Id |
Subject |
Object |
Predicate |
Lexical cue |
T868 |
0-64 |
Sentence |
denotes |
HIV likely damages OLs through both direct and indirect actions. |
T869 |
65-140 |
Sentence |
denotes |
OLs lack CD4, and reports of OL infection by HIV are variable (Esiri et al. |
T870 |
141-162 |
Sentence |
denotes |
1991; Albright et al. |
T871 |
163-189 |
Sentence |
denotes |
1996; Wohlschlaeger et al. |
T872 |
190-298 |
Sentence |
denotes |
2009); thus, HIV infection of OLs is unlikely a major avenue of OL or white matter damage (discussed below). |
T873 |
299-486 |
Sentence |
denotes |
Alternatively, bystander damage to OLs through the production of “virotoxins” and “cellular toxins” (Nath 1999) by infected neighboring cells is more likely to be operative (Hauser et al. |
T874 |
487-503 |
Sentence |
denotes |
2009; Zou et al. |
T875 |
504-523 |
Sentence |
denotes |
2015; Jensen et al. |
T876 |
524-540 |
Sentence |
denotes |
2019; Zou et al. |
T877 |
541-547 |
Sentence |
denotes |
2019). |
T878 |
548-602 |
Sentence |
denotes |
ARVs also contribute to OL cytotoxicity (Jensen et al. |
T879 |
603-621 |
Sentence |
denotes |
2015; Festa et al. |
T880 |
622-641 |
Sentence |
denotes |
2019; Jensen et al. |
T881 |
642-648 |
Sentence |
denotes |
2019). |
T882 |
649-840 |
Sentence |
denotes |
HIV-1 Tat directly induces damage in isolated OLs through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/N-methyl-D-aspartic acid (NMDA) receptor-dependent mechanisms (Zou et al. |
T883 |
841-910 |
Sentence |
denotes |
2015) and is also associated with abnormal Kv1.3 activity (Liu et al. |
T884 |
911-917 |
Sentence |
denotes |
2017). |
T885 |
918-1014 |
Sentence |
denotes |
Immature OLs are preferentially targeted by Tat compared to differentiated OLs (Khurdayan et al. |
T886 |
1015-1032 |
Sentence |
denotes |
2004; Hahn et al. |
T887 |
1033-1049 |
Sentence |
denotes |
2012; Zou et al. |
T888 |
1050-1062 |
Sentence |
denotes |
2015, 2019). |
T889 |
1063-1311 |
Sentence |
denotes |
While the reasons why immature OLs are more susceptible to Tat are unclear, unlike mature OLs, Tat preferentially upregulates GSK-3β signaling in undifferentiated OLs by inhibiting Ca2+/calmodulin-dependent protein kinase II β (CaMKIIβ) (Zou et al. |
T890 |
1312-1318 |
Sentence |
denotes |
2019). |