Biomedical subjects

L Gazzolo

Publications and source records attributed to L Gazzolo.

At least 37 records · Page 2Linked to original sources

PubMed1993

Organization and expression of intermediate filaments in epithelial cells expressing the HTLV-I Tax protein.

Intermediate filaments (IF) represent major components of the cytoskeletal network. These proteins which are differentially expressed according to the cell type, constitute a dynamic structure which not only contributes to the cell architecture but also defines its state of differentiation. Furthermore, numerous observations have shown that the IF network is altered in cells transformed by tumorigenic viruses. We have previously demonstrated that HTLV-I (human T-cell leukemia virus type I) transformed T cells were characterized by a high level of vimentin transcripts and that the HTLV-I Tax regulatory protein was able to transactivate the vimentin promoter transfected into Jurkat and HeLa cells. To enlarge the scope of this study, we investigated the effects of the Tax protein on the expression and organization of IF of epithelial cells in which the IF network is composed of vimentin and cytokeratin. To this aim, we have developed a model of epithelial cells (HeLa) stably expressing the tax sequences which were introduced by using retrovirus-mediated gene transfer. Half of the Tax expressing HeLa clones were loosely adherent to the culture surface and were displaying remarkable morphological alterations, as ascertained by the presence of round-shaped or spindle-shaped cells. In these cells, expression of this viral protein correlated to a pronounced disruption in the distribution of both the vimentin and the cytokeratin networks, as shown by immunofluorescence and ultrastructural analysis. Indeed, vimentin filaments appeared to be concentrated in discrete spots throughout the cytoplasm, while the cytokeratin filaments appeared to form a dense ring around the nucleus. More importantly, mRNA and protein analysis indicate an enhanced expression of the cytokeratin 7 gene.(ABSTRACT TRUNCATED AT 250 WORDS)

Epithelium↗

PubMed1991

Enhanced resistance to HIV-1 replication in U937 cells stably transfected with the human IFN-beta gene behind an MHC promoter fragment.

Cells of the monocyte lineage act as a major reservoir for HIV, and ways of enhancing the resistance of mononuclear phagocytes to HIV replication would be useful for delaying the onset of AIDS in infected individuals. Seif et al. (J. Virol. 65:664, 1991) have recently shown the possibility of obtaining stable antiviral expression (SAVE), directed against three nonretroviral RNA viruses, and normal cell viability in a significant percentage of murine BALB/c 3T3 cells transformed with an IFN-beta expression plasmid under the control of the 0.6-kb XhoII-NruI promoter region of the murine H-2Kb MHC gene. In the present paper, we show that it is possible to establish SAVE in human promonocytic cells. Cells of the human promonocytic U937 line were stably transfected with a human IFN-beta expression plasmid carrying the neo- and human IFN-beta-coding sequences under the control of the H-2Kb promoter fragment previously used in murine cells. After selection with G418, two transformed clones were isolated that released small amounts of human IFN-beta into the culture medium, without affecting the expression of CD4 and leucocyte function-associated Ag-1 differentiation Ag. The presence of construct-derived IFN-beta mRNA was demonstrated by polymerase chain reaction amplification of cDNA, and the level of 2-5A synthetase, one of the major IFN-induced antiviral proteins, was shown to be constitutively increased. These clones were less permissive for HIV-1 than control clones transformed with the neo gene only. The antiviral state could be modulated by anti-IFN-beta antibodies, in that the continuous presence of antibodies in the culture medium abolished the enhanced resistance to HIV-1 replication, whereas the withdrawal of the antiserum restored the antiviral state, indicating that it did indeed result from the constitutive synthesis of human IFN-beta. These results demonstrate the possibility of restricting HIV-1 replication in human promonocytic cells by establishing SAVE. Further exploration of this method as a possible approach to somatic cell gene therapy of HIV infection appears worthwhile.

2',5'-Oligoadenylate Synthetase↗

PubMed1991

EGF promotes in vivo tumorigenic growth of primary chicken embryo fibroblasts expressing v-myc and enhances in vitro transformation by the v-erbA oncogene.

