Human T-cell Lymphotropic Virus I Research Articles

Simulation as an alternative to linear programming of human T-cell lymphotropic virus I (HTLV-I) model infection of CD4+ T-cells

Simulation as an alternative to linear programming of human T-cell lymphotropic virus I (HTLV-I) model infection of CD4+ T-cells

A Geometric Integration Based on Magnus Series Expansion for Human T-Cell Lymphotropic Virus I (HTLV-I) Infection of CD4+ T-Cells Model

A Geometric Integration Based on Magnus Series Expansion for Human T-Cell Lymphotropic Virus I (HTLV-I) Infection of CD4+ T-Cells Model

Detection of Active Epstein-Barr Virus Infection in Duodenal Mucosa of Patients With Refractory Celiac Disease.

Refractory celiac disease is characterized by mucosal damage in patients with celiac disease despite a gluten-free diet. Little is known about the mechanisms that cause persistent intestinal inflammation in these patients. We performed a case-control study of 17 consecutive patients diagnosed with refractory celiac disease from 2001 through 2014 (median age, 51 y; 10 women) and 24 patients with uncomplicated celiac disease (controls) to determine whether refractory disease is associated with infection by lymphotropic oncogenic viruses. We performed real-time PCR analyses of duodenal biopsy samples from all patients to detect Epstein-Barr virus (EBV), human herpesvirus-8, and human T-cell lymphotropic virus-I, -II, or -III. We used in situ hybridization and immunohistochemical analyses to identify infected cells and viral proteins. We did not detect human herpesvirus-8 or human T-cell lymphotropic viruses in any of the biopsy specimens. However, 12 of 17 (70.5%) biopsy specimens from patients with refractory celiac disease were positive for EBV, compared with 4 of 24 (16.6%) biopsy specimens from controls (P < .001). EBV was detected in inflammatory cells and enterocytes. An analysis of latency- and replication-associated proteins confirmed active infection. Further studies are needed to determine whether EBV infection contributes to the pathogenesis of refractory celiac disease and enteropathy-associated T-cell lymphoma.

Application of the multi-step differential transform method to solve a fractional human T-cell lymphotropic virus I (HTLV-I) infection of CD4+ T-cells

Application of the multi-step differential transform method to solve a fractional human T-cell lymphotropic virus I (HTLV-I) infection of CD4+ T-cells

Solutions of Fractional model of human T-cell lymphotropic virus I (HTLV-I) infection of CD4+ T-cells using HAM

In this paper, we introduce fractional-order model of (HTLV-I) infection of CD 4+ T-cells. Homotopy analysis method (HAM) is implemented to give approximate and analytical solutions of the presented problem. The fractional derivatives are described in the Caputo sense. The method introduces a promising tool for solving many linear and nonlinear fractional differential equations. In these schemes, the solution takes the form of a convergent series with easily computable components. Numerical results show that the approach is easy to implement and accurate when applied to ordinary differential equations of fractional order.

An approximate solution of a fractional order differential equation model of human T-cell lymphotropic virus I (HTLV-I) infection of [formula omitted] T-cells

In this paper, a fractional order differential system for modeling human T-cell lymphotropic virus I (HTLV-I) infection of CD4 + T-cells is studied and its approximate solution is presented using a multi-step generalized differential transform method. The method is only a simple modification of the generalized differential transform method, in which it is treated as an algorithm in a sequence of small intervals (i.e. time step) for finding accurate approximate solutions to the corresponding systems. The solutions obtained are also presented graphically.

