Hepatitis E virus mixed infection in immunocompetent patient.
Ontology highlight
ABSTRACT:
SUBMITTER: Smith DB
PROVIDER: S-EPMC3647676 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Hepatitis E virus (HEV) infection causes acute liver disease, but severe infections are rare in immunocompetent patients. We describe a case of HEV infection in a previously healthy male trauma patient in France who received massive transfusions. Genotyping confirmed HEV in a transfused platelet pool and the donor.
| S-EPMC5176217 | biostudies-literature
Project description:Lophomonas blattarum (L. blattarum) is a protozoan parasite living in intestinal tracts of termites and cockroaches. Chen and Meng from China repoted first case of pulmonary L. blattarum infection in 1993. 137 cases have only been reported in literature between 1993 to 2013. Majority of these infections occur in immunocompromised patients and have been reported from China. We report a case of this rare entity in an immunocompetent young Indian male.
| S-EPMC5112827 | biostudies-other
Project description:Hepatitis B virus (HBV) is the leading cause of liver disease and hepatic carcinoma (HCC). Approximately 350 million people worldwide are infected with HBV and at risk of chronicity. An efficient HBV-tolerant murine model that mimics HBV infection in humans is desirable for HBV-related research. In this study, we investigated and established a murine model by hydrodynamic injection (HDI) of pAAV/HBV into the tail vein of AAVS1 site element-transgenic mice. In 80% of the injected mice, the serum level of HBsAg reached 103-4 IU/ml and persisted for more than half a year. Next, the model was used to evaluate RNA interference (RNAi)-based antiviral therapy. Data obtained using the model demonstrated that this model will facilitate the elucidation of the mechanisms underlying chronic HBV infection and will also be useful for evaluating new antiviral drugs.
| S-EPMC5111840 | biostudies-other
Project description:An animal model for human hepatitis B virus (HBV) tolerance is needed to investigate the mechanisms. This model will also facilitate therapeutic strategies for the existing 350 million patients with chronic hepatitis B. We established a mouse model by hydrodynamic injection of an engineered, replication-competent HBV DNA into the tail veins of C57BL/6 mice. In 40% of the injected mice, HBV surface antigenemia persisted for > 6 months. Viral replication intermediates, transcripts, and proteins were detected in the liver tissues of the injected mice for up to 1 year. The tolerance toward HBV surface antigen in this model was shown to be due to an insufficient cellular immunity against hepatitis B core antigen, as was documented in humans. This animal model will accelerate further genetic and mechanistic studies of human chronic hepatitis B infection.
| S-EPMC1635544 | biostudies-literature
Project description:Human immunodeficiency virus (HIV) and hepatitis C virus (HCV) share the same transmission routes; therefore, coinfection is frequent. An estimated 5-10 million individuals alone in the western world are infected with both viruses. The majority of people acquire HCV by injection drug use and, to a lesser extent, through blood transfusion and blood products. Recently, there has been an increase in HCV infections among men who have sex with men. In the context of effective antiretroviral treatment, liver-related deaths are now more common than Acquired Immune Deficiency Syndrome-related deaths among HIV-HCV coinfected individuals. Morbidity and mortality rates from chronic HCV infection will increase because the infection incidence peaked in the mid-1980s and because liver disease progresses slowly and is clinically silent to cirrhosis and end-stage-liver disease over a 15-20 year time period for 15%-20% of chronically infected individuals. HCV treatment has rapidly changed with the development of new direct-acting antiviral agents; therefore, cure rates have greatly improved because the new treatment regimens target different parts of the HCV life cycle. In this review, we focus on the epidemiology, diagnosis and the natural course of HCV as well as current and future strategies for HCV therapy in the context of HIV-HCV coinfection in the western world.
| S-EPMC4161799 | biostudies-literature
Project description:The bacterial genus Gordona includes seven species of mycolic acid-containing actinomycetes which are cultured from environmental sources and rarely from clinical samples. They have been implicated in primary pulmonary diseases, nosocomial wound infections, and central nervous system infections in two immunocompromised patients. We isolated Gordona terrae from the cerebrospinal fluid sample of an immunocompetent patient with meningitis and multiple brain abscesses and detected Gordona terrae DNA in the abscesses. The outcome was good at the 4-year follow-up, after prolonged treatment with trimethoprim-sulfamethoxazole. Phenotypic identification of this isolate was confirmed by analysis of the 16S rRNA gene sequence, which shared 100% homology with that of G. terrae reference strains. Physicians and clinical microbiologists must be aware of the occurrence of Gordona species infection not only among immunocompromised patients but among all patients. Accurate identification of Gordona species may be accomplished by molecular techniques.
