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Biomedical subjects

M Barral-Netto

Publications and source records attributed to M Barral-Netto.

At least 37 records · Page 2Linked to original sources
PubMed1997

Parasite-driven in vitro human lymphocyte cytotoxicity against autologous infected macrophages from mucosal leishmaniasis.

Parasite-specific cytotoxicity in human leishmaniasis was evaluated in an autologous system. PBL from cutaneous leishmaniasis (CL) or mucosal leishmaniasis (ML) patients were exposed to Leishmania amazonensis-infected autologous macrophages for 7 days and then used as effector cells in a cytotoxic assay using 51Cr-labeled autologous infected macrophages as targets. Results are reported as LU per 10(7) PBMC. Cytotoxic activity is present in ML (9.7 +/- 2.1 LU/10(7) PBMC) but not in CL (1.5 +/- 2.4 LU/10(7) PBMC) patients' lymphocytes, and the differences were highly significant (p < 0.0001). Both CD8+ T cells and NK cells exhibited cytotoxic activity. Addition of rIL-12, but not of IFN-gamma, during the generation of effector cells increased cytotoxic responses against infected macrophages. On the other hand, addition of mAb against human IL-12 or IFN-gamma during the stimulation of PBL significantly decreased the cytotoxic responses. Addition of IL-10 led to diminished cytotoxic responses, whereas the addition of anti-IL-10 did not significantly increase the cytotoxic responses. The observation of parasite-driven autologous cytotoxic responses in patients with ML, the destructive form of leishmaniasis, but not in CL, suggests that this phenomenon is involved in tissue pathology rather than in protection. Understanding the regulation of cytotoxic responses in leishmaniasis may be relevant to strategies aimed at limiting pathologic tissue destruction.

Animals↗
PubMed1997

Molecular cloning and characterization of ConBr, the lectin of Canavalia brasiliensis seeds.

ConBr, a lectin isolated from Canavalia brasiliensis seeds, shares with other legume plant lectins from the genus Canavalia (Diocleinae subtribe) primary carbohydrate recognition specificity for D-mannose and D-glucose. However, ConBr exerts different biological effects than concanavalin A, the lectin of Canavalia ensiformis seeds, regarding induction of rat paw edema, peritoneal macrophage spreading in mouse, and in vitro human lymphocyte stimulation. The primary structure of ConBr was established by cDNA cloning, amino acid sequencing, and mass spectrometry. The 237-amino-acid sequence of ConBr displays Ser/Thr heterogeneity at position 96, indicating the existence of two isoforms. The mature Canavalia brasiliensis lectin monomer consists of a mixture of predominantly full-length polypeptide (alpha-chain) and a small proportion of fragments 1-118 (beta-chain) and 119-237 (gamma-chain). Although ConBr isolectins and concanavalin A differ only in residues at positions 58, 70, and 96, ConBr monomers associate into dimers and tetramers in a different pH-dependent manner than those of concanavalin A. The occurrence of glycine at position 58 does not allow formation of the hydrogen bond that in the concanavalin A tetramer exists between Asp58 of subunit A and Ser62 of subunit C. The consequence is that the alpha carbons of the corresponding residues in ConBr are 1.5 A closer that in concanavalin A, and ConBr adopts a more open quaternary structure than concanavalin A. Our data support the hypothesis that substitution of amino acids located at the subunit interface of structurally related lectins of the same protein family can lead to different quaternary conformations that may account for their different biological activities.

Amino Acid Sequence↗
PubMed1996

Variation of cytokine patterns related to therapeutic response in diffuse cutaneous leishmaniasis.

Diffuse cutaneous leishmaniasis is a rare entity characterized by disseminated cutaneous nodules associated with specific anergy to leishmanial antigens. A low but not absent IFN-gamma expression by cells present in cutaneous lesions has been documented during the active phase of diffuse cutaneous leishmaniasis. In this study we confirm this observation, and extend it by showing a similar pattern in peripheral blood mononuclear cells and the variation of mRNA cytokine expression pattern during different stages of the disease. During active disease, patients did not express mRNA for IFN-gamma, while expressing mRNA for IL-2, IL-4, and IL-10. In contrast, an expression of IFN-gamma and low IL-10 was observed after treatment-induced transient healing of cutaneous lesions. In three patients we have been able to analyze a third PBMC sample obtained after clinical relapse, documenting in all of them decreased IFN-gamma expression with no expression of IL-10. Although there was an association between the appearance of IFN-gamma expression and clinical improvement, with marked expression of IFN-gamma mRNA and decreased expression of mRNA for IL-10 after treatment, this was not sufficient to prevent relapse in these patients. Therefore, it is possible that factors other than the cytokines characteristic of the Th1 and Th2 balance are implicated in the inability of diffuse cutaneous leishmaniasis patients to mount an anti-Leishmania immune response causing clinical improvement.