Screening of Deceased Organ Donors: No Easy Answers

Transmission of infection to recipients of solid organs is uncommon but well documented. Improved technologies for the diagnosis of infectious diseases suggest possible changes to paradigms used in the screening of organ donors to prevent disease transmission with transplantation. Available microbiologic assays, including molecular tests, are generally designed for use as diagnostic tools in individuals believed to have a specific infection based on clinical or epidemiological criteria. By contrast, these assays often lack the performance characteristics required for screening of deceased organ donors. This challenge is apparent with the analysis of assays for human T-cell lymphotropic virus-I and -II in low-risk populations. Changing epidemiologic patterns associated with the spread of novel pathogens or altered patterns of immigration will necessitate flexibility in the "list" of potential pathogens. Individual benefits from transplantation generally outweigh the risk of transmission of infection. However, this favorable experience will not obviate the need to continuously improve screening practices.

Homotopy Perturbation Method for Solving Human T-Cell Lymphotropic Virus I(HTLV-I) Infection of Cd4+ T-Cells Model

In this article, homotopy perturbation method is implemented to give approximate and analytical solutions of nonlinear ordinary differential equation systems such as human Tcell lymphotropic virus I (HTLV-I) infection of CD4+ T-cells model. The proposed scheme is based on homotopy perturbation method (HPM), Laplace transform and Padé approximants. The results to get the homotopy perturbation method (HPM) is applied Padé approximants. Our proposed approach showed results to analytical solutions of nonlinear ordinary differential equation systems. Some plots are presented to show the reliability and simplicity of the methods.

Adult T‐cell Leukemia/Lymphoma in an Adolescent Presenting with Skin Lesions

Adult T-cell leukemia/lymphoma is a T-cell malignancy caused by the human T-cell lymphotropic virus-I. Adult T-cell leukemia/lymphoma is primarily a disease of adults due to the long latency period between initial infection and development of leukemia. We present a case of acute adult T-cell leukemia/lymphoma in an adolescent. Skin lesions had appeared 3 years earlier and were the initial sign of human T-cell lymphotropic virus-I infection and T-cell malignancy. Her disease failed to respond to both intensive chemotherapy and antiviral therapy. Cutaneous lesions are sometimes the initial sign of adult T-cell leukemia/lymphoma and early recognition is imperative.

Virally associated arthritis 2008: clinical, epidemiologic, and pathophysiologic considerations.

Several viruses have been associated with the development of inflammatory arthritis, including the hepatitis viruses (hepatitis B virus and hepatitis C virus), HIV, the parvovirus B19, the human T-cell lymphotropic virus-I, and the alphaviruses. Here, we review the epidemiology, the pathophysiological mechanisms, the pertinent clinical and laboratory findings as well as the principles of therapy of the most common virus-associated arthritides. We believe that the knowledge of these key diagnostic and therapeutic features of virus-associated arthritides is important for the rheumatologist of the 21st century.

Molecular aspects of HTLV-I infection and adult T-cell leukaemia/lymphoma

Human T-cell lymphotropic virus-I (HTLV-I) is the cause of adult T-cell leukaemia/lymphoma. Various viral proteins, especially, but not exclusively, Tax have been implicated in oncogenesis, mostly through in vitro studies....

Reducing the risk of transfusion‐transmissible viral infection through blood donor selection: the Australian experience 2000 through 2006

Selection of voluntary donors who are at low risk of transfusion-transmissible viral infection (TTVI) is central in maintaining the safety of the blood supply. Evaluation of its effectiveness and the dynamics of the process may offer opportunities to further improve transfusion safety. The impact of donor selection on prevalence of TTVI was analyzed in all allogeneic donations in Australia between July 2000 and June 2006 by interviewing donors found to have a TTVI. The presence and disclosure of infective risks was reassessed. A total of 6.3 million donations were tested; of these, 1,449 (0.02%) were repeat-reactive for a TTVI and were discarded. This comprised 605 (42%) positive for the presence of hepatitis B, 818 (56%) positive for the presence of hepatitis C, 18 (1%) positive for the presence of human immunodeficiency virus, and 20 (1%) positive for the presence of human T-cell lymphotropic virus-I and/or -II (HTLV-I/II). This prevalence was 50 to 350 times lower than in the Australian population. In 1,158 cases (80%), an infective risk was identified; 509 donors (44%) had more than one. The most common identified were country of birth and parental ethnicity (n = 682, 26% of risks), tattoos and/or piercings (n = 448, 18%), and intravenous drug use (n = 302, 12%). In 302 cases (21%) disclosure at predonation screening would have resulted in deferral. Factors influencing nondisclosure included temporal remoteness and perceptions that laboratory testing rendered disclosure unnecessary. These findings affirm the effectiveness of current stringent donor selection criteria in reducing the residual risk of TTVI. Ongoing donor education regarding the importance of risk disclosure is required.