| S-EPMC229584 | biostudies-other
Project description:Progress toward understanding Zika virus (ZIKV) pathogenesis is hindered by lack of immunocompetent small animal models, in part because ZIKV fails to effectively antagonize Stat2-dependent interferon (IFN) responses in mice. To address this limitation, we first passaged an African ZIKV strain (ZIKV-Dak-41525) through Rag1-/- mice to obtain a mouse-adapted virus (ZIKV-Dak-MA) that was more virulent than ZIKV-Dak-41525 in mice treated with an anti-Ifnar1 antibody. A G18R substitution in NS4B was the genetic basis for the increased replication, and resulted in decreased IFN-β production, diminished IFN-stimulated gene expression, and the greater brain infection observed with ZIKV-Dak-MA. To generate a fully immunocompetent mouse model of ZIKV infection, human STAT2 was introduced into the mouse Stat2 locus (hSTAT2 KI). Subcutaneous inoculation of pregnant hSTAT2 KI mice with ZIKV-Dak-MA resulted in spread to the placenta and fetal brain. An immunocompetent mouse model of ZIKV infection may prove valuable for evaluating countermeasures to limit disease.
| S-EPMC5953559 | biostudies-literature
Project description:ObjectiveThe impact of hepatitis B virus (HBV) preS/S-gene mutations on occult HBV infection (OBI) is not fully understood. This study characterized multiple novel HBV preS/S-gene mutants obtained from an OBI patient.MethodsPreS/S-gene mutants were analyzed by clonal sequencing. Viral replication and expression were analyzed by transfecting HBV genomic recombinants into HepG2 cells.ResultsTwenty-one preS/S-gene mutants were cloned from four sequential serum samples, including 13 mutants that were not previously documented: (1) sI/T126V+sG145R; (2) preS1 nt 3014-3198 deletion; (3) preS1 nt 3046-3177 deletion; (4) preS1 nt 3046-3177 deletion+s115-116 "INGTST" insertion; (5) preS1 nt 3046-3177 deletion+s115-116 "INGTST" insertion+sG145R; (6) preS1 nt 3115-3123 deletion+sQ129N; (7) preS1 nt 3115-3123 deletion+s126-127 "RPCMNCTI" insertion; (8) s115-116 "INGTST" insertion; (9) s115-116 "INGTST" insertion+sG145R; (10) s126-127 "RPCMNCTI" insertion; (11) preS1 nt 2848-2862 deletion+preS2 initiation codon M→I; (12) s122-123 "KSTGLCK" insertion+sQ129N; and (13) preS2 initiation codon M→I+s131-133TSM→NST. The proportion of preS1 nt 3046-3177 deletion and preS2 initiation codon M→I+s131-133TSM→NST mutants increased in the viral pool with prolonged disease. The 13 novel OBI-related mutants showed a 51.2-99.9% decrease in HBsAg levels compared with that of the wild type. Additional N-glycosylation-associated mutations, sQ129N and s131-133TSM→NST, but not s126-127 "RPCMNCTI," greatly attenuated anti-HBs binding to HBsAg. Compared with the wild type, replication and surface antigen promoter II activity of the preS1 nt 3046-3177 deletion mutant decreased by 43.3% and 97.0%, respectively.ConclusionPreS/S-gene mutations may play coordinated roles in the presentation of OBI and might be associated with disease progression. This has implications for HBV diagnosis and vaccine improvement.
| S-EPMC4868315 | biostudies-literature
Project description:The complement system bridges innate and adaptive immunity against microbial infections, with viral infection being a major trigger. Activation of the classical, alternative, and lectin pathways have been reported in chronic hepatitis C virus (HCV) infection and/or cryoglobulinemia. HCV infection leads to dysregulation of complement-mediated immune responses. Clinical and experimental evidence support involvement of complement in intra- and extrahepatic manifestations of HCV infection, such as liver fibrosis and type II cryoglobulinemia. In this review, we summarize studies that have investigated the interplay between HCV and the complement system to establish chronic infection and autoimmunity, as well as the association between HCV pathogenesis and abnormal complement profiles. Several unanswered questions are highlighted which suggest additional informative lines of investigation.
| S-EPMC5992393 | biostudies-literature
Project description:Acute hepatitis E virus (HEV) infections are usually self-limiting in immunocompetent patients. HEV persistence has been described only in immunosuppressed patients such as solid-organ transplant recipients, patients with hematological diseases, or patients with human immunodeficiency virus (HIV) infection.A 61-year-old patient was admitted in hospital for jaundice and asthenia.The patient had underlying cirrhosis and developed a chronic HEV infection.Ribavirin therapy was initiated.Ribavirin therapy for 12 months allowed the clearance of the virus and HEV viral load remained undetectable thereafter. This patient had taken no immunosuppressive drugs, was not suffering from any autoimmune disease and was not infected with HIV. We studied the patient's anti-HEV immune response months after the viral clearance. His peripheral blood mononuclear cells (PBMC) were stimulated in vitro by HEV peptides. The patient had a mild T lymphopenia, but polyclonal stimulation of PBMC showed a robust T cell response. The response of his anti-HEV specific interferon-? producing T cells was low.Other studies are now needed to identify the population with a chronic evolution of HEV infection despite no apparent immunodepression.
| S-EPMC5626257 | biostudies-literature