Adolescent↗
PubMed1996

In vivo protective effect of the lectin from Canavalia brasiliensis on BALB/c mice infected by Leishmania amazonensis.

In vivo administration of Canavalia brasiliensis lectin (at the time of infection, or maintained throughout the infection) reduced the lesions of highly susceptible BALB/c mice infected by Leishmania amazonensis. At the doses used C. brasiliensis lectin (ConBr) does not interfere with penetration or fate of Leishmania in the macrophages in vitro. Since Interferon-gamma (IFN-gamma) is the major macrophage activating factor, and considered a critical element in the successful immune response against leishmaniasis, we explored its participation in this phenomenon. ConBr either in vivo or in vitro induced IFN-gamma production in normal or in leishmania-infected BALB/c mice. However we were unable to change the course of disease by in vivo IFN-gamma administration (although IFN-gamma preparations were effective in inducing a leishmanicidal effect in vitro on L. amazonensis-infected peritoneal macrophages). Additionally, IFN-gamma neutralization with anti-IFN-gamma monoclonal antibody did not alter the protection conferred by ConBr administration. These data show that lectin administration in vivo is protective in the otherwise unchecked L. amazonensis infection of BALB/c mice, and suggest that such effect is not mediated by IFN-gamma.

Animals↗
PubMed1996

Cytotoxicity in patients with different clinical forms of Chagas' disease.

There are few studies on cell-mediated cytotoxicity in human Chagas' disease. In the present study, we evaluated peripheral blood mononuclear cell (PBMC) cytotoxicity activity from chagasic patients with different clinical forms of disease. To verify the cytotoxic response, we performed cell lysis assays using 51Cr-labelled K562 cells as targets. Results are reported as lytic units (LU = number of cells required for 30% lysis) per million PBMC. Exposure of patients' PBMC to Trypanosoma cruzi antigen led to an increase in cytotoxic activity compared with unstimulated patient cells against K562. Asymptomatic cardiomyopathy patients had higher responses (37.8 +/- 5.0 LU/10(6) PBMC; mean +/- s.d.) than indeterminate (11.5 +/- 3.6 LU/10(6) and symptomatic cardiomyopathy (7.8 +/- 2.5 LU/10(6)). Normal control PBMC stimulated with T. cruzi antigen had 4.36 +/- 1.31 LU/10(6)) PBMC against K562. Addition of recombinant interferon-gamma (IFN-gamma) did not lead to significant increase in cytotoxicity in any group of patients. On the other hand, recombinant human IL-12 significantly increased cytotoxic responses from symptomatic cardiomyopathy patients and normal controls who presented low levels of cytotoxicity induced by T. cruzi antigen. The combined use of IL-12 and a neutralizing anti-IFN-gamma antibody did not change IL-12-induced cytotoxic responses, showing the direct role of this cytokine on natural killer (NK) cells. NK cells were the main cells responsible for the lysis of K562 target cells as evidenced by testing cell subsets following magnetic cell sorting. These data demonstrate that chagasic patients with different clinical forms of disease have PBMC which respond to T. cruzi antigen with a cytotoxic response, and this response is up-regulated by IL-12.

Adult↗
PubMed1996

Interleukin-12 restores interferon-gamma production and cytotoxic responses in visceral leishmaniasis.

