| Summary: | Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of illnesses, such as adult T-cell leukemia/lymphoma, myelopathy/tropical spastic paraparesis (a neurodegenerative disorder), and other diseases. Therefore, HTLV-1 infection is a serious public health concern. Currently, diseases caused by HTLV-1 cannot be prevented or cured. Hence, there is a pressing need to comprehensively understand the mechanisms of HTLV-1 infection and intervention in host cell physiology. HTLV-1-encoded non-structural proteins that reside and function in the cellular membranes are of particular interest, because they alter cellular components, signaling pathways, and transcriptional mechanisms. Summarized herein is the current knowledge about the functions of the membrane-associated p8<sup>I</sup>, p12<sup>I</sup>, and p13<sup>II</sup> regulatory non-structural proteins. p12<sup>I</sup> resides in endomembranes and interacts with host proteins on the pathways of signal transduction, thus preventing immune responses to the virus. p8<sup>I</sup> is a proteolytic product of p12<sup>I</sup> residing in the plasma membrane, where it contributes to T-cell deactivation and participates in cellular conduits, enhancing virus transmission. p13<sup>II</sup> associates with the inner mitochondrial membrane, where it is proposed to function as a potassium channel. Potassium influx through p13<sup>II</sup> in the matrix causes membrane depolarization and triggers processes that lead to either T-cell activation or cell death through apoptosis.
|
|---|
