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Abstract Physiological Basis Behavioral variant frontotemporal dementia is a common symptom of young-onset dementia with a portion of patients presenting pathologically and genetically with amyotrophic lateral sclerosis. The human endogenous retrovirus K is elevated in ALS serum and is associated with ALS TDP-43 pathology, according to previous studies. Methods We analyzed the HERV-K env gene in sporadic bvFTD, sporadic ALS, and control serum by ddPCR. Result Here, we show that HERV-K env levels are noticeably elevated in bvFTD in comparison to control serum, differentiating situations with an AUC value of 0. 867. HERV-K env levels are also elevated in bvFTD's superior frontal cortex, with the HERV-K reverse transcriptase protein and TDP-43 deposit localized to the neuronal cytoplasm, and TDP-43 deposit are also localized to the neuronal cytoplasm.
Source link: https://doi.org/10.1038/s43856-021-00060-w
paraphrase transcriptase activity in patients has been consistently found in studies of ALS. After multiple-testing correction, there was one ERV locus that showed significant rise expression in post-mortem motor cortex tissue samples in the discovery study. HML6_3p21. 31c was consistently elevated in ALS in motor cortex and cerebellum tissue tissue, according to six replication post-mortem studies. There were no significant differences between ALS and controls in ERV family expression between ALS and controls. Our findings support the theory that specific ERV loci are involved in ALS pathology.
Source link: https://doi.org/10.1038/s41598-021-93742-3
Abstract Atypical Teratoid Rhabdoid Tumor is a rare pediatric central nervous system cancer caused by deletion or mutation of SMARCB1 (a tumor suppressor gene). In this research, we found that SMARCB1 controls Human Endogenous Retrovirus K expression. In both the intracellular and extracellular compartments of all AT/RT cell lines and 95 percent of AT/RT patient tissues tested, we found HML-2 env expression in both the intracellular and extracellular compartments, as well as in 95% of AT/RT patient tissues. HML-2 transcription increased after a SMARCB1 knock-down in neural stem cells, which resulted in an increase in HML-2 transcription. We discovered that SMARCB1 binds near the HML-2 promoter, inhibiting transcription by chromatin immunoprecipitation, as shown by chromatin immunoprecipitation; the restoration of SMARCB1 expression in AT/RT cell lines has significantly reduced HML-2 expression. HML-2 knock-down with shRNA, siRNA, and CRISPR-dCas9 all decreased Ras expression as measured by qRT-PCR, meaning that HML-2 modulates MAPK/ERK signaling in AT/RT cells.
Source link: https://doi.org/10.1038/s41598-021-92223-x
In both pregnancy trimester and the postpartum period, antibodies against HHV-6A/B were significantly higher in P-MS than in P-HC. Taking into account MSRV env mRNA expression, the prevalence in the first trimester of pregnancy was significantly higher in P-MS patients who suffered with relapses during pregnancy. When it comes down, high IgM antibody titres against HHV-6A/B and MSRV mRNA expression during the first trimester of pregnancy may have served as relapse predictors for the gestation/postpartum periods.
Source link: https://doi.org/10.1038/s41598-021-87941-1
Abstract: We present a recombinant baculoviral vector-based DNA vaccination system against Middle East respiratory syndrome coronavirus and the acute respiratory syndrome coronavirus-2. The human endogenous retrovirus envelope gene, a non-replicating baculovirus envelope gene, was introduced as a DNA vaccine vector for gene delivery into human cells by a non-replicating baculovirus envelope gene. DNA encoding SARS-CoV2 S-full or S1 or a MERS-CoV NTD domain-fused SARS-CoV2 RBD was introduced into AcHERV's genome for COVID19 vaccine construction.
