Human T-cell Leukemia-lymphoma Virus Research Articles

Effects of interferon inducible protein 16 (IFI16) on viral protein and pro-inflammatory cytokine expression in human T-cell leukemia virus type 1 (HTLV-1)-positive T cells

Objective To investigate the effects of interferon inducible protein 16 (IFI16), a cytosolic DNA sensor, on the expression of human T-cell leukemia virus type 1 (HTLV-1) proteins and pro-inflammatory cytokines in adult HTLV-1-positive T cells. Methods IFI16 expression in different HTLV-1-positive T cell lines was detected by immunoblot assay. Specific siRNA targeting the IFI16 gene was constructed and the gene silencing efficiency was detected by immunoblot assay. Expression of HTLV-1 Tax protein at mRNA and protein levels was respectively detected by real-time PCR and immunoblot assay after knocking down the expression of IFI16 in HTLV-1-positive T cells with siRNA. Expression of interferon (IFN)-α, IFN-γ, tumor necrosis factor (TNF)-α, Tax and Env were detected by real-time PCR. Results Compared with the HTLV-1-negative T cell line Jurkat, IFI16 expression was enhanced in the HTLV-1-positive T cell lines MT2, MT4 and C8166. Tax expression was increased, while that of IFN-α, IFN-γ and TNF-α was decreased in MT2 and MT4 cells after silencing the expression of IFI16 with siRNA. Conclusions IFI16 expression was increased in HTLV-1-positive MT2 and MT4 cells. Meanwhile, IFI16 promoted the production of interferon and pro-inflammatory cytokines and inhibited the expression of HTLV-1 proteins. Key words: Interferon inducible protein 16 (IFI16); Human T-cell leukemia lymphoma virus type 1 (HTLV-1); Interferon; T lymphocyte; TNF-α

Inflammatory Alteration of Human T Cells Exposed Continuously to Asbestos.

Asbestos is a known carcinogen and exposure can lead to lung cancer and malignant mesothelioma. To examine the effects of asbestos fibers on human immune cells, the human T cell leukemia/lymphoma virus (HTLV)-1 immortalized human T cell line MT-2 was employed. Following continuous exposure to asbestos fibers for more than eight months, MT-2 sublines showed acquisition of resistance to asbestos-induced apoptosis with decreased death signals and increased surviving signals. These sublines showed various characteristics that suggested a reduction in anti-tumor immunity. On the other hand, inflammatory changes such as expression of MMP7, CXCR5, CXCL13 and CD44 was found to be markedly higher in sublines continuously exposed to asbestos compared with original MT-2 cells. All of these molecules contribute to lung inflammation, T and B cell interactions and connections between mesothelial cells and T cells. Thus, further investigation focusing on these molecules may shed light on the role of chronic inflammation caused by asbestos exposure and the occurrence of malignant mesothelioma. Finally, regarding peripheral T cells from healthy donors (HD) and asbestos-exposed patients with pleural plaque (PP) or malignant pleural mesothelioma (MPM), following stimulation of CD4+ T cells, T cells from MPM patients showed reduced potential of interferon (IFN)-γ expression. Moreover, levels of interleukin (IL)-6, one of the most important cytokines in chronic inflammation, in cultured supernatants were higher in PP and MPM patients compared with HD. Overall, asbestos-induced chronic inflammation in the lung as well as the pleural cavity may facilitate the onset of asbestos-induced cancers due to alterations in the interactions among fibers, immune cells such as T and B cells and macrophages, and mesothelial and lung epithelial cells. Further investigations regarding chronic inflammation caused by asbestos fibers may assist in identifying molecular targets for preventive and therapeutic strategies related to the effects of asbestos exposure.

Deoxynivalenol- and zearalenone-contaminated feeds alter gene expression profiles in the livers of piglets.