We report that the activation of the endogenous chicken EGF receptor leads to the tumorigenic growth in vivo of early passage chicken embryo fibroblasts (CEFs) that express a nonsarcomagenic oncogene, v-myc. To provide a continuous paracrine source of this growth factor in vivo, we employed irradiated Rat-1 cells which had been stably transfected with a synthetic cDNA to human EGF. Expression of another non-sarcomagenic nuclear oncogene, v-erbA, prones the CEFs to in vitro transformation by EGF, but does not cause EGF dependent tumorigenicity in vivo. The short period of incubation in the in vivo assay employed by our study (10 days), together with the genetic stability of primary chicken embryo fibroblasts, make it very likely that the reported alterations in cellular behaviour are a direct and primary effect of the expression of the relevant oncogenes and their cooperation with the EGF induced response. Dose response and ligand binding assays suggest that the EGF response is transmitted via the chicken c-erbB molecule, which by virtue of its preference for TGF-alfa is distinct from the mammalian EGF receptors studied so far. The level of expression of the endogenous chicken EGF receptor is within the same range as that reported for primary human fibroblasts (5-7 x 10(3) per cell). The cooperative effect of v-myc with chicken c-erbB probably takes place at a post receptor level, as its expression did not affect the steady state level or affinity for ligand of the chicken EGF receptor.

Animals↗

PubMed1991

Constitutive IL-2 expression in HTLV-I-infected leukaemic T cell lines.

An IL-2 autocrine growth circuit has been proposed as a major mechanism in HTLV-I-related leukaemogenesis. We have developed a polymerase chain reaction combined with reverse transcription RT-PCR to detect IL-2 transcripts and a sensitive immunostaining method for IL-2 protein. Combination of these two methods with in situ hybridization demonstrated that most cells of the T cell line IARC 301.5, whose proliferation is stimulated by autocrine IL-2, constitutively synthesize IL-2. This pattern was also found in the HTLV-I T cell lines HUT, MT2 and C 8166/45, and in the HTLV-I-negative T cell lines Jurkat and HSB2 but not MOLT4. Four non-lymphoid cell lines and cultured fibroblasts were negative, in agreement with the T cell specificity of IL-2 synthesis. Hence, most T cell lines tested, whether HTLV-I-infected or not, constitutively synthesize IL-2, suggesting a possible common feature of leukaemic T cell lines. The presence of IL-2 transcript and protein in most cells of the reacting cell lines is consistent with an autocrine process possibly involved at some stage in acquiring growth autonomy.

Antibodies, Monoclonal↗

PubMed1991

Molecular and cellular events at the onset of the lymphoproliferative process induced by HTLV-I (human T-cell leukemia virus, type I).

The human retrovirology opened its first chapter, 10 years ago, with the isolation and characterization of HTLV-I (Human T-cell leukemia virus, type I), a type C retrovirus, which was found to be etiologically linked first to adult T-cell leukemia and second to neurological disorders. Epidemiological data have indeed shown that patients who developed these diseases represent a small percentage of HTLV-I infected individuals living in restricted geographical areas. Experiments performed at molecular and cellular levels have revealed that HTLV-I plays an essential role in the initiation of the lymphoproliferative process. Indeed, viral particles deliver a mitogenic signal to human resting T lymphocytes. After proviral integration, two regulatory proteins--Tax and Rex--are controlling the replicative cycle of HTLV-I. The Tax protein trans-activates the proviral transcription and the Rex protein is essential in the synthesis of viral structural proteins. Furthermore, the Tax protein induces the transcription of several cellular genes involved in T-cell activation and proliferation. Studies are now aimed at identifying HTLV-I target cells among precursors of the T cell lineage and at unravelling the role of HTLV-I in the secondary events leading to leukemogenesis.

Gene Products, rex↗

PubMed1990

Tax1 induction of the HTLV-I 21 bp enhancer requires cooperation between two cellular DNA-binding proteins.

Activation of the HTLV-I promoter by the viral Tax1 transactivator is mediated by a 21 bp sequence motif imperfectly repeated three times and composed of three exactly conserved domains (A, B and C from 5' to 3'). We show here that the Tax1 response requires the integrity of the B domain and of at least one of the flanking A or C domains. We have identified three cellular proteins which bind specifically to the 21 bp motif. One of these is the already well-characterized transcription factor ATF. The other two, namely HEB1 and HEB2, are specific for the 21 bp motif. HEB1 can bind to either domain A or C, but binding of ATF and HEB2 is determined by domain B. However, neither domain B alone, nor ATF/CREB binding sites respond significantly to Tax1. We therefore propose that Tax1 induction of the 21 bp enhancer element requires interaction with the two different cellular proteins identified in this study: HEB1 and HEB2, rather than binding of the ATF factor.

