| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T405 |
0-107 |
Sentence |
denotes |
There is currently no specific pharmacotherapy to combat SARS-CoV-2 infection and its pathological effects. |
| T406 |
108-503 |
Sentence |
denotes |
Actually, the use of plasma from convalescent COVID-19 patients or of SARS-CoV-2-specific neutralizing antibodies has been shown to be a promising option for the treatment of critically COVID-19 patients [32,33,34,35,36,37,172,173]; however, it has some limitations that might be overcome by vaccine strategies or by the production of specific anti SARS-Co-V-2 therapeutic monoclonal antibodies. |
| T407 |
504-680 |
Sentence |
denotes |
Despite the promising data that demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates [174], we cannot be sure to get a vaccine against SARS-CoV-2 (see [175]). |
| T408 |
681-931 |
Sentence |
denotes |
Indeed, animals immunized with inactivated SARS-CoV vaccines developed a severe (asthma-like) lung eosinophilic immunopathology when challenged with SARS-CoV, further indicating a central role of eosinophil “balanced numbers” in this pathology [176]. |
| T409 |
932-1115 |
Sentence |
denotes |
Vaccines might generate antibodies against viral ligand/ACE2 complex that finally blocks ACE2 activity during SARS-CoV infection and consequent downstream asthma-like events/symptoms. |
| T410 |
1116-1427 |
Sentence |
denotes |
On the other hand, fatal outcomes in SARS-CoV infection correlated with a cytokine storm involving elevated Th2 serum cytokines (including IL-4, IL-5 and IL-10), suggesting that an increase of Th2 cytokines possibly mediated by virus-specific CD4 T cells might be crucial in the severe forms of infection [110]. |
| T411 |
1428-1842 |
Sentence |
denotes |
In addition to cytokine profile (such as IL-10), eosinopaenia, tachycardia, normo/hypotension (although COVID-19 and hypoxia increase Ang II and many patients are “hypertensive” and/or receiving anti-hypertensive medications) and hypoxia in SARS-CoV-2 patients are compatible with downstream events stemming from both an excessive ACE2 pathway upregulation and activation of positive feedback loops (see Figure 2). |
| T412 |
1843-2039 |
Sentence |
denotes |
ACE2 and (anti-inflammatory) IL-10 hyperproduction may ultimately trigger subsequent compensatory (and deleterious) responses, leading to both renin/ACE and pro-inflammatory cytokine upregulation. |
| T413 |
2040-2159 |
Sentence |
denotes |
In line with this hypothesis, a longitudinal study showed that IL-6 increases late during the COVID-19 progression [3]. |
