Publications by authors named "Sachin Kumar Tripathi"

We have previously found that human apolipoprotein E (apoE) is enriched on the envelope of infectious hepatitis B virus (HBV) and plays an important role in HBV infection and morphogenesis. Recently, we have demonstrated that the low-density lipoprotein receptor (LDLR) is required for efficient HBV infection. LDLR is a known apoE-binding receptor.

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Introduction: In Uttar Pradesh, India, there are many fatal head injuries as a result of road traffic accidents (RTAs). Studying the pattern and distribution of intracranial hemorrhages, a frequent complication of severe head trauma might provide vital information on the efficacy of traffic safety regulations. To improve road safety tactics and lower fatal head injuries in Uttar Pradesh, this study intends to assess the effect of road safety measures on the frequency and distribution of intracranial hemorrhages in fatal head injury patients.

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Introduction: The Gonds tribe, indigenous to the Sonbhadra region in Uttar Pradesh, India, faces unique challenges and disparities in women's health, particularly in the domains of menstrual health, pregnancy, and postpregnancy care. This study aims to shed light on the demographic patterns of these critical aspects of women's health among the Gonds tribe, providing valuable insights for healthcare interventions and policy development.

Aim: This study explores the demographic and socioeconomic factors affecting Gond women's health, focusing on menstrual hygiene and life stages before, during, and after pregnancy.

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Hepatitis C virus (HCV) infects the human liver, and its chronic infection is one of the major causes of Hepatocellular carcinoma. Translation of HCV RNA is mediated by an Internal Ribosome Entry Site (IRES) element located in the 5'UTR of viral RNA. Several RNA Binding proteins of the host interact with the HCV IRES and modulate its function.

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Host factors play essential roles in viral infection, and their interactions with viral proteins are necessary for establishing effective pathogenesis. p53 is a host factor that maintains genomic integrity by controlling cell-cycle progression and cell survival. It is a well-known tumor suppressor protein that gets activated by various stress signals, thereby regulating cellular pathways.

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Host protein HuR translocation from nucleus to cytoplasm following infection is crucial for the life cycle of several RNA viruses including hepatitis C virus (HCV), a major causative agent of hepatocellular carcinoma. HuR assists the assembly of replication-complex on the viral-3'UTR, and its depletion hampers viral replication. Although cytoplasmic HuR is crucial for HCV replication, little is known about how the virus orchestrates the mobilization of HuR into the cytoplasm from the nucleus.

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Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver diseases, such as fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Several cellular entities, including paraspeckles and their related components, are involved in viral pathogenesis and cancer progression. NEAT1 lncRNA is a major component of paraspeckles that has been linked to several malignancies.

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We have earlier shown that p53-FL and its translational isoform ∆40p53 are differentially regulated. In this study, we have investigated the cellular effect of ∆40p53 regulation on downstream gene expression, specifically miRNAs. Interestingly, ∆40p53 showed antagonistic regulation of miR-186-5p as compared to either p53 alone or a combination of both the isoforms.

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The cellular lipid pool plays a central role in hepatitis C virus (HCV) life cycle, from establishing infection to virus propagation. Here, we show that a liver abundant long noncoding RNA, highly upregulated in liver carcinoma (HULC), is upregulated during HCV infection and manipulates the lipid pool to favour virus life cycle. Interestingly, HULC was found to be crucial for the increase in number of lipid droplets in infected cells.

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