ObjectiveThe Fusarium mycotoxins of deoxynivalenol (DON) and zerolenone (ZEN) cause health hazards for both humans and farm animals. Therefore, the main intention of this study was to reveal DON and ZEN effects on the mRNA expression of pro-inflammatory cytokines and other immune related genes in the liver of piglets.MethodsIn the present study, 15 six-week-old piglets were randomly assigned to the following three different dietary treatments for 4 weeks: control diet, diet containing 8 mg DON/kg feed, and diet containing 0.8 mg ZEN/kg feed. After 4 weeks, liver samples were collected and sequenced using RNA-Seq to investigate the effects of the mycotoxins on genes and gene networks associated with the immune systems of the piglets.ResultsOur analysis identified a total of 249 differentially expressed genes (DEGs), which included 99 upregulated and 150 downregulated genes in both the DON and ZEN dietary treatment groups. After biological pathway analysis, the DEGs were determined to be significantly enriched in gene ontology terms associated with many biological pathways, including immune response and cellular and metabolic processes. Consistent with inflammatory stimulation due to the mycotoxin-contaminated diet, the following Kyoto encyclopedia of genes and genomes pathways, which were related to disease and immune responses, were found to be enriched in the DEGs: allograft rejection pathway, cell adhesion molecules, graft-versus-host disease, autoimmune thyroid disease (AITD), type I diabetes mellitus, human T-cell leukemia lymphoma virus infection, and viral carcinogenesis. Genome-wide expression analysis revealed that DON and ZEN treatments downregulated the expression of the majority of the DEGs that were associated with inflammatory cytokines (interleukin 10 receptor, beta, chemokine [C-X-C motif] ligand 9), proliferation (insulin-like growth factor 1, major facilitator superfamily domain containing 2A, insulin-like growth factor binding protein 2, lipase G, and salt inducible kinase 1), and other immune response networks (paired immunoglobulin-like type 2 receptor beta, Src-like-adaptor-1 [SLA1], SLA3, SLA5, SLA7, claudin 4, nicotinamide N-methyltransferase, thyrotropin-releasing hormone degrading enzyme, ubiquitin D, histone H2B type 1, and serum amyloid A).ConclusionIn summary, our results demonstrated that high concentrations DON and ZEN disrupt immune-related processes in the liver.

Increased seroreactivity to human T cell lymphoma/leukemia virus-related endogenous sequence-1 Gag peptides in patients with human T cell lymphoma/leukemia virus myelopathy.

Previously, we had shown that although only 8% of patients with large granular lymphocytic leukemia (LGLL) were infected with human T cell lymphoma/leukemia virus (HTLV)-2, almost half had antibodies to HTLV Gag and Env peptides. Herein, we investigated whether this could be due to cross-reactive antibodies to two homologous peptides in the Gag protein of the endogenous retrovirus HTLV-related endogenous sequence-1 (HRES-1). In addition, we had previously shown that patients with HTLV neurodegenerative diseases had increased seroreactivity to homologous HERV-K10 endogenous retrovirus peptides. Hence, in this study we also examined whether these patients had increased seroreactivity to the aforementioned HRES-1 Gag peptides. Sera from 100 volunteer blood donors (VBD), 53 patients with LGLL, 74 subjects with HTLV-1 or 2 infection (58 nonmyelopathy and 16 myelopathy), and 83 patients with multiple sclerosis (MS) were evaluated. The HTLV-positive myelopathy (HAM) patients had a statistically increased prevalence of antibodies to both HRES-1 Gag peptides (81%) vs. the VBD (0%), LGLL patients (13%), and MS patients (1%), and the HTLV-positive nonmyelopathy subjects (21%). The data suggest that cross-reactivity to HRES-1 peptides could be involved in the pathogenesis of HAM. The difference between the VBD and LGLL patients was also statistically significant, also suggesting a possible association in a minority of patients.

Seroprevalence and correlates of human T-cell lymphoma/leukemia virus type 1 antibodies among pregnant women at the University of Nigeria Teaching Hospital, Enugu, Nigeria.