Base Sequence↗

PubMed1990

Human T cell leukemia virus type I induces DNA synthesis and immunoglobulin secretion in human lymphocyte cultures.

Viral particles obtained from HTLV-I (human T cell leukemia virus, type I)-transformed T cell lines induced immunoglobulin production by normal peripheral blood lymphocytes. Conversely, no immunoglobulin could be detected in the supernatant medium in purified B cells cultivated with HTLV-I, suggesting that the presence of T cells is mandatory for HTLV-I to induce B cell polyclonal activation. The T cell help was mediated by soluble factors, as indicated in experiments showing that cell-free conditioned medium from T lymphocytes activated by HTLV-I was able to induce B cell proliferation and differentiation. Furthermore, a direct effect of HTLV-I on B cell proliferation was demonstrated when viral particles were added to purified B cells together with suboptimal doses of Staphylococcus aureus Cowan strain I (SAC). These observations show that an immediate early effect of HTLV-I infection was exerted on B cells, mainly in a T cell-dependent manner. Such an effect may account for the hypergammaglobulinemia observed in HTLV-I seropositive individuals, and in patients with HTLV-I-associated neurological disorders.

B-Lymphocytes↗

PubMed1990

Effect of human T-cell leukemia virus type I tax protein on activation of the human vimentin gene.

We report that the expression of the vimentin gene, a cytoskeletal growth-regulated gene, is activated in trans by the Tax (p40x) transactivator protein encoded by the human T-cell leukemia virus type I. Expression of the Tax protein activates a number of cellular genes, such as those coding for the alpha chain of the high-affinity interleukin-2 receptor and interleukin-2. These findings indicate that the Tax protein is involved in the unregulated T-cell growth associated with human T-cell leukemia virus type I infection. Higher levels of vimentin mRNA were expressed in two human T-cell leukemia virus type I-transformed T cell lines, C91/PL and C81-66/45, when compared with that in Jurkat T cells. We demonstrate that this activation is conferred by the vimentin upstream flanking sequences. Indeed, enhanced activity was detected when constructs with the vimentin promoter linked to the chloramphenicol acetyltransferase gene were transfected in HeLa cells and in two cell lines of hematopoietic origin (Jurkat T lymphoblastoid cells and U937 promonocytic cells) together with a Tax expression plasmid. By introducing a series of deletions in the vimentin promoter, we further restrict these sequences to 30 base pairs, located between 241 and 210 base pairs upstream of the mRNA cap site. A 40-base-pair oligonucleotide containing this regulatory region proved sufficient to confer Tax inducibility upon a heterologous promoter linked to chloramphenicol acetyltransferase. Importantly, this segment includes an 11-base-pair promoter segment that has homology with the binding site for the NF-kappa B transactivating factor. Our findings indicate that constitutive expression of the vimentin gene under the control of the Tax protein may be relevant in understanding the progression of the lymphoproliferative process associated with human T-cell leukemia virus type I infection.

Base Sequence↗

PubMed1989

Human T cell leukemia/lymphoma virus type I infection of a CD4+ proliferative/cytotoxic T cell clone progresses in at least two distinct phases based on changes in function and phenotype of the infected cells.

The effect of human T cell leukemia/lymphoma virus type I (HTLV-I) infection on the function and the phenotype of a human proliferating/cytotoxic T cell clone, specific for tetanus toxin, was investigated. During the period after infection, two distinct phases were observed, based on growth properties, phenotype, and functional activity of the infected cells. Phase I HTLV-I infected cells (0 to about 150 days after infection) proliferated in an IL-2-dependent way, but without the requirement for repetitive antigenic stimulation. No differences in expression of the CD2, CD3, CD4, Tp103, and CD28 Ag between these cells and the parental cells could be demonstrated, with the exception of the expression of IL-R p55 and HLA-DR Ag, which were constitutively expressed on the phase I cells. The phase I HTLV-I-infected cells, as well as the parental 827 cells reacted with a mAb specific for an epitope on the variable part of the TCR beta-chain, indicating that the TCR was not altered after HTLV-I infection. Like the parental clone, the phase I cells proliferated in response to tetanus toxin, but the tetanus toxin-specific response of the phase I cells did not require the presence of APC. Results of experiments, in which the levels of intracellular Ca2+ were measured, indicated that HTLV-I cells can acquire the capability to process Ag and present that to themselves. Phase I HTLV-I-infected T cells had lost their cytotoxic activity which was likely to be due to an effect on the lytic machinery rather than on Ag recognition by the TCR, inasmuch as it was found that phase I HTLV-I-infected T cells did no longer contain N-alpha-benzyloxy-L-lysine thiobenzylester-serine esterase activity. Furthermore, it was found that phase I HTLV-I-infected T cells had a diminished capacity to form conjugates with target cells. From a period of about 200 days after HTLV-I infection, phase II cells emerged that proliferated strongly in the absence of IL-2 and that had lost all functional activity. These cells did not express the CD3/T cell receptor complex on their surface. Phase I as well as phase II HTLV-I-infected cells were targets for CTL raised in the autologous donor.