American visceral leishmaniasis (AVL) is associated with the absence of lymphocyte proliferative responses and interleukin (IL)-2 and interferon-gamma (IFN-gamma) production upon stimulation with Leishmania antigen. In contrast, cure of AVL is associated with restoration of these T cell functions. In the present study, the ability of IL-12, a cytokine that acts on NK and T cells to restore cellular immune responses in AVL, was evaluated. Participants of the study included 12 patients with AVL and 7 subjects cured of AVL. The [3H]thymidine uptake and IFN-gamma production in cultures of peripheral blood mononuclear cells (from AVL patients) stimulated with Leishmania chagasi antigen were 882 +/- 1393 cpm and zero, respectively. Addition of IL-12 enhanced the proliferative response to 5097 +/- 6429 cpm (P < .001) and IFN-gamma production to 305 +/- 325 pg/mL (P < .01). IL-12 also restored cytotoxic activity against the K562 cell line. These results indicate that IL-12 has an important role in the regulation of the cellular immune response in human leishmaniasis.

Animals↗
PubMed1996

Biological behavior of Leishmania amazonensis isolated from humans with cutaneous, mucosal, or visceral leishmaniasis in BALB/C mice.

Leishmania amazonensis causes a wide spectrum of disease in humans. In this study, we evaluated BALB/c mice infected with five strains of L. amazonensis isolated from patients with either cutaneous, mucosal, or visceral leishmaniasis. Mice infected with cutaneous and mucosal isolates developed ulcerating footpad lesions with parasite-loaded macrophages and extensive tissue destruction. Skin metastases, early dissemination of parasites to the spleen, and high anti-Leishmania antibody levels were also noted. Mice infected with L. amazonensis strains isolated from patients with visceral disease had a controlled infection, with small footpad lesions with mononuclear cell infiltration, few infected macrophages, and granuloma formation. They had no skin metastases, delayed dissemination of the parasite to the spleen, lower levels of IgG and higher levels of IgG2a against L. amazonensis. These findings demonstrate an unexpected resistance of BALB/c mice to the infection with L. amazonensis isolated from patients with visceral leishmaniasis. This resistance seems to be due to differences in these parasites that may be related to the altered course of the disease in humans and in isogenic BALB/c mice.

Animals↗
PubMed1995

Serum soluble markers in the evaluation of treatment in human visceral leishmaniasis.

Visceral leishmaniasis (VL) has a fatal course if not properly treated. Recovery from VL is linked to cellular immune response. Unresponsiveness to antimonial therapy reinforces the importance of determining parameters for treatment assessment. We analysed the pre- and post-treatment serum levels of soluble CD4 (sCD4), sCD8, sIL-2R, soluble intercellular adhesion molecule-1 (sICAM-1) and neopterin in groups of VL patients either responsive or not to standard antimonial therapy. Pretreatment serum levels of all markers except for sICAM-1 were significantly higher in VL patients than in healthy subjects from the same area (P < 0.05). sICAM-1 levels were similar in healthy controls and in VL patients refractory to antimonial therapy (P = 0.25), but significantly higher in patients responsive to treatment (P = 0.02). The comparison of pre- and post-treatment concentrations showed that all markers, except sCD4 and sICAM-1, presented a significant fall (P < 0.05) in patients responsive to antimonial therapy. However, only neopterin presented with levels compatible with those of healthy subjects at the end of treatment (P = 0.30). In refractory patients sICAM-1 presented with post-treatment levels significantly higher than the pretreatment determinations (P = 0.03), while sCD4 experienced a significant drop (P = 0.01). All markers displayed clearly distinct behaviour according to the patient's response to therapy. This makes all soluble molecules studied suitable for use as indicators of antimonial therapy response. Additionally the comparison of pretreatment levels of the markers between responders and refractory patients to antimonial therapy showed that serum concentrations of sIL-2R and sICAM-1 significantly differed among these two groups (P = 0.02 in each case), suggesting that they may be used in future as predictors of antimonial therapy response.

Antimony↗
PubMed1995

Cytotoxicity in human mucosal and cutaneous leishmaniasis.

