Id |
Subject |
Object |
Predicate |
Lexical cue |
T299 |
0-80 |
Sentence |
denotes |
Respiratory syncytial virus, human immunodeficiency virus, and hepatitis C virus |
T300 |
81-334 |
Sentence |
denotes |
Respiratory syncytial virus (RSV), also known as human respiratory cell fusion virus (HRSV) and human orthopneumovirus, is a virus that causes respiratory infections in which infected mucosal cells fuse to form a syncytium (Schweitzer and Justice 2020). |
T301 |
335-464 |
Sentence |
denotes |
It is the leading cause of lower respiratory tract infections and hospital visits in infancy and childhood (Read and Bosco 2020). |
T302 |
465-635 |
Sentence |
denotes |
RSV infection results in bronchiolitis, which is classically caused by activated macrophages and eventually resolved by alternatively activated macrophages (Shirey et al. |
T303 |
636-642 |
Sentence |
denotes |
2010). |
T304 |
643-816 |
Sentence |
denotes |
The promotion of these two alternative macrophage fates appears to be related to RSV-induced COX-2 and LXA4 and RvE1-mediated protective measures (Fig. 4) (Richardson et al. |
T305 |
817-836 |
Sentence |
denotes |
2005; Shirey et al. |
T306 |
837-843 |
Sentence |
denotes |
2014). |
T307 |
844-1117 |
Sentence |
denotes |
Also, although it does not directly act on the virus, RvD1 inhibits inflammatory signal transduction by polyinosinic-polycytidylic acid, an analogue of RNAs derived from respiratory viruses such as RSV, and the action of RvD1 is mediated by FPR2/ALX and GPR32 (Hsiao et al. |
T308 |
1118-1124 |
Sentence |
denotes |
2014). |
T309 |
1125-1287 |
Sentence |
denotes |
These reports suggest the critical role of SPMs and lipid mediator class shift in the host’s response to RSV in the initial control and final infection clearance. |
T310 |
1288-1468 |
Sentence |
denotes |
Human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retroviruses) and are classified into two based on the genetic characteristics and viral antigen, HIV-1 and HIV-2. |
T311 |
1469-1585 |
Sentence |
denotes |
HIV infection may progress to acquired immunodeficiency syndrome (AIDS), a progressive failure of the immune system. |
T312 |
1586-1704 |
Sentence |
denotes |
Over time, AIDS causes life-threatening opportunistic infections and a condition in which cancer thrives (Douek et al. |
T313 |
1705-1724 |
Sentence |
denotes |
2009; Powell et al. |
T314 |
1725-1731 |
Sentence |
denotes |
2016). |
T315 |
1732-2045 |
Sentence |
denotes |
When co-cultured with HIV-1 infected mononuclear cells and human glial cells (astrocytoma, glial and primary human astrocyte), tumour necrosis factor alpha (TNF-α) and interleukin-1β are produced, and large amounts of LTB4, LTD4, LXA4, and PAF, were also found in media from this co-culture (Fig. 4) (Genis et al. |
T316 |
2046-2052 |
Sentence |
denotes |
1992). |
T317 |
2053-2163 |
Sentence |
denotes |
So far, this is the only in vitro study to prove, that LXs are produced in direct response to viral infection. |
T318 |
2164-2239 |
Sentence |
denotes |
However, the role of LXs in this infection model has not been investigated. |
T319 |
2240-2465 |
Sentence |
denotes |
Synthetic peptides derived from human immunodeficiency virus type 1 gp120 activate the 7-transmembrane GPCR FPR2/ALX, down-regulating the expression and function of chemokine receptors CCR5 and CXCR4 in monocytes (Deng et al. |
T320 |
2466-2472 |
Sentence |
denotes |
1999). |
T321 |
2473-2563 |
Sentence |
denotes |
FPR2/ALX acts as an efficient core receptor for the primary isolate of HIV (Shimizu et al. |
T322 |
2564-2570 |
Sentence |
denotes |
2008). |
T323 |
2571-2681 |
Sentence |
denotes |
Viral entries through the alternative core receptors (CoR) CCR3 and FPR2/ALX depend on the HIV type 1 subtype. |
T324 |
2682-2827 |
Sentence |
denotes |
Viruses pseudotyped with subtype A and C Env proteins use the recently described alternative CoR FPR2 more efficiently than CCR3 (Nedellec et al. |
T325 |
2828-2834 |
Sentence |
denotes |
2009). |
T326 |
2835-2870 |
Sentence |
denotes |
ChemR23 also acts as a CoR for HIV. |
T327 |
2871-3010 |
Sentence |
denotes |
At this time, HIV-1 and HIV-2 appear to use the N-terminus and the second extracellular loop of ChemR23 during infection (Martensson et al. |
T328 |
3011-3017 |
Sentence |
denotes |
2006). |
T329 |
3018-3145 |
Sentence |
denotes |
As mentioned above, research is needed to determine the role of SPMs that act as ligands for FPR2 and ChemR23 in HIV infection. |
T330 |
3146-3292 |
Sentence |
denotes |
Hepatitis C virus (HCV) is a positive-sense single-stranded RNA virus of the family Flaviviridae with a small (55–65 nm size) envelope (Lee et al. |
T331 |
3293-3299 |
Sentence |
denotes |
2017). |
T332 |
3300-3454 |
Sentence |
denotes |
The HCV is the cause of hepatitis C and some cancers such as liver cancer (hepatocellular carcinoma, abbreviated HCC) and lymphoma in humans (Ferri et al. |
T333 |
3455-3483 |
Sentence |
denotes |
2015; Rusyn and Lemon 2014). |
T334 |
3484-3564 |
Sentence |
denotes |
To date, there appears to be no report on the effectiveness of SPMs against HCV. |
T335 |
3565-3712 |
Sentence |
denotes |
However, HCV peptide (C5A), an amphiphilic α-helix peptide of HCV, is an activator of the N-formyl peptide receptor in human phagocytes (Lin et al. |
T336 |
3713-3719 |
Sentence |
denotes |
2011). |
T337 |
3720-3810 |
Sentence |
denotes |
This suggests the possibility of interaction between RvD1 and LXA4, FPR families, and HCV. |
T338 |
3811-3933 |
Sentence |
denotes |
Vitamin D metabolites inhibit HCV and upregulate GPR37 gene expression, which induces cellular autophagy (Gutierrez et al. |
T339 |
3934-3940 |
Sentence |
denotes |
2014). |
T340 |
3941-4072 |
Sentence |
denotes |
PD1 was recently proposed as a new ligand for GPR37, and some studies suggest a possible relationship between PD1 and HCV (Fig. 4). |
T341 |
4073-4223 |
Sentence |
denotes |
SAA also has antiviral effects against HCV, however, it induces chronic inflammation through FPR2/ALX, causing liver damage (Abouelasrar Salama et al. |
T342 |
4224-4230 |
Sentence |
denotes |
2019). |
T343 |
4231-4396 |
Sentence |
denotes |
Although research has not been conducted yet, RvD1 and LXA4, which inhibit the action of SAA, are likely to suppress liver damage caused by SAA during HCV infection. |