Antigen-Presenting Cells↗

PubMed1989

Restriction of HIV-1 replication in promonocytic cells: a role for IFN-alpha.

A comparative study of the replication kinetics of human immunodeficiency virus type 1 (HIV-1) was performed in the promonocytic U937 cells and in the T lymphoblastoid H9 cells. If a productive HIV-1 infection of both cell types could be established, the time which elapses before most of the cells could express viral proteins is always proportionally longer for U937 cells than for H9 cells. Indeed, when U937 cells are infected with HIV-1, this nonproductive phase is followed by a lag phase during which the percentage of virus-producing cells is slowly increasing when compared to H9 cells. The restriction of HIV-1 replication in U937 cells might be consecutive to the lower adsorption of viral particles to these cells, even though the same percentage of U937 and H9 cells was expressing the CD4 molecule. Furthermore, we demonstrate that HIV-1 replication in U937 cells is mainly restricted by endogenous IFN-alpha. Indeed, addition of anti-IFN-alpha antibodies at the time of infection, during the nonproductive phase of the viral replication cycle, or during the lag phase leads to an earlier expression of viral proteins and/or to a rapid increase in the percentage of virus-producing cells. Likewise, the treatment of cultures of HIV-1 chronically infected U937 cells with the same antibodies induces an increased production of viral particles. Thus, IFN-alpha appears to be involved in the persistence of HIV-1 in the monocytes/macrophages of infected individuals.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1989

Immunohistochemical study of normal skin of HIV-1-infected patients shows no evidence of infection of epidermal Langerhans cells by HIV.

Langerhans cells (LC) are dendritic epidermal antigen-presenting cells expressing the surface molecule CD4, which renders them theoretical cellular targets for direct infection by the human immunodeficiency virus (HIV). To date, somewhat conflicting results have been reported concerning the in vivo infection of LC by HIV as well as the numerical alteration of these cells in the course of HIV infection. In the present work we studied clinically normal skin of a group of 44 HIV-1-seropositive patients classified according to the Centers for Disease Control (CDC) stages II (n = 14), III (n = 9), and IV (n = 21). Monoclonal antibodies (MAb) to HIV p18, p24, and gp120 and to HLA-DR and CD1a antigens (specific for LC) were applied on frozen skin sections using an amplification biotin-streptavidin-fluorescein technique. The MAb to HIV p18 cross-reacted with a cytoplasmic antigen of epidermal basal keratinocytes also present on HIV-seronegative skin specimens. No other reactivity was observed with any of the three anti-HIV MAb. The quantitative study showed that no significant correlations could be established between the number of LC (evaluated independently by HLA-DR and CD1a antigens) and the number of peripheral blood CD4+ve lymphocytes or the CDC disease stage. These results cast some doubt on the previously reported in vivo infection and numerical decrease in LC in HIV infection. The precise involvement of LC in HIV infection awaits further investigation.

Acquired Immunodeficiency Syndrome↗

PubMed1989

Peripheral T-lymphocyte activation by human T-cell leukemia virus type I interferes with the CD2 but not with the CD3/TCR pathway.