Global stability and periodic solution of a model for HTLV-I infection and ATL progression

Human T-cell lymphotropic virus I (HTLV-I) infection is linked to the development of adult T-cell leukemia/lymphoma (ATL), among many illness. The healthy CD4 + T cells infect HTLV-I through cell-to-cell contact with infected T-cells. The infected T cells can remain latent and harbor virus for several years before virus production occurs. Actively infected T cells can infect other T cells and can convert to ATL cells, whose growth is assumed to follow a classical logistic growth function. In this paper, we consider the classical mathematical model with saturation response of the infection rate. By stability analysis we obtained the condition for the infected T cells die out and the condition for HTLV-I infection becomes chronic. At the same time, we also obtained the condition for a unique endemic equilibrium is globally stable in the interior of the feasible region.

Infusional Adriamycin Based Chemotherapy Significantly Improves the Survival of Human T-Cell Lymphotropic Virus-I Induced Acute Type Adult T-Cell Leukemia Lymphoma.

Introduction: In this retrospective analysis, we provide a comprehensive account of the pathophysiology, clinical course and outcomes with various therapeutic regimens in HTLV-1 associated Adult T-cell Lymphoma/Leukemia- The Brooklyn Experience.Patients and Methods:We retrospectively reviewed the medical records of all patients identified as having acute type Human T-cell Lymphotropic Virus (HTLV-I) associated Adult T-cell Leukemia/Lymphoma (ATLL), from 1995 to 2005. The diagnosis was made according to REAL and WHO classification and based on clinical presentation, tissue biopsy and positive HTLV-I serology. Since all patients expired during the study, we used analysis of variance to examine the mean survival of these patients and the relationship between types of therapy and the survival.Results:We identified 44 patients with diagnosis of acute type ATLL. The most common disease presentation was lymphomatous in 70% (n=31) and leukemic presentation in 8% (n=3) both leukemia and lymphomatous presentation at diagnosis was seen in 22% (n=10) of patients. The mean survival for the entire group of patients was 31 weeks. The median survival was 16 weeks (range from 1 to 314 weeks). Patients who presented initially without hypercalcemia had a mean survival that was significantly higher than the patients with hypercalcemia 54 weeks versus 20 weeks, p<0.01. Treatment with infusional adriamycin chemotherapy significantly improved survival mean 99 ± 2.2 weeks, compared to CHOP 28 ± 2 weeks and much better than non-adriamycin regimens 21 ± 3 weeks p<0.001. Treatment with infusional adriamycin consistently improved survival in the patients without hypercalcemia 56± 6.6 weeks versus CHOP 21 ± 3.4 versus non-adriamycin containing regimens 10 ± 2.5 weeks, p=0.001. The presence or absence at diagnosis of central nervous system disease, pleural effusion, ascites, extensive liver or skin involvement or blood group were not independently associated with survival after adjusting for either hypercalcemia or infusional adriamycin chemotherapy. In multivariate analysis the presence of hypercalcemia was no longer significant after the therapy with infusional adriamycin.Conclusions: Hypercalcemia portends poor prognosis in all forms of HTLV-1 associated ATLL and should be included in any risk stratification schema for this disease. Our review demonstrates a statistically significant improvement in median overall survival with infusional adriamycin based chemotherapy over traditional CHOP, CVP or the AZT and interferon combination. This superiority in outcomes was evident in patients with or without hypercalcemia at presentation. Although overall survival remains relatively low in the acute form of this disease and most patients remain incurable with current therapies, our findings suggest that the incorporation of infusional adriamycin based regimens in future treatment modalities to include specific and non-specific molecular targeted therapies, would be a prudent strategy in development of more effective therapies for this disease.

