HTLV-1, the Other Pathogenic Yet Neglected Human Retrovirus: From Transmission to Therapeutic Treatment

Abstract

Going back to their discovery in the early 1980s, both the Human T-cell Leukemia virus type-1 (HTLV-1) and the Human Immunodeficiency Virus type-1 (HIV-1) greatly fascinated the virology scene, not only because they were the first human retroviruses discovered, but also because they were associated with fatal diseases in the human population. In almost four decades of scientific research, both viruses have had different fates, HTLV-1 being often upstaged by HIV-1. However, although being very close in terms of genome organization, cellular tropism, and viral replication, HIV-1 and HTLV-1 are not completely commutable in terms of treatment, especially because of the opposite fate of the cells they infect: death versus immortalization, respectively. Nowadays, the antiretroviral therapies developed to treat HIV-1 infected individuals and to limit HIV-1 spread among the human population have a poor or no effect on HTLV-1 infected individuals, and thus, do not prevent the development of HTLV-1-associated diseases, which still lack highly efficient treatments. The present review mainly focuses on the course of HTLV-1 infection, from the initial infection of the host to diseases development and associated treatments, but also investigates HIV-1/HTLV-1 co-infection events and their impact on diseases development.

Human T-cell Lymphotropic Virus Type I Associated with Amyotrophic Lateral Sclerosis Syndrome: Immunopathological Aspects and Treatment Options

“…The different workgroups have attracted controversies regarding their use and have reported improvement in response rates and relief of symptoms in patients with high viral loads [2]. The results of a recent study that evaluated patients for several years highlighted the improvement in disability scales in the group that took prednisone in both the short and long term when compared with untreated patients [8,9]. Initial schemes involve methylprednisolone 100 mg IV per day for three days, followed by oral prednisone 15 mg per day [2,8,9].…”

“…The results of a recent study that evaluated patients for several years highlighted the improvement in disability scales in the group that took prednisone in both the short and long term when compared with untreated patients [8,9]. Initial schemes involve methylprednisolone 100 mg IV per day for three days, followed by oral prednisone 15 mg per day [2,8,9]. There are alternative proposals with anti-inflammatory drugs such as cyclosporine, pentoxifylline, danazol, and interferons [8,10].…”

“…Initial schemes involve methylprednisolone 100 mg IV per day for three days, followed by oral prednisone 15 mg per day [2,8,9]. There are alternative proposals with anti-inflammatory drugs such as cyclosporine, pentoxifylline, danazol, and interferons [8,10]. Flow charts of treatment for the disease show a regular response to steroids or improvement in progression and propose alternatives to continue with interferon, cyclosporin A, danazol, and vitamin C [10].…”

“…Flow charts of treatment for the disease show a regular response to steroids or improvement in progression and propose alternatives to continue with interferon, cyclosporin A, danazol, and vitamin C [10]. New therapeutic options that focus on eliminating infected cells and reducing the proviral load have emerged; the antigens of the virus are not recognized by the immune system and drugs such as valproic acid, by the mechanism of action that inhibits the enzyme histone deacetylase, induce the expression of the proviral gene HTLV-I, generating recognition by the immune system and leading to cytotoxic-type response [8,10]. Regarding the goal of reducing viral load, some of the work done have been controversial.…”

Morphological alterations in minor salivary glands of HTLV1+ patients: A pilot study

“…The pathogenesis of these manifestations seems to be related to the capacity of HTLV‐1 to cause immune activation, similar to what happens in the medullary region of those affected by HAM/TSP. The virus integrates into the DNA of T CD4 + lymphocytes, which, once infected, will cause activation of T CD8 + lymphocytes and consequent release of several cytokines, which are responsible for the destruction of infected cells and, concomitantly, of the adjacent tissues …”