Regulation of host gene expression by J paramyxovirus.

Paramyxoviruses are negative-sense, single-stranded RNA viruses that are associated with numerous diseases in humans and animals. J paramyxovirus (JPV) was first isolated from moribund mice (Mus musculus) with hemorrhagic lung lesions in Australia in 1972. In 2016, JPV was classified into the newly established genus Jeilongvirus. Novel jeilongviruses are being discovered worldwide in wildlife populations. However, the effects of jeilongvirus infection on host gene expression remains uncharacterized. To address this, cellular RNA from JPV-infected mouse fibroblasts was collected at 2, 4, 8, 12, 16, 24, and 48 hours post-infection (hpi) and were sequenced using single-end 75 base pairs (SE75) sequencing chemistry on an Illumina NextSeq platform. Differentially expressed genes (DEGs) between the virus-infected replicates and mock replicates at each timepoint were identified using the Tophat2-Cufflinks-Cuffdiff protocol. At 2 hpi, 11 DEGs were identified in JPV-infected cells, while 1,837 DEGs were detected at 48 hpi. A GO analysis determined that the genes at the earlier timepoints were involved in interferon responses, while there was a shift towards genes that are involved in antigen processing and presentation processes at the later timepoints. At 48 hpi, a KEGG analysis revealed that many of the DEGs detected were involved in pathways that are important for immune responses. qRT-PCR verified that Rtp4, Ifit3, Mx2, and Stat2 were all upregulated during JPV infection, while G0s2 was downregulated. After JPV infection, the expression of inflammatory and antiviral factors in mouse fibroblasts changes significantly. This study provides crucial insight into the different arms of host immunity that mediate Jeilongvirus infection. Understanding the pathogenic mechanisms of Jeilongvirus will lead to better strategies for the prevention and control of potential diseases that may arise from this group of viruses.

Clinical Course of Vitreomacular Traction Managed Initially by Observation.

BACKGROUND AND OBJECTIVE: To investigate the clinical course and outcomes of patients with vitreomacular traction (VMT) managed initially by observation. PATIENTS AND METHODS: This noncomparative case series included patients with a diagnosis of VMT based on clinical symptoms and findings on spectral-domain optical coherence tomography (SD-OCT) between 2005 and 2014. VMT was documented using a standardized grading system based on the degree of distortion of the foveal contour. Data were collected at five retina clinics using standardized collection forms. Visual acuity, changes in SD-OCT findings, and timing of the release of VMT as seen on SD-OCT were recorded. RESULTS: The study included 230 eyes of 185 patients. Mean age was 72.5 years, and mean follow-up was 32 months. At baseline, VMT grading was grade 1 in 92 eyes (40%), grade 2 in 118 eyes (51.3%), and grade 3 in 20 eyes (8.7%). By last follow-up, spontaneous release of VMT occurred in 73 eyes (31.7%). Spontaneous release of VMT occurred at a mean of 18 months (median: 10.9 months) after initial visit. Mean logMAR best corrected visual acuity (BCVA) was 0.28 (20/55) (range: 20/20 to 20/400) at baseline and 0.25 (20/51) (range: 20/20 to 20/400) at last follow-up. Pars plana vitrectomy was performed in 10 eyes (4.1%) for macular hole (six eyes) and increased VMT (four eyes); BCVA was at least 20/40 in eight of the 10 eyes at last follow-up. CONCLUSION: Patients with VMT generally had a favorable clinical course when managed initially by observation. Spontaneous release of VMT occurred in approximately one-third of patients. At last follow-up, pars plana vitrectomy was performed in fewer than 5% of patients.

Complement, age-related macular degeneration and a vision of the future.

Age-related macular degeneration (AMD) is one of the most well-characterized late-onset, complex trait diseases. Remarkable advances in our understanding of the genetic and biological foundations of this disease were derived from a recent convergence of scientific and clinical data. Importantly, the more recent identification of AMD-associated variations in a number of complement pathway genes has provided strong support for earlier, paradigm-shifting studies that suggested that aberrant function of the complement system plays a key role in disease etiology. Collectively, this wealth of information has provided an impetus for the development of powerful tools to accurately diagnose disease risk and progression and complement-based therapeutics that will ultimately delay or prevent AMD. Indeed, we are poised to witness a new era of a personalized approach toward the assessment, management, and treatment of this debilitating, chronic disease.