Human T-cell leukemia virus type I (HTLV-I) is etiologically associated with adult T-cell leukemia, an aggressive lymphoproliferative disorder, and with chronic neurological diseases. In vitro it can infect several types of cells but transforms only human T lymphocytes. We have previously shown that HTLV-I viral particles, even when noninfectious, were able to activate human resting T lymphocytes, suggesting that this activation step may be important in the initiation of the lymphoproliferative process. In the present study, we first demonstrate that in contrast to other mitogenic stimuli, HTLV-I has the unique property to activate human resting T cells in the absence of accessory cells. We then investigate the relationship between HTLV-I-induced T-cell activation and the classical well-known pathways of activation, namely, the CD3/TCR and CD2 pathways. Competitive blocking experiments were performed in which the effects of monoclonal antibodies (MAb) to the CD3/TCR complex or to the CD2 molecule were evaluated on the HTLV-I activation of T cells and compared with that obtained on phytohemagglutinin (PHA)-stimulated cells. It was found that anti-CD3 or -TCR MAb strongly suppress the proliferative response of T cells to PHA, but are significantly less efficient in inhibiting the activation initiated by HTLV-I. By contrast, MAb recognizing specific epitopes of the CD2 molecule inhibit the proliferative response of T cells to PHA or to HTLV-I to the same extent. The results provide evidence that HTLV-I virions interfere mainly with activation via CD2 but not via the CD3/TCR complex. Considering the earlier expression of the CD2 molecule on human T-cell precursors, these observations might be relevant to the characterization of the differentiation stage at which viral infection could interfere with the development and the maturation of T lymphocytes.

Antibodies, Monoclonal↗

PubMed1988

Human T-cell leukemia virus type I-induced proliferation of human thymocytes requires the presence of a comitogen.

HTLV-I has recently been shown to be a direct activator of resting human peripheral T cells. In order to determine the susceptibility of T-cell precursors to HTLV-I mitogenic activity we have exposed human thymic T cells to uv-inactivated HTLV-I. Unlike mature T cells, thymocytes were not directly susceptible to HTLV-I-induced activation although agglutination of cells did occur after exposure to HTLV-I alone. However, in the presence of another stimulus, phyto-hemagglutinin or anti-CD3 monoclonal antibodies and accessory cells, thymocytes proliferated when exposed to HTLV-I. Concanavalin A did not induce HTLV-I comitogenic activity. HTLV-I-induced thymocyte proliferation was enhanced by autologous or heterologous accessory cells. This proliferation was shown to be mediated by the interleukin-2/interleukin-2 receptor pathway. Simultaneous stimulation by HTLV-I and nonmitogenic doses of phytohemagglutinin were required both for the production of interleukin-2 and for the expression of the interleukin-2 receptor. These data demonstrated functional differences between peripheral T cells and thymocytes.

Adult↗

PubMed1987

Malondialdehyde production from spermine by homogenates of normal and transformed cells.

The oxidation of spermine in vitro by a mixture of polyamine oxidase and diamine oxidase from pig kidney gives rise to malondialdehyde via 3-aminopropanol as the intermediate. Conversely, with spermidine, under similar experimental conditions, no evidence could be obtained for malondialdehyde formation within the limits of sensitivity of the assay (2.0 nmol). The activities of both these enzymes show about a 2-fold increase in normal rat kidney cells (LA31 NRK) transformed by the temperature sensitive mutant of Rous sarcoma virus (LA31) and incubated at the non permissive temperature (39 degrees C) compared to the activities in LA31 NRK at the permissive temperature (33 degrees C). These same enzymatic activities show no temperature dependent changes in normal rat kidney cells (NRK) or in these same cells infected by the wild type virus (NRK B77). In extracts derived from Friend erythroleukemic cells induced to differentiate by dimethyl sulfoxide or hexamethylene bis acetamide, spermine oxidation takes place more efficiently than in non induced cells. A rise in diamine oxidase activity is seen in LA31 NRK (39 degrees C) 12 h after the temperature shift, whereas morphological manifestations of normalcy are seen only at 48 h. The Km of diamine oxidase is 10(-6) M for putrescine and 10(-3) M for 3-aminopropanol. A possible mechanism involving the well documented acetylation of putrescine [23,26] is proposed for diverting intracellular putrescine away from cytosolic diamine oxidase and towards intramitochondrial monoamine oxidase.

Aldehydes↗

PubMed1987

Loss of interleukin-2 requirement for the generation of T colonies defines an early event of human T-lymphotropic virus type I infection.

