Viral Antigens
Product List
HTLV-1 Envelope
HTLV-1 Envelope Recombinant
The E.Coli derived recombinant protein contains the C- terminus of gp46 and most of p21E of HTLV-1. This non-fusion, E. coli-derived protein, starts from HTLV-1 env. Amino acid 165, and is ending in amino acid 440, Mw 27 kDa.
HTLV-1 gp21
HTLV-1 gp21 Recombinant
The E.Coli derived recombinant protein contains the gp21 immunodominant region, 1-152 amino acids, the MW is 17.9 kDa. Fused with a His tag at C-Terminus.
HTLV-1 gp46 mosaic
HTLV-I gp46 Mosaic Recombinant
The E.Coli derived recombinant mosaic protein contains the gp46 immunodominant region, 21-313 amino acids; Mw on SDA-PAGE is 34.2kDa and fuse to 6 histidines at C-terminus.
HTLV-1 mosaic
HTLV-1 Mosaic Recombinant
The E.Coli derived recombinant mosiac protein contains the gp21 and gp46 immunodominant regions, 374-400 amino acids and 190-201 amino acids. The protein is fused with GST at N-terminus.
HTLV-1 p24
HTLV-1 p24 Recombinant
HTLV-1 p24 is purified by proprietary chromatographic technique.
HTLV-1 p24 core
HTLV-1 p24 Core Recombinant
The protein contains 214 amino acids having an Mw of 24kDa.
Introduction
Human T-cell lymphotropic virus (HTLV) is a retrovirus belonging to the family Retroviridae and the genus Deltaretrovirus. It is classified into four types: HTLV-1, HTLV-2, HTLV-3, and HTLV-4. HTLV-1 and HTLV-2 are the most studied and are associated with various diseases in humans. HTLV-1 is known to cause adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) .
HTLV-1 is an enveloped, single-stranded RNA virus that displays CD4 T-cell tropism. It spreads primarily through direct cell-to-cell contact, and viral RNA is not found in plasma. The virus integrates into the host genome as a provirus, leading to lifelong infection . HTLV-1 is primarily found in blood, breast milk, and semen, and it is transmitted through these bodily fluids . The virus is endemic in regions such as the Caribbean, South America, Japan, and parts of Africa .
HTLV-1 primarily infects CD4+ T cells and can cause their malignant transformation. The virus’s Tax protein plays a central role in modulating the expression of viral and cellular genes, leading to uncontrolled T-cell proliferation and genomic instability . HTLV-1 also affects immune responses and pathogen recognition by altering cytokine production and immune cell signaling pathways .
HTLV-1’s Tax protein interacts with various cellular proteins and signaling pathways, including the NF-κB pathway, to promote T-cell proliferation and survival . The virus spreads through direct cell-to-cell contact, forming a virological synapse that facilitates the transfer of viral particles between cells . HTLV-1 also employs other mechanisms, such as the formation of cellular conduits and extracellular viral assemblies, to ensure its persistence and spread .
The expression and activity of HTLV-1 are regulated by both viral and host factors. The Tax protein activates viral gene expression and NF-κB signaling, while the Hbz protein counteracts some of Tax’s functions . Additionally, microRNAs and long non-coding RNAs play roles in regulating HTLV-1 transcription and latency . Post-translational modifications of viral proteins also contribute to the regulation of HTLV-1 activity .
HTLV-1 has significant implications in biomedical research, particularly in understanding retroviral oncogenesis and immune evasion mechanisms. Diagnostic tools for HTLV-1 include immunoassays and confirmatory tests such as western blot and line immunoassay . Therapeutic strategies for HTLV-1-associated diseases focus on antiviral drugs, immune modulation, and targeted therapies to inhibit viral replication and T-cell transformation .
HTLV-1 establishes lifelong infection by integrating its genome into the DNA of infected T cells. The virus persists in the host by inducing pro-proliferative changes in infected cells, maintaining the proviral load . HTLV-1’s role in the life cycle includes initial infection, latency, and reactivation, which can lead to diseases such as ATL and HAM/TSP . The virus’s ability to evade immune responses and persist in the host contributes to its pathogenicity and long-term impact on health .