CD8+ T cells and lysis of parasitized macrophages seem to be important in the resistance to murine leishmaniasis. In the present study, we evaluated peripheral blood mononuclear cell (PBMC) from patients with either cutaneous (CL) or mucosal (ML) leishmaniasis in cell lysis assays using 51-Cr-labeled Daudi or K562 cells, or autologous antigen-pulsed macrophages as targets. Results are reported as lytic units (number of cells required for 30% lysis) per million PBMC. Exposure of patient PBMC (n = 12) to lysate from Leishmania amazonensis promastigotes led to an increase in cytotoxic activity compared to unstimulated patient cells against Daudi (81.8 +/- 14.9 vs 13.6 +/- 5 lytic units (LU) per million PBMC; mean +/- SEM) and K562 (65.7 +/- 8.4 vs 13.1 +/- 5 LU/10(6) PBMC). ML had higher responses than CL in both targets (80.4 +/- 11.0 vs 46.4 +/- 11.6 LU/10(6) PBMC for K562, and 104.3 +/- 23.8 vs 59.3 +/- 14.3 LU/10(6) PBMC for Daudi). Normal control PBMC, stimulated with L. amazonensis antigen had 6.32 +/- 3.72 LU/10(6) PBMC against Daudi cells and 9.06 +/- 2.78 LU/10(6) PBMC against K562. The cell responsible for lysis of the K562 cells was characterized as NK, by means of cell separation employing magnetic beads coupled to antibodies. Addition of recombinant TGF-beta or recombinant human IL-10 reduced L. amazonensis-induced cytotoxicity by 90% and 70%, respectively. Cytotoxicity of antigen-stimulated PBMC was also demonstrated against autologous L. amazonensis antigen-pulsed macrophages in the range of 6.7 to 41.7 LU/10(6) PBMC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Polar and subpolar diffuse cutaneous leishmaniasis in Brazil: clinical and immunopathologic aspects.

BACKGROUND: Diffuse cutaneous leishmaniasis (DCL) is a rare manifestation of human leishmaniasis, characterized by multiple, slowly progressive nodules or plaques without ulceration, involving almost the entire body. It has been suggested, that DCL results from a lack of cell-mediated immunity to leishmanial antigen, leading to uncontrolled parasite growth. METHODS: We have performed detailed clinical, histopathologic, and immunologic investigations in six patients with DCL. Biopsies were taken from the nodules, processed, and examined for determination of the macrophagic pattern present, based on the intensity of vacuolation and the frequency of vacuolated cells, the parasite index, and the presence of eosinophils. Immunologically, patients were evaluated by their response to intradermal skin test to PPD or leishmania antigen, determination of antileishmania antibodies by immunofluorescent assay, and lymphocyte proliferation assay. RESULTS: There seemed to be a negative relation between nodules and skin ulcerations, whereas the highest number of parasites were observed in patients with the greatest number of vacuolated macrophages. The delayed hypersensitivity skin test to leishmanial antigen was negative, and antileishmania IgG antibodies were positive in all patients. CONCLUSIONS: Although all cases fulfill the criteria for being classified as DCL, they present a wide spectrum. Three cases were clearly at the unresponsive pole, and three other cases belonged to the subpolar form of DCL, exhibiting varying weak signs of antiparasite responsiveness.

Adolescent↗
PubMed1995

Lymphadenopathy as the first sign of human cutaneous infection by Leishmania braziliensis.

This paper describes the presence of transitory lymphadenopathy as an initial sign of cutaneous leishmaniasis, and sometimes the only manifestation of Leishmania braziliensis infection. Ten patients with lymphadenopathy living in an area of L. braziliensis transmission had Leishmania cultivated from their lymph nodes previous to any other manifestation of cutaneous leishmaniasis. Seven of the 10 developed leishmanial ulcers later in the course of infection, whereas lymphadenopathy regressed in three cases and no other sign of infection developed. Results of tests for anti-Leishmania antibodies and an intradermal skin test were positive in four and five patients, respectively, at the time of the diagnosis. The documentation of Leishmania amastigotes in the lymph nodes before any clinical evidence of cutaneous disease indicates that early spread of L. braziliensis from the skin to lymph nodes occurs before a local lesion develops. All medical doctors examining patients coming from endemic areas of leishmaniasis should be aware that lymph node enlargement, even in the absence of a typical ulceration, may be indicative of leishmanial infection and warrants further investigation.

Adult↗
PubMed1995

Transforming growth factor-beta in human cutaneous leishmaniasis.

