“…GLUT1, heparin sulfate proteoglycan(HSPG) and neuropilin-1 are the three molecules that are reported as key players for the interaction between the viral envelop and the cell membrane, and for the entry into the cells [24][25][26]. It has been proposed that HTLV-1 particles first contact HSPG, then neuropilin-1 recruits HTLV-1/ HSPG complex to present them to GLUT1.…”
Section: Mechanisms Of Htlv-1 Transmissionmentioning
“…GLUT1, heparin sulfate proteoglycan(HSPG) and neuropilin-1 are the three molecules that are reported as key players for the interaction between the viral envelop and the cell membrane, and for the entry into the cells [24][25][26]. It has been proposed that HTLV-1 particles first contact HSPG, then neuropilin-1 recruits HTLV-1/ HSPG complex to present them to GLUT1.…”
Section: Mechanisms Of Htlv-1 Transmissionmentioning
“…The replication cycle of HTLV-1 begins with the interaction between the viral Env glycoproteins and the specific cellular receptor proteins. At least three cellular receptors have been found to facilitate viral attachment and entry into the cell, and these include the glucose transporter 1 (GLUT1) [24,25], neuropilin-1 (NRP-1) [26][27][28], and heparan sulfate proteoglycans (HSPG) [29][30][31]. During the membrane fusion process and after entry of the viral capsid into the cytoplasm, the viral genomic RNA is reverse transcribed into DNA, by the viral particle-associated reverse transcriptase.…”
Section: Htlv-1 Genetic Architecture and Viral Replicationmentioning
“…An absence or decrease in PG-core proteins may therefore reduce the expression of GAGs and potentially cause an insufficient interaction between bacteria and host cells, thereby preventing infection [25]. We therefore compared PG-core protein gene expression (Fig.…”
This study investigated the proteoglycan (PG)-dependent mechanism ofImmunofluorescent co-staining with antibodies against chlamydial LPS and heparin did not identify bacterial and heparin co-localization on Jurkat cells. We also confirmed that when C. pneumoniae was statically infected to human CD4 + peripheral blood lymphocytes known not expressing detectable level of heparin, the bacteria attached to and formed inclusion bodies in the cells. Thus, the attachment mechanism of C.pneumoniae to Jurkat cells with low PG expression is unique when compared withHEp-2 cells and potentially independent of GAGs such as heparin.
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