Source link: https://doi.org/10.1038/s41541-021-00303-w
Ascl1 converts proliferative astroglia from the early postnatal cerebral cortex to interneuron-like cells in an in vitro way. In vivo, we investigated whether Ascl1 could similarly trigger neuronal reprogramming of glia in the postnatal mouse cerebral cortex. In vivo Ascl1-transduced glial cells were converted into doublecortin-immunoreactive neurons with only marginal effectiveness, in contrast to the effective reprogramming that was observed in vitro. Compared to glial fibrillary acidic protein-positive astrocytes, we saw a dramatic decline in the relative number of retrovirus-positive oligodendrocyte progenitor cells. This rise in OPCs was not due to Ascl1-mediated astrocyte-to-OPC fate conversion, according to genetic fate mapping, which showed that this rise in OPCs was not related to Ascl1-mediated astrocyte-to-OPC conversion. Ascl1 is a selective promoter of OPC proliferation, rather than inducing neuronal reprogramming of glia in the early postnatal cortex, according to our findings.
Source link: https://doi.org/10.3389/fnins.2022.919462
Human endogenous retroviruses originating from exogenous retroviral infections of germ cells millions of years ago have the ability to cause human disease. Particularly in advanced HCC, Syncytin-1 expression was up-regulated in HCC compared to nearby non-tumorous tissues, particularly in advanced HCC. Syncytin-1 overexpression was positively associated with HCC patients with serum HBsAg positives, according to a new report. Syncytin-1 enhanced cell proliferation, metastasis, and tumorigenicity in HCC, according to experimental studies in vitro and in vivo. According to the HCC's review, the mitogen-activated protein kinase pathway was involved in the disease. According to our clinical findings, the phosphorylation MEK1/2 and ERK1/2 were elevated in HCC when compared to nearby non-tumorous tissues. It showed the linear correlation between Syncytin-1 expression and elevated MEK1/2 and ERK1/2 phosphorylation levels in HCC. Syncytin-1 promoted HCC progression and doxorubicin resistance via the inflammation-activated MEK/ERK pathway in conclusion.
Source link: https://doi.org/10.1038/s41420-021-00562-5
Abstract The Vietnamese native pig u2014a porcine breed with a small body u2014 has been used as a biomedical animal model. Here, we show that, in comparison to other breeds, VnPs have fewer copies of porcine endogenous retroviruses, which pose a danger to xenotransplantation of pig organs to humans. The most accurate porcine reference genome was used to calculate nrPERV loci based on the most recent porcine reference genome, RetroSeq. In the inferred areas, LTRs were detected using de novo sequencing read assembly near the loci containing the target site duplication sequences.
Source link: https://doi.org/10.1038/s41598-022-14654-4
Several live-attenuated vaccinations for companion animals made using the Crandell-Rees feline kidney cell line were infected with a replication-competent feline ERV strain named RD-114 virus, according to We previously reported that several live-attenuated vaccines prepared using the Crandell-Rees feline kidney cell line were contaminated with a replica-competent feline ERV related to a replication-competent feline kidney cell line Multiple RD-114 virus-related proviruses in CRFK cells can also be produced by recombination of several RD-114 virus-related proviruses. We also found that the infectious RD-114 virus can be derived by recombination of several RD-114 virus-related proviruses. We also succeeded in establishing RDRS knockout CRFK cells that do not produce infectious RD-114 virus as a result of this. In RDKO_CRFK cells, the growth kinetics of feline herpesvirus type 1, calicivirus, and panleukopenia virus differed from those in parental cells, but all of them had high titers above 10 7 TCID 50 /mL. This study found that RDRS env gene knockout CRFK cells could be useful as a cell line for the manufacture of live-attenuated vaccines or biological products with no risk of infectious ERV contamination.
Source link: https://doi.org/10.1038/s41598-022-10497-1
In colorectal cancer samples, many TEs, including the pluripotency-related human endogenous retrovirus H, are abnormally present, according to this study. Transcriptional upregulation of HERVH has been attributed to mutations in many tumor suppressors, including ARID1A. Increasing transcription in various HERVH loci increases thanks to a lack of ARID1B's compensatory activity. Suppression of HERVH in CRC cells and patient-derived organoids reduces tumor formation. HERVH transcripts colocalize with nuclear BRD4 foci, modulating their metabolism and co-regulating multiple target genes.
Source link: https://doi.org/10.1038/s41467-022-31197-4
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