Transforming growth factor (TGF)-beta has several downregulatory functions on the immune system: inhibition of interleukin-2 receptor induction, decrease of interferon-gamma-induced class II antigen expression, inhibition of macrophage activation, as well as cytotoxic and lymphokine-activated killer cell generation. TGF-beta has also been recognized as an important immunoregulator in murine leishmaniasis, for which it increases susceptibility to disease. In the present study we evaluate the involvement of TGF-beta in human leishmaniasis in vitro and in patients with cutaneous leishmaniasis. Human macrophages produce active TGF-beta after infection by Leishmania amazonensis (480 +/- 44.7 pg/ml; mean +/- SEM), L. donovani chagasi (295 +/- 7.6 pg/ml), or L. braziliensis (196 +/- 15.7 pg/ml). When TGF-beta was added to cultures of human macrophages infected with L. braziliensis it led to an increase of approximately 50% in parasite numbers as compared with untreated cultures. Exogenous TGF-beta added to macrophage cultures was able to reverse the effect of interferon-gamma in controlling Leishmania growth. Even at 100 IU/ml interferon-gamma the presence of TGF-beta increases the number of intracellular parasites. On the other hand, TNF-alpha at high concentration (100 IU/ml) totally blunts the suppressive effect of TGF-beta. Immunostaining for TGF-beta was observed in the dermis, produced by fibroblasts and occasionally by inflammatory cells in the biopsies from human leishmaniasis lesions, being present in most of the biopsies taken from patients with early cutaneous leishmaniasis (less than 2 months of ulcer development) and in cases of active mucosal leishmaniasis. Taken together these observations suggest an important role for TGF-beta in human leishmaniasis, with its production by infected macrophages being probably related to parasite establishment in the early stages of the disease.

Animals↗
PubMed1995

Up-regulation of T helper 2 and down-regulation of T helper 1 cytokines during murine retrovirus-induced immunodeficiency syndrome enhances susceptibility of a resistant mouse strain to Leishmania amazonensis.

Resistance to and recovery from leishmania infection is dependent on cell-mediated immunity. C57BL/6 mice are resistant to Leishmania amazonensis (La) infection but susceptible to LP-BM5 murine leukemia virus (MuLV) infection. MuLV infection leads to a state of immunodeficiency characterized by severe compromise of cell-mediated immunity. When infected with La alone, C57BL/6 mice developed a small transient lesion that evolved to spontaneous healing or a lesion with extremely slow growth. Lesions were predominantly comprised of a lympho-macrophagic infiltrate with few parasitized macrophages. When infected with La and, 4 weeks later, with MuLV (La-MuLV), the mice developed a large uncontrolled nonhealing lesion containing vacuolated and heavily parasitized macrophages. In contrast, mice infected with MuLV first and La 4 weeks later (MuLV-La) developed a small but persistent lesion, characterized histologically by a small number of heavily parasitized macrophages and few lymphocytes. Eight weeks after MuLV infection, both had similar immunological profiles with decreased lymphocyte proliferation, diminished production of interferon-gamma, and high production of interleukins 4 and 10. At the time of L. amazonensis infection, La-MuLV animals have a normal T cell function whereas in MuLV-La mice this function is already impaired; this may influence the recruitment of macrophages to the site of leishmania injection.

Animals↗
PubMed1994

Transforming growth factor-beta in tegumentary leishmaniasis.

1. The course of infection with the protozoan parasite Leishmania is determined in part by its early replication in macrophages, the exclusive host cells for these organisms. Resistance to and recovery from leishmanial infection is related to cell-mediated immune responses in all forms of human and murine leishmaniasis. 2. Factors contributing to the early inhibition or proliferation of Leishmania are poorly understood, but cytokines such as IFN gamma, IL-10 or transforming growth factor beta (TGF-beta) are known to influence the replication of Leishmania in macrophages. 3. TGF-beta is a multipotential cytokine with diverse effects on cells of the immune system, including down-regulation of certain macrophage functions. Infection of murine or human macrophages by Leishmania induces the production of active TGF-beta. Recombinant TGF-beta added to murine or human macrophage cultures leads to increased intracellular replication of Leishmania. Exogenous TGF-beta administered in vivo promotes enhancement of infection, whereas its neutralization by monoclonal antibodies decreases the level of in vitro infection, and protects susceptible mice. 4. Susceptible animals treated with anti-TGF-beta monoclonal antibodies change their immune response, not increasing the expression of IL-4 while increasing the expression of IFN gamma mRNA in their draining lymph nodes. Resistant animals treated with TGF-beta also change their pattern of immune response as indicated by an increase of the important Th2 cytokine IL-10 mRNA in the draining lymph node. 5. TGF-beta has profound effects on the host response to Leishmania in both mouse and man, and probably is an important parasite escape mechanism.

