Recombinant HTLV-1 Gp62 Protein (Melanesia mel5)

Simultaneous infection by human immunodeficiency viruses (HIV) and human T-lymphotropic viruses (HTLV) are not uncommon since they have similar means of transmission and are simultaneously endemic in many populations. Besides causing severe immune dysfunction, these viruses are neuropathogenic and can cause neurological diseases through direct and indirect mechanisms. Many pieces of evidence at present show that coinfection may alter the natural history of general and, more specifically, neurological disorders through different mechanisms. In this review, we summarize the current evidence on the influence of coinfection on the progression and outcome of neurological complications of HTLV-1/2 and HIV-1.

HTLV-1, the first human oncogenic retrovirus, is a type C retrovirus that belongs to the Deltaretrovirus genus. The HTLV-1 genome has 8.5 kbp length, and consists of major genes such as gag, pol, pro, env, and pX region. This retrovirus is considered as one of the most deadly infectious agent for peripheral-blood mononuclear cells (PBMC). The infection of HTLV-1 can lead to dangerous complications, such as infective dermatitis (ID), uveitis, arthritis, lymphadenitis, arthropathies, Sjogren's Syndrome (SS), and particularly HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) or Adult T-Cell Leukemia Lymphoma (ATLL). At the moment, Zidovudine (AZT) plus IFN-alpha is the only treatment available for HTLV-1 infections. Based on scientific studies, alongside the therapeutic regimens, intrinsic mechanisms also play a determinant role in reducing the signs of disease. Programmed cell death-1 (PD-1) signaling pathway, one of the most important checkpoints, has recently received interest, such as the development of a novel generation of anti-tumors. In the present study, we discuss the role of PD-1 signaling pathway in HTLV-1 infection as well as its application as a novel approach for treatment of HTLV-1 infections.