Parkinsonism in the course of HTLV‐I‐associated myelopathy

Parkinsonian syndromes may represent a complication of viral infection. Human T cell lymphotropic virus I (HTLV-I) is a cause of a chronic myelopathy in which encephalic involvement has been also found. We report on the case of a 60-year-old man with HTLV-I-associated myelopathy, complicated with bradykinesia, resting tremor, and cogwheel rigidity. These findings suggest that parkinsonian features may represent a neurological disorder associated with HTLV-I infection.

Dynamics of human T-cell lymphotropic virus I (HTLV-I) infection of CD4 + T-cells

Stilianakis and Seydel ( Bull. Math. Biol., 1999) proposed an ODE model that describes the T-cell dynamics of human T-cell lymphotropic virus I (HTLV-I) infection and the development of adult T-cell leukemia (ATL). Their model consists of four components: uninfected healthy CD4 + T-cells, latently infected CD4 + T-cells, actively infected CD4 + T-cells, and ATL cells. Mathematical analysis that completely determines the global dynamics of this model has been done by Wang et al. ( Math. Biosci., 2002). In this note, we first modify the parameters of the model to distinguish between contact and infectivity rates. Then we introduce a discrete time delay to the model to describe the time between emission of contagious particles by active CD4 + T-cells and infection of pure cells. Using the results in Culshaw and Ruan ( Math. Biosci., 2000) in the analysis of time delay with respect to cell-free viral spread of HIV, we study the effect of time delay on the stability of the endemically infected equilibrium. Numerical simulations are presented to illustrate the results. To cite this article: P. Katri, S. Ruan, C. R. Biologies 327 (2004).

Serological findings amongst first-time blood donors in Yaoundé, Cameroon: is safe donation a reality or a myth?

Blood safety remains an issue of major concern in transfusion medicine in developing countries where national blood transfusion services and policies, appropriate infrastructure, trained personnel and financial resources are lacking. This is aggravated by the predominance of family and replacement, rather than regular benevolent, nonremunerated donors. Thus, in order to identify and encourage healthy, regular and benevolent nonremunerated donors, consenting first-time blood donors in the Yaoundé University Teaching Hospital were screened for human immunodeficiency virus (HIV), hepatitis B surface antigen (HBSAg), hepatitis C virus (HCV), human T-cell lymphotropic virus-I (HTLV-I) and syphilis using standard methods. Of 252 first-time donors recruited, 66 (26.2%) were positive for at least one of the infections screened. There were 7.9% positive for HIV, 10.7% for HBSAg, 4.8% for HCV and 9.1 and 1.6%, respectively, for syphilis and HTLV-I. About 30% of the 66 infected persons had co-infections. HIV-positive donors had a significantly increased risk of being positive for antibodies to syphilis (OR = 7.27; 95% CI = 2.23-23.51; P = 0.0007), not observed for HBV, HCV and HTLV-I. These results suggest that blood transfusion is still very unsafe in this community and that it is imperative that emphasis be laid on donor education. Furthermore, donors with a history of sexually transmitted infections should be totally excluded from all donations.

