), fusion (F), hemagglutinin (H), and large (L) proteins (24). The P gene encodes two additional proteins, V and C, by a process of RNA editing and an alternative translational initiation in a different reading frame, respectively (4, 9). The V and C proteins are nonessential products (58, 62) but play important roles in MV virulence (12,54,70,74,75). Although the V protein has been shown to counteract the cellular interferon (IFN) response (7,13,50,52,69), molecular mechanisms by which the C protein contributes to virus virulence are poorly understood. We have recently shown that a recombinant MV that lacks C protein expression (MV⌬C) replicates poorly in certain cell lines, and its growth defect is related to translational inhibition and strong IFN induction (47).Host antiviral responses are initiated by detecting pathogenassociated molecular patterns, such as cytoplasmic singlestranded RNA (ssRNA) bearing a 5Ј triphosphate and doublestranded RNA (dsRNA) (19, 71). The retinoic acid inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (mda-5) products are known to be intracellular receptors (sensors) for these virus-derived RNA molecules (32). Recently, some RNAs processed by RNase L have also been shown to be re...

We discuss the possibility of the existence of tetraquark states made of four quarks in the string (flux tube) model. The new particle is composed of a diquark and an antidiquark which are connected by a color flux. It is shown that the vibrational and rotational excited states of the string explain some nonqq mesons observed experimentally. Moreover we discuss the decay widths of such tetraquarks with the use of the Schwinger mechanism.