Animals↗
PubMed1993

Antigen-reactive gamma delta T cells in human leishmaniasis.

The importance of Ag-specific gamma delta T lymphocytes in human immune responses to pathogenic organisms is unknown. In the present study the expression of gamma delta TCR on T lymphocytes from patients with cutaneous, mucosal, or visceral leishmaniasis was examined. All of these patient groups had elevated levels of gamma delta T cells in peripheral blood. Patients' gamma delta T cells included CD8+ as well as null cells. The percentage of T cells expressing gamma delta TCR was increased significantly by stimulation in vitro with certain parasite Ag. T-cell lines generated by stimulation with promastigote lysates of Leishmania amazonensis or L. braziliensis typically contained 25 to 60% gamma delta T cells. In contrast, two immunodominant surface Ag of L. amazonensis, gp63 and gp42, did not expand gamma delta T cells from infected patients, although both Ag elicited strong alpha beta T-cell responses. gamma delta T cells isolated from a Leishmania-specific T-cell line responded to stimulation with promastigote lysate. Of particular interest, gamma delta T cells from PBMC of a patient with mucosal leishmaniasis responded to stimulation with a recombinant 70 kDa heat shock protein of L. chagasi. This study demonstrated that several clinical forms of leishmaniasis induced elevated numbers of gamma delta T cells that responded specifically to Leishmania Ag in vitro. Therefore, this component of the T-cell response to Leishmania may impact the outcome of clinical disease.

Animals↗
PubMed1993

Transforming growth factor beta as a virulence mechanism for Leishmania braziliensis.

Transforming growth factor beta (TGF-beta) has potent down-regulating effects on macrophages and is thus capable of influencing the fate of intramacrophage parasites, including leishmanias. We report the development of a mouse model for the study of the human pathogen Leishmania braziliensis and demonstrate, both in vitro and in vivo, a key regulatory role for TGF-beta in the pathogenesis of infection with this parasite. Recombinant TGF-beta added to cultures of murine peritoneal macrophages led to increased intracellular L. braziliensis replication, whereas addition of neutralizing anti-TGF-beta monoclonal antibody decreased levels of infection. Macrophages infected with L. braziliensis produced biologically active TGF-beta, with a direct correlation between amounts of TGF-beta induced by two parasite isolates and their relative virulence. In vivo, treatment with recombinant TGF-beta rendered avirulent parasites virulent and activated latent L. braziliensis infection. Activation of parasite replication was observed in mice which had been infected with L. braziliensis 15 weeks previously but had not developed lesions or had healed lesions, depending on the parasite isolate used to infect the mice. The exacerbation of L. braziliensis infection in vivo was associated with an increase of interleukin 10 mRNA in the draining lymph node. These results demonstrate that TGF-beta is able to alter the course of in vitro and in vivo infections with L. braziliensis, the latter being characterized by an increase in interleukin 10, an important Th2 helper-T-cell cytokine.

Actins↗
PubMed1993

Aggravation of both Trypanosoma cruzi and murine leukemia virus by concomitant infections.

Given the dissemination of acquired immunodeficiency syndrome (AIDS) in Latin America, where Chagas' disease is endemic, there is a present and increasing risk of concurrent infections with human immunodeficiency virus (HIV) and Trypanosoma cruzi. We used the model of murine acquired immunodeficiency syndrome (MAIDS) caused by a murine leukemia virus (MuLV) that induces immunologic alterations with similarities to those accompanying human HIV infection to study aspects of concomitant infections. The MuLV infection was found to reactivate T. cruzi infection in C57Bl/10 mice, as indicated by elevated parasitemia and lymphocytic infiltration in the myocardium. The T cells from these animals did not respond to T. cruzi antigens (lymphocyte proliferation, interferon-gamma, or interleukin-2 [IL-2] production) but had increased levels of IL-10. Trypanosoma cruzi-specific antibody was decreased but not absent in dually infected animals. In a second set of experiments, we infected MAIDS-resistant B6D2 mice with MuLV, followed by infection with T. cruzi. These animals had higher parasitemia than those infected with T. cruzi alone. More interestingly, only dually infected animals developed MAIDS. The present report describes the activation of T. cruzi infection by MuLV as well as the aggravation of MuLV infection by T. cruzi. These results may be relevant to coinfections with retrovirus and protozoan parasites in humans.

Acute Disease↗