Down-regulation of SHP1 and up-regulation of negative regulators of JAK/STAT signaling in HTLV-1 transformed cell lines and freshly transformed human peripheral blood CD4+ T-Cells

Adult T-cell leukemia (ATL) is an aggressive malignancy that is associated with human T-cell lymphotropic virus I (HTLV-I) infection. HTLV-I transformed T-cell lines and fresh ATL cells are characterized by constitutive activation of the interleukin-2 receptor (IL-2R) signaling pathway however, the mechanism(s) responsible for constitutive IL-2R activation are unknown. To further examine the cause of this signaling pathway deregulation, we measured mRNA and protein expression levels by real-time PCR and Western blots, respectively, of four negative regulators of the IL-2R signaling pathway including src homology 2 (SH2)-containing phosphatase (SHP1), cytokine-inducible (CIS) SH2-containing protein, suppressor of cytokine signaling-1 (SOCS1) and protein inhibitor of activated signal transducer and activator of transcription 3 (STAT3) (PIAS3) in six HTLV-1 negative and seven HTLV-1 positive T-cell leukemia lines. The activation status of the JAK/STAT pathway was also examined. SHP1 mRNA and protein expression levels were selectively down regulated in all HTLV-1-infected transformed cell lines, while CIS, SOCS1, and PIAS3 protein expression were markedly but variably upregulated and the cells showed evidence of constitutive STAT3 activation. In acutely HTLV-1 infected primary CD4+ T-cells there was a gradual loss of SHP1 expression over 10 weeks in culture which correlated with progression from immortalization to transformation and loss of IL-2 dependence for growth. Two transformed cell lines that were established following HTLV-1 infection showed loss of SHP1 expression and overexpression of CIS, SOCS1, PIAS3. However, this overexpression was not adequate to block constitutive activation of the JAK/STAT pathway. Thus, multiple levels of IL-2 receptor signal deregulation are found in HTLV-1 transformed cells, which may be a result of early loss of SHP1 expression.

Mathematical analysis of the global dynamics of a model for HTLV-I infection and ATL progression

Mathematical analysis is carried out that completely determines the global dynamics of a mathematical model for the transmission of human T-cell lymphotropic virus I (HTLV-I) infection and the development of adult T-cell leukemia (ATL). HTLV-I infection of healthy CD4 + T cells takes place through cell-to-cell contact with infected T cells. The infected T cells can remain latent and harbor virus for several years before virus production occurs. Actively infected T cells can infect other T cells and can convert to ATL cells, whose growth is assumed to follow a classical logistic growth function. Our analysis establishes that the global dynamics of T cells are completely determined by a basic reproduction number R 0. If R 0⩽1, infected T cells always die out. If R 0>1, HTLV-I infection becomes chronic, and a unique endemic equilibrium is globally stable in the interior of the feasible region. We also show that the equilibrium level of ATL-cell proliferation is higher when the HTLV-I infection of T cells is chronic than when it is acute.

The contrasting roles of IL-2 and IL-15 in the life and death of lymphocytes: implications for the immunotherapy of rheumatological diseases

Chapter summaryInterleukin-15 (IL-15) is a 14-15-kDa member of the 4α helix bundle family of cytokines that stimulate T and NK (natural killer) cells. IL-15 and IL-2 utilize heterotrimeric receptors that include the cytokine-specific private receptors IL-2Rα and IL-15Rα, as well as two receptor elements that they share, IL-2Rβ and γc. Although IL-2 and IL-15 share two receptor subunits and many functions, at times they provide contrasting contributions to T-cell-mediated immune responses. IL-2, through its pivotal role in activation-induced cell death (AICD), is involved in peripheral tolerance through the elimination of self-reactive T cells. In contrast, IL-15 in general manifests anti-apoptotic actions and inhibits IL-2-mediated AICD. IL-15 stimulates the persistence of memory phenotype CD8+ T cells, whereas IL-2 inhibits their expression. Abnormalities of IL-15 expression have been described in patients with rheumatoid arthritis or inflammatory bowel disease and in diseases associated with the retrovirus HTLV-I (human T-cell lymphotropic virus I). Humanized monoclonal antibodies that recognize IL-2Rα, the private receptor for IL-2, are being employed to inhibit allograft rejection and to treat T-cell leukemia/lymphoma. New approaches directed toward inhibiting the actions of the inflammatory cytokine, IL-15, are proposed for an array of autoimmune disorders including rheumatoid arthritis as well as diseases associated with the retrovirus HTLV-I.