Factors associated with viral load suppression in HIV-infected pregnant women in Rio de Janeiro, Brazil.

Viral load (VL) near delivery is a determinant of mother-to-child transmission (MTCT) of HIV. To evaluate factors associated with an undetectable VL near delivery in HIV-infected pregnant women receiving highly active antiretroviral therapy (HAART) and non-HAART regimens, HIV-infected pregnant women with a detectable VL at entry and having used antiretrovirals for ≥4 weeks before delivery were selected. Multivariate analysis was employed using binary logistic unconditional models; the dependent variable was having a VL <400 copies/mL near delivery. VL suppression was achieved in 403/707 women (57%): 65.4% in the HAART group, but only 26% in the non-HAART group P = 0.001. Duration of HAART was correlated with VL suppression, with maximum benefit seen after ≥12 weeks of therapy (odds ratio [OR]: 2.51; 95% confidence interval [CI]: 1.72-3.65). CD4+ cell count near delivery (OR: 1.53; 95% CI: 1.06-2.20) and baseline VL (OR: 0.74; 95% CI: 0.58-0.94) were also independently associated with VL suppression. Overall MTCT rate was 1.6%. HAART for ≥12 weeks, baseline VL and CD4 cell count near delivery were independently associated with viral suppression near delivery.

Genotypic and phenotypic evidence of different drug-resistance mutation patterns between B and non-B subtype isolates of human immunodeficiency virus type 1 found in Brazilian patients failing HAART.

We have investigated the phenotypic and genotypic susceptibility of 14 HIV-1 strains isolated from individuals failing HAART therapy to protease inhibitors (PI). Proviral and plasma viral pol gene fragment were amplified, sequenced and subtyped. Nine samples clustered with protease subtype B reference strains and the remaining samples were classified as non-B subtype corresponding to subtype F (n = 4) and subtype A (n = 1). Although all patients were treated with similar P1 drug regimen, the non-B subtype isolates did not present the L90M and 184V mutations and used mainly G48V and V82A/F to achieve drug resistance. A strong cross-resistance phenotype among all four PI was associated with the mutation L90M in the subtype-B isolates, and with G48V and V82A/F in the non-B counterparts. This observation revealed that the non-B viruses tested had specific genotypic characteristics contrasting with the subtype-B isolates.

Papular-purpuric "gloves and socks" syndrome due to parvovirus B19: report of a case with unusual features.

We present a case of papular-purpuric "gloves and socks" syndrome (PPGSS) in an adult male with acute parvovirus B19 infection. The patient displayed the classical features of fever, oral lesions, and purpura on hands and feet, but the purpuric lesions on the feet evolved to superficial skin necrosis, a feature not previously described in this syndrome. We believe this is the first reported case of PPGSS occurring in Brazil.

Drug-resistant reverse transcriptase genotyping and phenotyping of B and non-B subtypes (F and A) of human immunodeficiency virus type I found in Brazilian patients failing HAART.

Development of drug resistance is the inevitable consequence of incomplete suppression of virus plasma levels in HIV-1-infected patients treated with highly active antiretroviral therapy. Resistance mutations previously characterized have been found in B subtype viruses of developed countries. Moreover, mutation profiles for non-B and more divergent B subtype viruses found in developing countries shall be analyzed together with their ex vivo phenotyping in order to establish an exact correlation between the genotyping data and the clinical management counseling for those uncommon virus subtypes. In the present study, we evaluated the mutation profile for individuals infected with B subtype and non-B subtype viruses. Viral DNA fragments corresponding to the RT gene were amplified, sequenced, and subtyped. Phenotyping analysis for reverse transcriptase nucleoside (NRTI) and nonnucleoside inhibitor susceptibility was performed using the recombinant virus assay technology. Brazilian non-B subtypes (subtype F, n = 4, and subtype A, n = 1) isolates showed essentially the same B subtype mutation profile, presenting an NRTI drug resistance with similar MIC50% and MIC90% values for all drugs analyzed regardless of their subtypes. A strong cross-resistance phenotype among AZT, 3TC, and abacavir could be seen in all isolates analyzed. A novel result was that some RT sequences not only revealed the presence of G333D/E mutations but also correlated to the presence of mutation T386I that could abrogate the M184V-surpassing effect of L210W or L210W plus G333D/E. These findings suggest that Brazilian non-B subtype HIV-1 strains use an identical RT drug resistance mutation pattern when compared to B isolates and will contribute to the validation of the genotypic and phenotypic tests in these predominant worldwide-spread viral variants.

