HTLV-1 and HTLV-2: highly similar viruses with distinct oncogenic properties

Ciminale, Vincenzo; Rende, Francesca; Bertazzoni, Umberto; Romanelli, Maria Grazia

doi:10.3389/fmicb.2014.00398

Cited by 51 publications

(57 citation statements)

References 112 publications

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“…The reasons why HTLV-2 is less virulent than HTLV-1 remain unclear. A higher expression of gene products inducing viral latency by HTLV-2 (p28 and tRex) and some differences between Tax-1 and Tax-2 may play a major role in HTLV pathogenesis [118].…”

Section: Viral Characteristics and Pathogenesismentioning

confidence: 99%

Infection with human retroviruses other than HIV-1: HIV-2, HTLV-1, HTLV-2, HTLV-3 and HTLV-4

Nicolás

Ambrosioni

Paredes

et al. 2015

Expert Review of Anti-infective Therapy

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HIV-1 is the most prevalent retrovirus, with over 30 million people infected worldwide. Nevertheless, infection caused by other human retroviruses like HIV-2, HTLV-1, HTLV-2, HTLV-3 and HTLV-4 is gaining importance. Initially confined to specific geographical areas, HIV-2, HTLV-1 and HTLV-2 are becoming a major concern in non-endemic countries due to international migration flows. Clinical manifestations of retroviruses range from asymptomatic carriers to life-threatening conditions, such as AIDS in HIV-2 infection or adult T-cell lymphoma/leukemia or tropical spastic paraparesis in HTLV-1 infection. HIV-2 is naturally resistant to some antiretrovirals frequently used to treat HIV-1 infection, but it does have effective antiretroviral therapy options. Unfortunately, HTLV still has limited therapeutic options. In this article, we will review the epidemiological, clinical, diagnostic, pathogenic and therapeutic aspects of infections caused by these human retroviruses.

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Section: Viral Characteristics and Pathogenesismentioning

confidence: 99%

Infection with human retroviruses other than HIV-1: HIV-2, HTLV-1, HTLV-2, HTLV-3 and HTLV-4

Nicolás

Ambrosioni

Paredes

et al. 2015

Expert Review of Anti-infective Therapy

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“…15, 29, 30 The pathogenic determinant of T-cell lymphomas is the (6) human T-cell lymphoma virus which is prevalent in selected geographical areas. 15, 31 Lastly, the (7) Merkel cell polyomaviruses are identified in a rare aggressive form of skin cancer, Merkel cell carcinoma in immunosuppressed individuals. 15 Of note, with the exception of HCV, all the known human oncogenic viruses contain at least one oncogene in their genomes and may directly transform healthy cells to tumor-forming cells.…”

Section: Human Carcinogenic Pathogensmentioning

confidence: 99%

Microbiome and potential targets for chemoprevention of esophageal adenocarcinoma

Neto

Whitaker

Pei

2016

Seminars in Oncology

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Esophageal cancer is one of the deadliest cancers, with a dismal prognosis. It is increasingly recognized that esophageal cancer is a heterogeneous disease. It can be subdivided into two distinct groups: squamous cell carcinoma and adenocarcinoma, based on histological appearance. In the Western world, the incidence of squamous cell carcinoma was considerably higher than esophageal adenocarcinoma (EA) until the 1990s when, due to a dramatic increase, the incidence of EA surpassed that of squamous cell carcinoma. EA typically follows a well-established stepwise evolution from chronic inflammation due to reflux esophagitis (RE) that progresses to metaplasia (Barrett’s esophagus- BE) to dysplasia, which often culminates in EA. The pathophysiology of EA is complex and involves diverse factors, including gastroesophageal reflux, gastric acid secretion, dysfunction of the antireflux barrier, gastric emptying disturbances, and abnormalities in esophageal defense mechanisms. The current understanding of the etiology of EA is mainly derived from epidemiological studies of risk factors such as cigarette smoking, obesity, gastroesophageal reflux disorders (GERD), and low fruit and vegetable consumption. Numerous studies have been done but the factors that drive the dynamic increase in the incidence of EA remain elusive. The advent of widespread antibiotic use occurred in the 1950s, preceding the surge of EA. Based on this temporal sequence, it has been hypothesized that antibiotics alter the microbiome to which the esophagus is exposed in patients who have GERD and that chronic exposure to this abnormal microbiome (i.e., changes in species diversity or abundance) accounts for the increase in EA. If changes in the proposed factors alter the stepwise progression (RE-BE-dysplasia- EA), they may represent potential targets for chemoprevention. New discoveries will help improve our understanding of the biology and pathogenesis of these cancers, and aid in finding novel therapeutic targets.

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“…It was also the last. With the possible exception of the related, but distinct, HTLV-2, discovered by the Gallo group in a different type of T-cell leukemia a few years later (51), which forced the renaming of HTLV to HTLV-1, and whose role in oncogenesis remains to be established (52), no other directly oncogenic human retrovirus has been found. More recently, infections with two other related viruses, HTLV-3 and HTLV-4, have been reported in a few individuals in sub-Saharan Africa, apparently the result of zoonotic infection from local primates (53).…”

Section: Impact Of the Discoverymentioning

confidence: 99%

“…Of these, about 5% will succumb to ATL, and another 5% will acquire another disease caused by the same virus, HTLV-associated myelopathy/tropical spastic paraparesis, a serious neurological condition. The large majority of infected individuals remain healthy carriers for life (52). Although the molecular mechanisms of HTLV oncogenesis are a very active area of research (55), knowledge gained has not yet led to any new treatment or prevention measures, beyond screening of the donated blood supply.…”

Section: Impact Of the Discoverymentioning

confidence: 99%

The discovery of HTLV-1, the first pathogenic human retrovirus

Coffin

2015

Proc. Natl. Acad. Sci. U.S.A.

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After the discovery of retroviral reverse transcriptase in 1970, there was a flurry of activity, sparked by the "War on Cancer," to identify human cancer retroviruses. After many false claims resulting from various artifacts, most scientists abandoned the search, but the Gallo laboratory carried on, developing both specific assays and new cell culture methods that enabled them to report, in the accompanying 1980 PNAS paper, identification and partial characterization of human T-cell leukemia virus (HTLV; now known as HTLV-1) produced by a T-cell line from a lymphoma patient. Follow-up studies, including collaboration with the group that first identified a cluster of adult T-cell leukemia (ATL) cases in Japan, provided conclusive evidence that HTLV was the cause of this disease. HTLV-1 is now known to infect at least 4-10 million people worldwide, about 5% of whom will develop ATL. Despite intensive research, knowledge of the viral etiology has not led to improvement in treatment or outcome of ATL. However, the technology for discovery of HTLV and acknowledgment of the existence of pathogenic human retroviruses laid the technical and intellectual foundation for the discovery of the cause of AIDS soon afterward. Without this advance, our ability to diagnose and treat HIV infection most likely would have been long delayed.human retrovirus | adult T-cell leukemia

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HTLV-1 and HTLV-2: highly similar viruses with distinct oncogenic properties

Cited by 51 publications

References 112 publications

Infection with human retroviruses other than HIV-1: HIV-2, HTLV-1, HTLV-2, HTLV-3 and HTLV-4

Infection with human retroviruses other than HIV-1: HIV-2, HTLV-1, HTLV-2, HTLV-3 and HTLV-4

Microbiome and potential targets for chemoprevention of esophageal adenocarcinoma

The discovery of HTLV-1, the first pathogenic human retrovirus

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