Existence and uniqueness of global solutions to fully nonlinear first order elliptic systems

Let $F : \mathbb{R}^n \times \mathbb{R}^{N\times n} \rightarrow \mathbb{R}^N$ be a Caratheodory map. In this paper we consider the problem of existence and uniqueness of weakly differentiable global strong a.e. solutions $u: \mathbb{R}^n \longrightarrow \mathbb{R}^N$ to the fully nonlinear PDE system \label{1} \tag{1} F(\cdot,Du ) \,=\, f, \ \ \text{ a.e. on }\mathbb{R}^n, when $f\in L^2(\mathbb{R}^n)^N$. This problem has not been considered before. By introducing an appropriate notion of ellipticity, we prove existence of solution to \eqref{1} in a tailored Sobolev "energy" space (known also as the J.L. Lions space) and a uniqueness a priori estimate. The proof is based on the solvability of the linearised problem by Fourier transform methods and a "perturbation device" which allows to use of Campanato's notion of near operators, an idea developed for the 2nd order case.Comment: Journal: Nonlinear Analysis, revised, 15 page

Innate Sensing of Foamy Viruses by Human Hematopoietic Cells

Foamy viruses (FV) are nonpathogenic retroviruses that have cospeciated with primates for millions of years. FV can be transmitted through severe bites from monkeys to humans. Viral loads remain generally low in infected humans, and no secondary transmission has been reported. Very little is known about the ability of FV to trigger an innate immune response in human cells. A few previous reports suggested that FV do not induce type I interferon (IFN) in nonhematopoietic cells. Here, we examined how human hematopoietic cells sense FV particles and FV-infected cells. We show that peripheral blood mononuclear cells (PBMCs), plasmacytoid dendritic cells (pDCs), and the pDC-like cell line Gen2.2 detect FV, produce high levels of type I IFN, and express the IFN-stimulated gene MxA. Fewer than 20 FV-infected cells are sufficient to trigger an IFN response. Both prototypic and primary viruses stimulated IFN release. Donor cells expressing a replication-defective virus, carrying a mutated reverse transcriptase, induced IFN production by target cells as potently as wild-type virus. In contrast, an FV strain with env deleted, which does not produce viral particles, was inactive. IFN production was blocked by an inhibitor of endosomal acidification (bafilomycin A1) and by an endosomal Toll-like receptor (TLR) antagonist (A151). Silencing experiments in Gen2.2 further demonstrated that TLR7 is involved in FV recognition. Therefore, FV are potent inducers of type I IFN by pDCs and by PBMCs. This previously underestimated activation of the innate immune response may be involved in the control of viral replication in humans

Viral and subviral derived small RNAs as pathogenic determinants in plants and insects

The phenotypic manifestations of disease induced by viruses and subviral infectious entities are the result of complex molecular interactions between host and viral factors. The viral determinants of the diseased phenotype have traditionally been sought at the level of structural or non-structural proteins. However, the discovery of RNA silencing mechanisms has led to speculations that determinants of the diseased phenotype are caused by viral nucleic acid sequences in addition to proteins. RNA silencing is a gene regulation mechanism conserved within eukaryotic kingdoms (with the exception of some yeast species), and in plants and insects it also functions as an antiviral mechanism. Non-coding RNAs of viral origin, ranging in size from 21 to 24 nucleotides (viral small interfering RNAs, vsiRNAs) accumulate in virus-infected tissues and organs, in some cases to comparable levels as the entire complement of host-encoded small interfering RNAs. Upon incorporation into RNA-induced silencing complexes, vsiRNAs can mediate cleavage or induce translational inhibition of nucleic acid targets in a sequence-specific manner. This review focuses on recent findings that suggest an increased complexity of small RNA-based interactions between virus and host. We mainly address plant viruses, but where applicable discuss insect viruses as well. Prominence is given to studies that have indisputably demonstrated that vsiRNAs determine diseased phenotype by either carrying sequence determinants or, indirectly, by altering host-gene regulatory pathways. Results from these studies suggest biotechnological applications, which are also discussed