BackgroundHuman T-cell lymphoma/leukemia virus (HTLV)-1 is a retrovirus transmitted vertically from mother to child parenterally and sexually by infected lymphocytes.ObjectiveThe objective of this study was to determine the seroprevalence of HTLV-1 antibodies and associated risk factors for HTLV-1 infection among pregnant women in University of Nigeria Teaching Hospital, Enugu, southeast Nigeria.Materials and methodsA cross-sectional study was carried out from July to October 2010. Two hundred pregnant women were recruited consecutively from the antenatal clinic. Five milliliters of blood was collected from each of the participants into a plain sterile bottle and allowed to clot. The serum obtained was stored at −20°C until required for analysis. The serum samples were then analyzed for antibodies to HTLV-1 using a one-step incubation double-antigen sandwich enzyme-linked immunosorbent assay kit. Participants’ demographic characteristics and degree of exposure to the risk factors associated with HTLV-1 infection were captured using a questionnaire. Statistical analysis of results was done using SPSS version 17.ResultsThe average age of the pregnant women was 28.94 years (standard deviation 4.17). The age-group with the highest representation was those between the ages of 26 and 30 years. Thirty-six percent of the population was above 30 years old. The result of the tests showed that only one respondent, a 31-year-old pregnant woman tested positive for HTLV-1 antibodies. Therefore, the seroprevalence of HTLV-1 antibodies among pregnant women attending the antenatal clinic at University of Nigeria Teaching Hospital was 0.5%, with a 95% confidence interval of 0%–2.8%. Some of the sociodemographic risk factors of HTLV-1 infection found to be applicable to the 31-year-old woman who tested positive included positive history of previous sexually transmitted diseases, high parity, low socioeconomic status, female sex, and age above 30 years. The pregnant women that participated in this study were exposed to risk factors and behaviors associated with HTLV-1 infection. Some of the pregnant women (17.5%) had contracted sexually transmitted diseases, and 80.5% did not use condoms during coitus.ConclusionThe seroprevalence obtained in this study was low, though it is 100% for anyone infected. More prospective and multicenter studies are required to determine the infectivity of HTLV-1 among pregnant women in Nigeria.

Increased seroreactivity to HERV-K10 peptides in patients with HTLV myelopathy

BackgroundPreviously, we had shown that persons infected with human T-cell lymphoma leukemia virus 1 or 2 (HTLV-1 or 2) had an increased prevalence of antibodies to a peptide in the Pol protein of the retrovirus HERV-K10, homologous to a peptide in HTLV gp21 envelope protein. The prevalence rate was higher in those with myelopathy vs. non-myelopathy. We have now extended our observations to a cohort restricted to North America in whom the diagnosis of HTLV myelopathy was rigorously confirmed to also test for reactivity to another HERV-K10 peptide homologous to the HTLV p24 Gag protein.MethodsSera from 100 volunteer blood donors (VBD), 53 patients with large granular lymphocytic leukemia (LGLL), 74 subjects with HTLV-1 or 2 infection (58 non-myelopathy and 16 myelopathy) and 83 patients with multiple sclerosis (MS) were evaluated in ELISA assays using the above peptides.ResultsThe HTLV myelopathy patients had a statistically significant increased prevalence of antibodies to both HERV-K10 peptides (87.5%) vs. the VBD (0%), LGLL patients (0%), MS patients (4.8%), and the HTLV positive non-myelopathy subjects (5.2%).ConclusionThe data suggest that immuno-cross-reactivity to HERV-K10 peptides and/or transactivation of HERV-K10 expression by the HTLV Tax protein may be involved in the pathogenesis of HTLV-associated myelopathy/tropical spastic paraparesis and spastic ataxia.

Registry of inherited coagulopathies in Brazil: first report

Inherited coagulopathies are bleeding disorders, which require treatment for life. Keeping an updated registry on these diseases is crucial for planning care, documenting prevalence of diseases and evaluating effectiveness of resources. We have analysed data from 26 treatment centres on coagulopathies in Brazil. Information included socio-demographic data, diagnosis of coagulopathies, severity of haemophilias A and B, presence and quantification of inhibitors in haemophilia, type of von Willebrand disease (VWD) and infection status for viral diseases. On 1 July 2007, there were 10 982 patients with inherited coagulopathies in Brazil, of which 6881 (62.7%) corresponded to haemophilia A, 1291 (11.7%) to haemophilia B, 2333 (21.2%) to VWD, 258 (2.4%) to other coagulopathies and 219 (2.0%) to undiagnosed bleeding disorders. Haemophilia A and B inhibitors were present in 9.9% and 1.9% of the patients, respectively. Human immunodeficiency virus infection was present is 6.5%, 4.8% and 1% of patients with haemophilia A, B and VWD, respectively. Hepatitis C virus infection was present in 34.9%, 29.7% and 12% of patients with haemophilia A, B and VWD, respectively. Infection by hepatitis B and human T-cell leukemia-lymphoma virus was also reported. This is the first report on the registry of patients with inherited coagulopathies in Brazil, supposed to be the third largest population of patients with haemophilia.