Accessory cells and/or soluble factors, together with interleukin 2 (IL2), are required for the proliferation and differentiation of phytohemagglutinin (PHA)-activated T lymphocytes. Human T-lymphotropic virus, type I (HTLV-I), a human retrovirus isolated from patients with adult T cell leukemia, can transform T cells in vitro. We investigated the role of HTLV-I-transformed T cell lines as accessory cells in promoting the growth of T colony-forming cells. We found that T cells isolated by E rosetting and then activated with PHA, when seeded with as few as 5 X 10(3) irradiated HTLV-I-producing cells, could generate colonies in the absence of IL2. We analyzed further the effects of HTLV-I virions on T colony formation. Infection of T cells with semipurified HTLV-I viral particles promoted colony formation, in the absence of IL2, of accessory cells or soluble factors. The same results were obtained either with monocyte-depleted T lymphocytes, or with T4 or T8 lymphocytes. Furthermore, T lymphocytes in the presence of heat-inactivated HTLV-I (devoid of replicative potential) could form colonies independently of IL2. Finally, experiments with sera positive for HTLV-I antibodies (to abolish binding of viral particles to cellular receptors) indicated that HTLV-I promoted IL2-independent colony formation, only by "touching" T colony-forming cells. These results taken together demonstrate that the loss of the exogenous IL2 (and other growth-helping factors) requirement defines an early event of HTLV-I infection. The results also suggest that viral attachment to T cells possibly supplies an accessory function triggering autocrine secretion of IL2 by these cells.

Cell Division↗

PubMed1986

Detection of HTLV-I (human T-cell lymphotropic virus, type I) proviral DNA in leukemic cells from a French patient with Sezary syndrome.

Human T-lymphotropic type I (HTLV-I) proviral sequences were detected in leukemic cells of a patient living in Marseilles (south of France) and suffering from Sezary syndrome. He did not have any travel history outside France and did not receive blood transfusion or hepatitis B vaccination. This case of HTLV-I positive Sezary syndrome is the first one described outside the known endemic regions for HTLV-I. Moreover, this patient was found to be negative for viral antibodies. This observation should therefore stimulate new and thorough analysis of the association of this human retrovirus with leukemia and lymphoma in the Mediterranean region, both by seroepidemiological and molecular biology techniques.

Aged↗

PubMed1986

[Adult T-cell lymphoma/leukemia associated with HTLV-I virus in Martinique: apropos of 2 cases].

Two HTLV-I associated adult T cell leukemia cases were observed in patient from Martinique (French West Indies). These case are similar to the clinical entity, described by Takatsuki in 1977 in Japan and by Catovsky in Caribbean patients, characterized by a lymphadenopathy, skin lesions and visceral involvement, hypercalcemia, an aggressive course, and poor prognosis. The malignant cells with T4 phenotype and often suppressive function, were pleomorphic, mature, with prominent nuclear irregularities. Systematic research of HTLV-I virus or antibodies in patients with this clinical picture, to measure the influence of this virus in T cell lymphoproliferative diseases in France and in French West Indies is required.

Adult↗

PubMed1985

Type-I and type-III HTLV antibodies in hospitalized and out-patient Zairians.

Sera from 182 Zairians (99 females and 83 males), aged 5 to 71 years, including maternity and child care consultants, out-patients suffering from minor injuries and patients hospitalized for tuberculosis, malaria or trauma, were analyzed for specific antibodies to HTLV-I and HTLV-III. Following pre-screening by the ELISA technique, reactive sera were further analyzed for specificity to HTLV-I or HTLV-III antigens by competition and/or Western blotting experiments. African sera, possibly because they have higher immunoglobulin levels than US and European sera, are highly reactive in ELISA systems and confirmatory assays are essential to rule out false-positive results. Confirmed antibody prevalence for HTLV-I was 13.2% (II females and 13 males) and increased with age, suggesting continuous exposure to the virus throughout life. Confirmed antibody prevalence for HTLV-III was 6.0% (8 females and 3 males) and showed a peak age range between 21 and 40 years, suggesting heterosexual transmission. Individuals positive for HTLV-I antibodies were not the same as individuals positive for HTLV-III antibodies, suggesting that infection with one virus did not increase susceptibility to infection by the other virus. Further investigations of the epidemiology and of the immunovirology of HTLV-III in Zaire, in relation to acquired immuno-deficiency syndrome (AIDS)-associated pathologies, should enlighten the question of the significant percentage of HTLV-III-infected individuals who do not manifest symptoms of AIDS.

Acquired Immunodeficiency Syndrome↗