Disseminated American muco-cutaneous leishmaniasis caused by Leishmania braziliensis braziliensis in a patient with AIDS: a case report.

The authors report a case of culture-proven disseminated American muco-cutaneous leishmaniasis caused by Leishmania braziliensis braziliensis in an HIV positive patient. Lesions began in the oropharynx and nasal mucosa eventually spreading to much of the skin surface. The response to a short course of glucantime therapy was good.

Cellular and humoral immune responses of a patient with American cutaneous leishmaniasis and AIDS.

The lymphocyte responsiveness to leishmanial antigens and its influence on the course of cutaneous leishmaniasis was studied in a patient with AIDS-associated American cutaneous leishmaniasis caused by Leishmania braziliensis. The patient had cutaneous disseminated erythematous papules or nodules and mucosal lesions as well as moniliasis and weight loss. The patient had a poor delayed-type hypersensitivity to leishmanial antigens, showing 3 mm of induration. The cellular immune responses were studied in vitro by lymphocyte proliferative assays induced by leishmanial antigens and concanavalin A. The T cell phenotypes were analysed by flow cytometry. The peripheral blood mononuclear cells before proliferation showed an inversion of the CD4/CD8 ratio (0.28:1). The lymphoproliferative responses to antigen and mitogen were very low (indices < 2.5). The blast-like cell phenotypes after antigen stimulation in culture were: CD3+ 44.8%, CD4+ 7.53% and CD8+ 17.45%. In AIDS patients the decrease in the pool of CD4+ cells, and consequent diminution of the CD4/CD8 ratio, produced by HIV infection provokes a generalized immune depression. The patient's disseminated clinical picture was probably related to the inability of his T cell-mediated immune responses to control the spread of Leishmania infection.

Hypergammaglobulinaemia in Leishmania donovani infected hamsters: possible association with a polyclonal activator of B cells and with suppression of T cell function.

Studies were carried out on the mechanisms by which B lymphocytes are polyclonally activated to secrete antibodies during visceral leishmaniasis. Crude extracts of Leishmania donovani, the aetiological agent of this disease, of Leishmania mexicana amazonensis, the etiological agent of cutaneous leishmaniasis, and of Herpetomonas muscarum, a related non-pathogenic organism, all contain components which cause strong in vitro polyclonal activation of hamster spleen cells leading to the production of antibodies. However, in vivo, only hamsters infected with L. donovani develop hypergammaglobulinaemia due to B cell polyclonal activation. Hamsters injected with the crude extracts of leishmania or infected with L. mexicana amazonensis do not manifest these alterations in their B cell response. Furthermore spleen cells of hamsters infected with L. donovani became unresponsive to stimulation with the T cell mitogen phytohaemagglutinin (PHA) by day 10 of infection, whereas their response to concanavalin A (Con A) was preserved. The decreased lymphocyte response to PHA coincided with the augmentation of the PFC/spleen ratio. In contrast, spleen cells from hamsters infected with L. mexicana amazonensis, responded normally to both mitogens throughout the course of infection. These results suggest that the hypergammaglobulinaemia present in visceral leishmaniasis may be the consequence of an inbalance of regulatory T cells, possibly associated with a direct stimulation of hamster B cells by L. donovani components.

[Transfer factor in diffuse cutaneous leishmaniasis. Experience with one case]. / Fato r de transferència na leishmaniose cutis difusa. Experiència de um caso.

Transfer factor was administered in one case of Diffuse Cutaneous Leishmaniasis ("DCL") with minimal therapeutical results after two courses of ten doses each. The patient was 34-year-old white man, born in the State of Pará --Amazon-- region, goldwasher, his disease started 9 years ago and consisted of disseminated papular and nodular lesions, some of them secondarily ulcerated and more closely clustered over the knees elbows and dorsa of the hands. Physical examination was normal except for the skin lesions and a perforation of the nasal septum. Some intradermal tests (Paracoccidiodin, Lepromin and PPD) were positive while the Montenegro (leishmanin) reaction was negative. Increased levels of IgG and IgM were found; IgA was normal even after the treatment. Transfer Factor was obtained from leishmanin positive and PPD strong reactors and the method of preparation is described. By the end of the first ten-doses course, lesions were reduced to dark atrophic residual macules but the histological sections displayed a surprising amount of parasites, predicting unavoidable relapse. For the second series, as the patient refused to be given Amphotericin B he was treated with hot baths and levamisole was administered in a 150 mg daily dosage and 45 days cycles. The leishmanin intradermal test did not became positive after the treatment and this fact is discussed.