<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(7)</volume><submitter>Yi J</submitter><pubmed_abstract>Cell-free DNA (cf-DNA) in blood represents a promising DNA damage response triggered by virus infection or trauma, tumor, etc. Hantavirus primarily causes two diseases: haemorrhagic fever with renal syndrome (HFRS) and Hantavirus cardiopulmonary syndrome (HCPS), depending on different Hantavirus species. The aim of this study was to evaluate plasma cf-DNA levels in acute phase of HFRS, and to correlate plasma cf-DNA with disease severity and plasma Hanttan virus (HTNV) load. We observed the appearance of cf-DNA in 166 plasma samples from 76 HFRS patients: the plasma cf-DNA levels peaked at the hypotensive stage of HFRS, and then decreased gradually. Until the diuretic stage, there was no significant difference in plasma cf-DNA level between patients and the healthy control. Exclusively in the febrile/hypotensive stage, the plasma cf-DNA levels of severe/critical patients were higher than those of the mild/moderate group. Moreover, the plasma cf-DNA value in the early stage of HFRS was correlated with HTNV load and disease severity. In most of the patients, plasma cf-DNA displayed a low-molecular weight appearance, corresponding to the size of apoptotic DNA. In conclusion, the plasma cf-DNA levels were dynamically elevated during HFRS, and correlated with disease severity, which suggests that plasma cf-DNA may be a potential biomarker for the pathogenesis and prognosis of HFRS.</pubmed_abstract><journal>Viruses</journal><pagination>2723-34</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4113790</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Increased plasma cell-free DNA level during HTNV infection: correlation with disease severity and virus load.</pubmed_title><pmcid>PMC4113790</pmcid><pubmed_authors>Yi J</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Jin B</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Zhuang R</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Ma Y</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Liu B</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Increased plasma cell-free DNA level during HTNV infection: correlation with disease severity and virus load.</name><description>Cell-free DNA (cf-DNA) in blood represents a promising DNA damage response triggered by virus infection or trauma, tumor, etc. Hantavirus primarily causes two diseases: haemorrhagic fever with renal syndrome (HFRS) and Hantavirus cardiopulmonary syndrome (HCPS), depending on different Hantavirus species. The aim of this study was to evaluate plasma cf-DNA levels in acute phase of HFRS, and to correlate plasma cf-DNA with disease severity and plasma Hanttan virus (HTNV) load. We observed the appearance of cf-DNA in 166 plasma samples from 76 HFRS patients: the plasma cf-DNA levels peaked at the hypotensive stage of HFRS, and then decreased gradually. Until the diuretic stage, there was no significant difference in plasma cf-DNA level between patients and the healthy control. Exclusively in the febrile/hypotensive stage, the plasma cf-DNA levels of severe/critical patients were higher than those of the mild/moderate group. Moreover, the plasma cf-DNA value in the early stage of HFRS was correlated with HTNV load and disease severity. In most of the patients, plasma cf-DNA displayed a low-molecular weight appearance, corresponding to the size of apoptotic DNA. In conclusion, the plasma cf-DNA levels were dynamically elevated during HFRS, and correlated with disease severity, which suggests that plasma cf-DNA may be a potential biomarker for the pathogenesis and prognosis of HFRS.</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jul</publication><modification>2024-11-12T04:52:39.941Z</modification><creation>2019-03-27T01:32:58Z</creation></dates><accession>S-EPMC4113790</accession><cross_references><pubmed>25029493</pubmed><doi>10.3390/v6072723</doi></cross_references></HashMap>