Use of replacement blood donors to study the epidemiology of major blood‐borne viruses in the general population of Maputo, Mozambique

The seroprevalence rates of human immunodeficiency virus (HIV), human T-cell leukemia/lymphoma virus (HTLV), hepatitis B virus (HBV), hepatitis D virus (HDV), and hepatitis C virus (HCV) in Mozambique are poorly documented. The epidemiology of these infections was studied in the Maputo region. All donors attending the blood bank during the study period were interviewed and underwent serological and molecular tests for markers of virus exposure. Thus, 1,578 consecutive replacement blood donors were investigated, as they undergo no selection (other than their relation with a patient needing a transfusion), and may thus provide reliable estimates of the prevalence rates in the general population. The age-standardized prevalence rates among 15- to 49-year-old men and women were, respectively, 12.3 and 15.4% for HIV and 0.9 and 1.2% for HTLV. Low educational status (P = 0.014) and tattooing/scarification (P = 0.023) were predictive of HIV infection in multivariate analysis. The age-adjusted prevalence rates of markers of hepatotropic virus among men and women were, respectively, 10.6 and 4.5% for hepatitis B surface antigen (HBsAg), 1.2 and 1.0% for anti-HCV, and 0 and 0% for anti-HDV. Two percent of donors had viral co-infections, involving most frequently the combination of HIV and HBsAg +. A significant association was found between anti-HIV and anti-HBc (P = 0.012). HBsAg was associated with the place of birth (P = 0.011) and a history of transfusion (P = 0.069). Smokers had higher seroprevalence rates than nonsmokers for HIV (P < 0.0001) and HBsAg (P = 0.045). Genotype A was the most frequent HBV genotype (86.3%) followed by E and D. HCV genotypes were 1a, 1b, 3a, and 5a. These results show that HBV vaccination and HIV-preventive measures need to be reinforced in Mozambique.

Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions

The human T-cell leukemia/lymphoma virus (HTLV) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX. To date, we know that this region encodes two essential transcriptional and post-transcriptional positive regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue). Here, we will review current knowledge of the functions of three additional proteins encoded in the pX region, p12I, p13II, and p30II.

Prevalence of Hepatitis C Infection in Patients with Non-Hodgkin's Lymphoma in South Florida and Review of the Literature

The etiology of non-Hodgkin's lymphoma is unknown in the majority of the cases. Although Epstein - Barr virus, human T-cell leukemia-lymphoma virus and human herpes virus-8 have been established as casual agents in the pathogenesis of specific types of lymphoma, the role of hepatitis C virus (HCV) in lymphomagenesis remains controversial, with marked geographic variability. We conducted an epidemiologic study to evaluate the prevalence of hepatitis C virus infection in patients with lymphoma in South Florida. Ninety consecutive patients with lymphoma and 96 consecutive control patients with solid tumors were tested for HCV. HCV infection was detected in 2 patients with NHL (2.2%) and in 4 control patients (4.1%). Our study does not support the association between HCV and lymphoma in South Florida, US.

Differential patterns of human cytomegalovirus gene expression in various T-cell lines carrying human T-cell leukemia-lymphoma virus type I: role of Tax-activated cellular transcription factors.

Replication of human cytomegalovirus (HCMV) was investigated in various T-cell lines expressing the tax gene product of human T-cell leukemia-lymphoma virus type I (HTLV-I). Differential patterns of HCMV replication were found in HTLV-I-carrying cell lines. HCMV gene expression was restricted to the immediate-early genes in MT-2 and MT-4 cells, whereas full replication cycle of the virus was observed in C8166-45 cells. Productive HCMV infection induced a cytopathic effect resulting in the lysis of infected cells. The results of electrophoretic mobility shift assay (EMSA) showed high levels of NF-kappaB-, CREB/ATF-1-, and SRF-specific DNA binding activity in all Tax-positive cell lines. In contrast, SP1 activity could be detected only in C8166-45 cells. Using an inducible system (Jurkat cell line JPX-9), a dramatic increase in NF-kappaB, CREB/ATF-1, SRF, and SP1 binding activity, as well as productive HCMV infection, were observed upon Tax expression. Overexpression of SP1 in MT-2 and MT-4 cells converted HCMV infection from an abortive to a productive one. These data suggest that the stimulatory effect of Tax protein on HCMV in T cells is accomplished through at least five host-related transcription factor pathways. The results of this study provide possible mechanisms whereby HCMV infections might imply suppression of adult T-cell leukemia.

