Recombinant HTLV type 1, 2

Name: Recombinant HTLV type 1, 2
SKU: DAG2735
Rating: 5 (1 reviews)

HTLV type 1, 2, recombinant protein from E. coli

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Summary

Product Overview

E. coli derived recombinant 56 kDa protein, (Purified/Coating; EIA), strain: BL21 DE3

Nature

Recombinant

Tag/Conjugate

Unconjugated

Purity

> 95% by determined by SDS-PAGE

Format

Liquid

Buffer

Tris-HCl buffer

Preservative

None

Storage

Store at 2-8°C for short term. Store at -20°C for long term. Avoid multiple freeze/thaw cycles

Introduction

The Human T-lymphotropic virus Type I (HTLV-1) is a human RNA retrovirus that is known to cause a type of cancer, referred to as adult T-cell leukemia and lymphoma, and a demyelinating disease called HTLV-I associated myelopathy/Tropical spastic paraparesis (HAM/TSP). HTLV-I is one of a group of closely related primate T lymphotropic viruses (PTLVs). Members of this family that infect humans are called Human T-lymphotropic viruses, and the ones that infect old-world primates are called Simian T-lymphotropic viruses. To date, four types of HTLVs (HTLV-I, HTLV-II, HTLV-III, and HTLV-IV) and four types of STLVs (STLV-I, STLV-II, STLV-III, and STLV-V) have been identified. The HTLVs are believed to originate from intraspecies transmission of STLVs. The original name for HIV, the virus that causes AIDS, was HTLV-III; this term is no longer in use.

Keywords

HTLV-1; HTLV-2; Human T-lymphotropic virus; HTLV type 1, 2

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Background

Human T-cell leukemia virus type 1 (HTLV-1) is a human retrovirus first discovered in 1980. Since then, several subtypes of HTLV have been discovered and HTLV-2 was first identified in patients with hairy cell leukemia. HTLV is a zoonotic virus similar to the simian T-cell leukemia virus found in monkeys. HTLV-1 and HTLV-2 are the most studied HTLV subtypes, and both show considerable homology in genomic structure, replication patterns, and properties of structural, regulatory, and accessory proteins. They share the same route of transmission through perinatal transmission, breastfeeding, and the transfer of infected lymphocytes through blood transfusions, sexual contact, and intravenous drug use. They both utilize GLUT-1 and NRP1 cell receptors to enter the cell. Both viruses also encode structural and enzymatic proteins common to retroviruses, as well as the regulatory proteins Tax and Rex, and both have RNA transcripts and proteins from the negative strand of the viral genome.

Infection with HTLV-1 can cause adult T-cell leukemia (ATL). In addition, HTLV-1-associated myelopathy (HAM)/tropical spastic paraplegia (TSP), rheumatoid arthritis, and systemic lupus erythematosus have been strongly associated with the virus. HTLV-1 is broadly infectious and is able to invade T lymphocytes, macrophages, and B lymphocytes, among others. In addition it destroys the host immune defense system and alters lymphocyte subpopulations, thus affecting the body's immune stability. After the virus invades the body, the incubation period can last for decades, and about 3% of HTLV-1-infected individuals eventually develop ATL. Once HTLV -1 infected individuals develop a significant clinical response, the course of the disease is often irreversible, treatment is limited, adverse reactions and side effects are evident, and the prognosis is poor. Therefore, the means of combating HTLV-1 viral infections appear to be of paramount importance.

The prevalence and incidence of HTLV-2 is much lower compared to HTLV-1. They are also very different in terms of clinical impact, with only HTLV-1 having a clear association with tumors. In contrast, HTLV-2, although consistently associated with elevated lymphocyte and platelet counts and increased overall cancer mortality, does not cause hematological disorders and is only occasionally associated with spinal cord disease. Notably, although HTLV-2 was initially identified in patients with hairy cell leukemia, no clinical correlation between it and lymphoproliferative disorders has been established.

Similarities and differences in the pathobiology of HTLV-1 and HTLV-2 Figure 1. Comparison of HTLV-1 and HTLV-2 pathobiology
(Source: Martinez MP, et al. 2019)

Alternative Names

Human T-cell leukemia virus type 1, 2

References

1. Martinez MP, et al. Comparative virology of HTLV-1 and HTLV-2. Retrovirology. 2019 Aug 7;16(1):21.
2. Ciminale V, et al. HTLV-1 and HTLV-2: highly similar viruses with distinct oncogenic properties. Front Microbiol. 2014 Jul 29;5:398.

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References

Case Report: An Uncommon Clinical Case of Fatal Adult T-Cell Leukemia/Lymphoma Associated with HTLV-1 and Suspected due to Cutaneous Lesions and Epidemiologic Data

AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE

Authors: de Assis, Isabelle Carvalho; Rodrigues Alberti, Joao Gabriel; Criado, Paulo Ricardo

Abstract

Adult T-cell leukemia/lymphoma (ATLL) is a peripheral T-cell neoplasm caused by the human T-cell leukemia virus type 1 (HTLV-1). It is characterized by a short survival time and lack of response to chemotherapy. We report a case of a 56-year-old woman, from the Brazilian northeast state of Bahia, who presented with a 2-month history of infiltrated papular and nodular skin lesions, especially on her forehead and also on her lower and upper limbs. Laboratory tests revealed positive serology for HTLV-1. Histopathological findings and the immunohistochemical profile confirmed the diagnosis of adult T-cell lymphoma/leukemia. A month after the diagnosis, the patient presented acute fatigue and pronounced paleness of the skin, dying of septic shock after her first chemotherapy cycle. The aim of this case report was to emphasize the importance of maintaining high clinical suspicion for ATLL, considering the epidemiological profile of the disease, especially for patients whose only early symptoms are cutaneous lesions.

Separation of the Epitopes in a Multi-Epitope Chimera: Helical or Flexible Linkers

PROTEIN AND PEPTIDE LETTERS

Authors: Kabiri, Mona; Tafaghodi, Mohsen; Saberi, Mohammad Reza; Moghadam, Maliheh; Rezaee, Seyed Abdolrahim; Sankian, Mojtaba

Abstract

Background: The engineered chimeric peptides including functional multi-epitope structures fused by various peptide linkers are widely applied in biotechnological research to improve the expression level and biological activity of chimera. Objective: The aim of our study was to evaluate the effect of helical and flexible linkers on solubility, expression level and folding of multi-epitope chimera containing four epitopes of Human T Lymphotropic Virus Type 1 (HTLV-1). Methods: For this purpose, the chimera sequences connected by the helical or flexible linker were inserted into different plasmid vectors and expressed in E. coli strains. The expressed products were analyzed using SDS-PAGE and Western blot techniques. Additionally, the molecular modeling study of the chimera with helical or flexible linker was performed using iterative threading assembly refinement (I-TASSER) to attain their three-dimensional structures. Results: Comparison of the chimera expression indicated that the insertion of a flexible (GGGGS)(3) linker among chimera epitopes could significantly enhance the level of expression, whereas, the low-level of chimera expression was observed for chimera containing the contiguous helical (EAAAK)(5) linker. According to the results of sequence alignment and plasmid stability test, the structure and function of a consecutive helical linker among chimera epitopes were similar to porins as the outer-membrane pore-forming proteins. The molecular modeling results confirmed our experimental study. Conclusion: This investigation illustrated the key role of linker design in determining the expression level of multi-epitope chimera and conformational folding.