ABSTRACT
The sacroiliac joints connect the base of the sacrum to the ilium. When inflamed, they are suspected to cause low back pain. Inflammation of the sacroiliac joints is called sacroiliitis. The severity of the pain varies and depends on the degree of inflammation. Sacroiliitis is a hallmark of seronegative spondyloarthropathies. The presence or absence of chronic sacroiliitis is an important clue in the diagnosis of low back pain. This article aims to provide a concise overview of the anatomy, physiology, and molecular biology of sacroiliitis to aid clinicians in the assessment and management of sacroiliitis. For this narrative review, we evaluated articles in English published before August 2019 in PubMed. Then, we selected articles related to the painful manifestations of the sacroiliac joint. From the retrieved articles, we found that chronic sacroiliitis may be caused by various forms of spondyloarthritis, such as ankylosing spondyloarthritis. Sacroiliitis can also be associated with inflammatory bowel disease, Crohn’s disease, gout, tuberculosis, brucellosis, and osteoarthritis, indicating common underlying etiological factors. The pathophysiology of sacroiliitis is complex and may involve internal, environmental, immunological, and genetic factors. Finally, genetic factors may also play a central role in progression of the disease. Knowing the genetic pre-disposition for sacroiliitis can be useful for diagnosis and for formulating treatment regimens, and may lead to a substantial reduction in disease severity and duration and to improved patient performance.
ABSTRACT
The functional receptor for type III interferons [IFNs] is a heterodimer of IFNLR1 and IL10R2. IFNLR1 is expressed in a highly tissue specific manner, with epithelial and liver tissue as the prime expressing tissues in humans. However, knowledge about the molecular pathways responsible for regulating the expression of IFNLR1 is yet unknown. In this study, various bioinformatics tools were used to predict the scores of signal peptides of IFN-lamda-R1 and IFN-lamda-R1, which was considered as an important difference in the expression of both receptors or participation in regulating the IFNLR1 gene. In silico study revealed that the signal peptide of IFN-lamda-R1 had more potential than the signal peptide of IFN-lamda-R1 but changing the signal peptide of wild type IFN-lamda-R1 with the signal peptide of IFN-lamda-R1 in wet lab had barely shown any differences. Selective expression of IFN-lamda-R1 was considered to be a plus point towards the targeted anti-viral activity of IFN-lamda-s but artificial control on its expression will surely make IFN-lamda-s a better drug with enhanced activity. The results of this study may help us in contributing some understanding towards the mechanisms involved in the selective expression of IFNLR1 and exceptionalities involved
ABSTRACT
Hepatitis B virus [HBV] is a well known agent of liver diseases. HBV disease burden varies across the globe with regions from low to high endemicity. Pakistan lies in the intermediate endemic zone, with high rate of mortality due to liver disease, cirrhosis and hepatocellular carcinoma. There is a wide range of heterogeneity in relation to HBV genotypes and sub- genotypes and in their patterns of pathogenesis virulence and response to antiviral therapy. A large number of HBV genomic variations are associated with clinical outcomes such as hepatocellular carcinoma and liver cirrhosis. Thus, the present study aims to analyze PreS2 gene sequence from HBV isolates and their phylogeny. To investigate this, a study was conducted on twenty one HBV chronically infected individuals, serum samples were subjected to PCR with specific primers for PreS2 region of HBV genotype D and then sequenced. Point mutations: A39V, P41H and L42I were found in cell permeability domain of PreS2 protein. However, MHC class I and II epitopes were conserved in all sequences. Phylogenetic analysis was carried out by comparing the nucleotide sequence with 22 reference sequences of HBV sub- genotype D retrieved from the GeneBank. Phylogenetic analysis showed that two of our isolates, ASAB1[2266] and ASB3[PIMS 7] shared cluster 1 with China D1, Pakistan D1, Iran D1, and Turkey D1. Meanwhile, ASAB2 [HF2] was grouped in cluster 2 with Lebanese D2 and Brazil D2