The Human T-Cell Lymphoma/Leukemia Viruses

The primate T-cell lymphoma/leukemia viruses belong to an oncogenic genus of complex retroviruses. Members of this genus have been shown to be pathogenic in man. The human T-cell lymphoma/leukemia virus (HTLV) type I has been linked in the etiology of T-cell malignancies and “autoimmune-like” neurologic and rheumatic disorders; a related virus, HTLV-II, is becoming increasingly associated with similar disorders. Cell transformation is thought to be caused predominantly by the effects of the viral regulatory protein, Tax. An additional induced host cell molecule, adult T-cell lymphoma-derived factor, may contribute to cell immortalization. Like the DNA tumor viruses, HTLV activates transcription of cellular proto-oncogenes and inhibits cellular mechanisms of tumor suppression, cell cycle arrest, and apoptosis. However, individuals who are able to mount a strong cell-mediated immune response and limit viral entry into uninfected cells do not develop associated malignancies. Unfortunately, HTLV-induced malignancies are difficult to treat with conventional chemotherapy, and disease progression is often rapid with a median survival of less than 2 years. There are, however, some novel approaches that have yet to be fully tested that may have greater efficacy in the treatment of HTLV-induced diseases. In the future, better screening and detection methods, along with new vaccines and therapies, may contribute to the increased prevention and control of HTLV infection and its associated diseases.

Generation of HTLV‐I‐Transformed T Cell Lines

Viral transformation of T cells is an effective method for obtaining large numbers of T cells that are easily maintained in the laboratory. Human T cell leukemia/lymphoma virus (HTLV-I), a type C retrovirus clearly implicated as the etiologic agent of adult T cell leukemia, can both infect and transform normal T cells. This unit presents a protocol in which human T cells are activated and then transformed with HTLV-I. Detection of virally transformed cells is discussed in the commentary.

Current therapeutic approaches in the treatment of Non-Hodgkin's lymphoma.

To review the causes, classification, treatment, and new treatment modalities of non-Hodgkin's lymphoma. Published literature and experimental therapies. The increasing incidence of non-Hodgkin's lymphoma can be attributed to a growth in the number of immunodeficiency and autoimmune disorders, infectious agents, and human T-cell leukemia-lymphoma virus. Treatment options include watch-and-wait, radiation, chemotherapy, biologic therapy, and stem cell/bone marrow transplant. New therapies include the use of monoclonal antibodies and radioimmunotherapy. Experimental therapies include high-dose radioimmunotherapy and stem cell transplantation, vaccines, and antisense antiangiogensis agents. Nurses will need to become versed in this modality, and will play an important part not only in therapy but also in patient education.

Human T-cell leukemia virus type 2 induces survival and proliferation of CD34+ TF-1 cells through activation of STAT1 and STAT5 by secretion of interferon-γ and granulocyte macrophage–colony-stimulating factor

Human T-cell leukemia-lymphoma virus (HTLV) type-2 can induce the survival and proliferation of CD34(+) TF-1 cells deprived of interleukin (IL)-3. This effect did not require productive infection and occurred when HTLV-2 was produced from T cells (CMo), but not from B cells (BMo), unless the latter virus was complexed with anti-HLA-DR monoclonal antibodies (mAbs). Cellular and molecular mechanisms triggered by HTLV-2 interaction with TF-1 cells were here investigated. Activation of signal transducer and activator of transcription (STAT) 5 protein occurred in TF-1 cells incubated either with IL-3 or with HTLV-2/CMo; in addition the virus, but not IL-3, activated STAT1. The effect of HTLV-2 required several hours, suggesting dependence on the induction of cellular factors. By screening a panel of secreted factors, granulocyte macrophage-colony-stimulating factor (GM-CSF), interferon (IFN)-gamma, and stem cell factor (SCF) were found induced by HTLV-2 in TF-1 cells. Of note is the fact that these molecules induce a variety of biologic effects through the activation of STAT proteins, including STAT1 and STAT5. Neutralization experiments indicated that GM-CSF and IFN-gamma, but not SCF, were responsible for HTLV-2-induced STAT activation, whereas anti-GM-CSF antibodies greatly inhibited TF-1 cell proliferation. Finally, incubation of BMo virus with anti-HLA-DR mAb rescued TF-1 cell survival in the absence of IL-3. Thus, HTLV-2 interaction with CD34(+) precursor cells may lead to the expression of cytokines that, by inducing autocrine activation of STATs, may influence the host's regenerative capacity and immune response to HTLV-2 and to other infectious agents.

