Increased expression of CD38 on endothelial cells in SARS-CoV-2 infection in cynomolgus macaques

Virology. 2024 Mar 14;594:110052. doi: 10.1016/j.virol.2024.110052. Online ahead of print.ABSTRACTSARS-CoV-2 infection causes activation of endothelial cells (ECs), leading to dysmorphology and dysfunction. To study the pathogenesis of endotheliopathy, the activation of ECs in lungs of cynomolgus macaques after SARS-CoV-2 infection and changes in nicotinamide adenine dinucleotide (NAD) metabolism in ECs were investigated, with a focus on the CD38 molecule, which degrades NAD in inflammatory responses after SARS-CoV-2 infection. Activation of ECs was seen from day 3 after SARS-CoV-2 infection in macaques, with increases of intravascular fibrin and NAD metabolism-associated enzymes including CD38. In vitro, upregulation of CD38 mRNA in human ECs was detected after interleukin 6 (IL-6) trans-signaling induction, which was increased in the infection. In the presence of IL-6 trans-signaling stimulation, however, CD38 mRNA silencing induced significant IL-6 mRNA upregulation in ECs and promoted EC apoptosis after stimulation. These results suggest that upregulation of CD38 in patients with COVID-19 has a protective role against IL-6 trans-signaling stimulation induced by SARS-CoV-2 infection.PMID:38507920 | DOI:10.1016/j.virol.2024.110052

Source: Virology - March 20, 2024 Category: Virology Authors: Cong Thanh Nguyen Misako Nakayama Hirohito Ishigaki Yoshinori Kitagawa Akemi Kakino Marumi Ohno Masashi Shingai Yasuhiko Suzuki Tatsuya Sawamura Hiroshi Kida Yasushi Itoh Source Type: research