Proposed signaling pathway to the actin cytoskeleton during HIV-1 entry in T lymphocytes

Proposed signaling pathway to the actin cytoskeleton during HIV-1 entry in T lymphocytes. (a) Mature free virions (step 1) are initially captured by unspecific binding to glycoproteins covering the target cell such as glycosaminoglycans (GAG, step 2) or cell surface molecules such as LFA-1 or DC-SIGN (step 3). Subsequent specific binding of gp120 to CD4 initiates signaling to moesin, Arp2/3 and filaminA (step 4), resulting in entry receptor clustering (step 5). This allows gp120 to engage chemokine entry coreceptors to initiate receptor signaling, whose downstream effects include activation of cofilin (step 6). Active cofilin and Arp2/3 locally loosen the cortical actin cytoskeleton and provide motility (steps 7 and 8), to facilitate release of the viral core into the cytoplasm and transport through the cortical actin, respectively (steps 9 and 10). (b) Schematic representation of the current understanding of signaling cascades induced by gp120 through binding to CD4 (left panel) and CXCR4/CCR5 (right panel) during HIV-1 entry. Note that these pathways may be distinct in HIV-1 target cells such as macrophages that lack expression of T cell specific factors such as Lck.

Publication

How HIV Takes Advantage of the Cytoskeleton in Entry and Replication. (2011) Bettina Stolp, et al. Viruses. 2011 Apr;3(4):293-311. Figure: F1. All organisms Mus musculus Drosophila melanogaster Homo sapiens Danio rerio

Disease mentions