Apoptosis in Lymphocytic Leukemias and Lymphomas

Most current classifications of lymphoid neoplasms define the tumors based on the cell of origin, phenotype, genetic abnormalities, and clinical features. Here it is proposed that human lymphocytic tumors can be categorized based on the propensity and capacity of the tumor cells to undergo apoptosis. The first category is defined by malignant cells that are resistant to apoptosis due to expression of anti-apoptotic factors such as bcl-2 and cellular inhibitors of apoptosis (IAPs). These tumors would include CLL and follicular lymphomas, as well as some malignancies in which the tumor cells are infected by viruses that co-opt cell survival pathways, such as human T-cell leukemia/lymphoma virus (HTLV)-1. The second category, in which the malignant cells are apoptosis-prone, would include tumors arising in the context of impaired cytotoxic T-cell function. These neoplasms would include some human immunodeficiency virus (HIV)-related lymphomas such as Burkitt's lymphoma, and post-transplantation lymphomas. The third category would include neoplasms of intermediate sensitivity to apoptosis, some of which are associated with infection such as mucosa-associated lymphoid tissue (MALT) lymphomas of the stomach. Although this classification is tentative, it should evolve in parallel with our understanding of pathogenic mechanisms in lymphoid neoplasia, and provides a novel framework with which to consider the appropriateness of specific therapeutic strategies. Distinctions among lymphocytic tumors in terms of the likelihood of response to therapies such as antisense to bcl-2 related proteins, inhibitors of NF-κB activity, and new approaches aimed at bolstering the host's immune response, would cross standard classifications based on the T or B-cell origin of the tumor cells.

Human T cell leukaemia/lymphoma virus infection in pregnant women in the United Kingdom: population study

Objective: To assess the prevalence of human T cell leukaemia/lymphoma virus (HTLV) infection in pregnant women in the United Kingdom.Design: Population study.Subjects: Guthrie card samples from babies born in 1997-8.Samples...

Prevalence of antibody to human T cell leukaemia/lymphoma virus in women attending antenatal clinic in southeast London: retrospective study

Infection with human T cell leukaemia/lymphoma virus (HTLV) type I occurs mainly in Japan, central and west Africa, and the Caribbean basin. Infection confers a lifetime risk of 2-4% for...

Erratum: In vitror infection of CD4+ T lymphocytes with HTLV-1 generates immortalized cell lines coexpressing lymphoid and myeloid cell markers

The human T cell leukemia/lymphoma virus (HTLV-I) is the etiologic agent of adult T cell leukemia (ATL). CD4+ lymphocytes are the preferential targets of infection, even though other cell types can be infected in vitro by the virus. Although ATL cells show CD3 and CD4 surface markers, some ATL-derived cell lines were reported to express also myeloid antigens. In order to analyze possible phenotypic changes induced by HTLV-I after infection of human lymphocytes, CD4+ cells were isolated from peripheral blood of three healthy donors, by separation through immunomagnetic beads.

In vitro infection of CD4+ T lymphocytes with HTLV-I generates immortalized cell lines coexpressing lymphoid and myeloid cell markers.

The human T cell leukemia/lymphoma virus (HTLV-I) is the etiologic agent of adult T cell leukemia (ATL). CD4+ lymphocytes are the preferential targets of infection, even though other cell types can be infected in vitro by the virus. Although ATL cells show CD3 and CD4 surface markers, some ATL-derived cell lines were reported to express also myeloid antigens. In order to analyze possible phenotypic changes induced by HTLV-I after infection of human lymphocytes, CD4+ cells were isolated from peripheral blood of three healthy donors, by separation through immunomagnetic beads. CD4+ lymphocytes were then infected by coculture with irradiated HTLV-I producing MT-2 cells. The phenotypic profile of infected cells was studied by flow cytometric analysis using monoclonal antibodies against lymphoid (CD3, CD4, TCR alpha/beta) and myelomonocitic markers (CD13, CD14, CD15, CD33, CD34). The results show that HTLV-I immortalized cell lines coexpressed CD13, CD33 and lymphoid markers. No expression of CD14, CD15 and CD34 was observed. These data suggest that the presence of both myeloid and lymphoid phenotype in HTLV-I infected T cells is the results of an induction rather than a selection mechanism.