Abstract
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 p8I, p12I, and p13II regulatory non-structural proteins. p12I resides in endomembranes and interacts with host proteins on the pathways of signal transduction, thus preventing immune responses to the virus. p8I is a proteolytic product of p12I residing in the plasma membrane, where it contributes to T-cell deactivation and participates in cellular conduits, enhancing virus transmission. p13II associates with the inner mitochondrial membrane, where it is proposed to function as a potassium channel. Potassium influx through p13II in the matrix causes membrane depolarization and triggers processes that lead to either T-cell activation or cell death through apoptosis.
Highlights
Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) [1,2,3,4]
Figure 3. pp88I I ininhhibibitists TT cceelll rreecceeppttoorr ((TTCCRR)) ssiiggnnaall transsdduuccttiioonn and nuclear factor of T cells (NFAT) aaccttiivvaattiioonn:: p8II iiss a proteolytic product of p12II inn the ER membranes, thhee proteinn trafffiics to plasma membrane and localizeess in the immunological synapse; p8II iinntteerraaccttss wwiitthh anndd inhibittss the phosphoryyllaattiioonn of the transmembrane protein called linker for activation of T cells (LAT) and by doing so, p8II ddiissaabblleessLLAAT to transmit signalss from TCR andd to interraacctt wwiitthh ootthheerr pprrootteeiinnss, ssuucchh aass pphhoosspphhoolliippaasseeCCggaammmmaa11, VVaavv pprrootteeiinnss, aanndd llyymmpphhooccyyttee--ssppeecciifificc pprrootteeiinn ttyyrroossiinnee kkiinnaassee ((sshhoowwnn iinn rreedd, ccyyaann aanndd ggrreeeenn)) oonn tthhee TTCCRR ssiiggnnaalliinngg ppaatthhwwaayy
This study showed that p13II causes inner mitochondrial membrane (IMM) depolarization, which increases proton transport through the pumps of the electron transport chain (ETC) and restores membrane potential while increasing oxygen consumption
Summary
Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) [1,2,3,4]. HTLV-1 functioning in the cell requires the expression of plus-strand-encoded proteins, which have essential roles.
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