Paracoccidioidomycosis in a patient with acquired immunodeficiency syndrome

The authors report a case of paracoccidioidomycosis and other opportunistic diseases in a patient with acquired immunodeficiency syndrome.     

Detection of Cryptosporidium--specific coproantigen in human immunodeficiency virus/acquired immunodeficiency syndrome patients by using a commercially available immunoenzymatic assay

The aim of this study was to verify the occurrence of Cryptosporidium infection in 52 human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) patients (group 1) and 38 clinically healthy individuals (group 2) by using enzyme immunoassay (EIA). All fecal samples collected were submitted to the Baermann, Lutz and Ritchie methods, the Safranin/Methylene Blue, and Weber's chromotrope modified Trichrome staining techniques, and EIA. In group 1, parasitological staining techniques and EIA were both positive for Cryptosporidium sp. infection in 3/52 (5.8%) samples and both negative in 45/52 (86.5%) samples, while 4/52 (7.7%) samples were positive in EIA and negative in parasitological staining techniques. Concerning group 2, all samples were negative by EIA and microscopy for Cryptosporidium infection. In conclusion, EIA may be an alternative method for detecting Cryptosporidium-specific coproantigen in HIV/AIDS patients.     

Disseminated dermatophytosis caused by Microsporum gypseum in two patients with the acquired immunodeficiency syndrome

Microsporum gypseum is not a common agent of human dermatophytosis. To the best of our knowledge, this fungus has not been described in human immunodeficiency virus (HIV)-infected patients. We report a tinea corporis infection with atypical presentation caused by M. gypseum in two patients with the acquired immunodeficiency syndrome (AIDS) studied at the São Paulo Hospital (São Paulo, Brazil).This revised version was published online in October 2005 with corrections to the Cover Date.     

Susceptibility to a mouse acquired immunodeficiency syndrome is influenced by theH-2

The development of a mouse acquired immunodeficiency syndrome (MAIDS) induced following LP-BM5 MuLV infection depends on host genetic factors. Susceptible mice, such as C57BL/6J mice, develop a profound impairment of lymphoproliferative response to mitogens and hyperplasia of lymphoid organs and succumb to infection within 6 months. These changes do not occur in resistant mice, such as A/J mice. Resistance to MAIDS is a dominant trait since (C57BL/6JxA/J)F₁ hybrid mice did not develop any immune dysfunctions following infection. Genetic regulation of the trait of resistance/susceptibility to MAIDS was determined in AXB/BXA recombinant inbred (RI) mouse strains (derived from resistant A/J and susceptible C57BL/6J progenitors). Two different criteria were used to determine their resistance or susceptibility to developing MAIDS: the gross pathologic evaluation of lymphoid organs at 13–15 weeks of infection, and survival. RI mouse strains segregated into two non-overlapping groups. The first group did not develop any significant pathology, and these mouse strains were considered as resistant to MAIDS. The second group showed the virus-induced pathological changes as well as an immunological dysfunction as seen in C57BL/6J progenitor mice, and these strains were thus considered as susceptible to MAIDS. This bimodal strain distribution pattern of resistance/susceptibility to MAIDS among the RI strains suggests that this phenotype is controlled by a single gene. Linkage analysis with other allelic markers showed a strong association between resistance/susceptibility to MAIDS and theH-2 complex. Possession of theH-2 ^b haplotype derived from C57BL/6J mice was associated with susceptibility to MAIDS, while theH-2 ^a haplotype conferred resistance to the disease. This finding was confirmed by demonstrating thatH-2 ^a congenics on the susceptible C57BL/10 background were as resistant to MAIDS as A/J mice which donated theH-2 ^a locus. Gene(s) within theH-2 complex thus represent the major regulatory mechanism of resistance/susceptibility to MAIDS.     

艾滋病合并咽喉马尔尼菲青霉菌病的研究

目的研究艾滋病(AIDS)患者合并咽喉马尔尼菲青霉菌病(Penicilliosis marneffei,PSM)的咽喉表现和诊疗方法。方法收集2002年5月~2007年3月,经真菌学、血清学和组织病理学证实的5例AIDS合并咽喉PSM患者。应用抗逆转录病毒药物治疗AIDS,用两性霉素B联合氟康唑静滴治疗PSM。结果咽痛、声嘶及粘膜溃疡是AIDS合并PSM的咽喉部症状体征。5例病变组织病理学检查发现细胞内PM菌体。真菌培养分离出双相性马尔尼菲青霉菌(Penicillium marneffei,PM)。经抗真菌治疗,2例体温下降,咽喉疼痛减轻,声嘶改善,扁桃体炎症消退,溃疡面缩小,全身症状减轻。最终4例机会性感染死亡,1例仍在随访中。结论AIDS合并咽喉PSM是根据病史、临床表现和实验检查三方面作出诊断;HIV/AIDS用抗逆转录酶病毒治疗,PM用两性霉素B联合氟康唑静滴治疗。     

降低我国艾滋病患者病死率的几个关键措施

随着人类免疫缺陷病毒(HIV)感染者逐渐进入获得性免疫缺陷综合征(AIDS)期,我国HIV感染者病死人数逐渐增加,已超过结核病与狂犬病的病死人数,位居第1.如何降低HIV/AIDS患者的病死率是我国目前亟待解决的重要课题.针对我国HIV/AIDS患者的特点,应采用多种措施.其中关键为:落实患者对药物的依从性,优化抗病毒治疗方案;扩大抗病毒治疗覆盖面,以增加接受抗病毒治疗的患者;加大检测力度,早诊断和早治疗以延长患者寿命,改善预后;注意对患者并发症的治疗,并科学分析病死原因.这些措施的实施需要社会各界共同参与和努力.     

Human immunodeficiency virus/acquired immunodeficiency syndrome and tropical diseases: a Brazilian perspective

The paper summarizes recent findings on the epidemiology and pathogenesis of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/Aids), highlighting the role of co-infections with major tropical diseases. Such co-infections have been studied in the Brazilian context since the beginning of the Aids epidemic and are expected to be more frequent and relevant as the Aids epidemic in Brazil proceeds towards smaller municipalities and the countryside, where tropical diseases are endemic. Unlike opportunistic diseases that affect basically the immunocompromised host, most tropical diseases, as well as tuberculosis, are pathogenic on their own, and can affect subjects with mild or no immunosuppression. In the era of highly active anti-retroviral therapies (HAART), opportunistic diseases seem to be on decrease in Brazil, where such medicines are fully available. Benefiting from HAART in terms of restoration of the immune function, putative milder clinical courses are expected in the future for most co-infections, including tropical diseases. On the other hand, from an ecological perspective, the progressive geographic diffusion of Aids makes tropical diseases and tuberculosis a renewed challenge for Brazilian researchers and practitioners dealing with HIV/Aids in the coming years.     

Serological response against Mycobacterium avium complex glycolipid antigens in patients with acquired immunodeficiency syndrome

In 43 MAC infected patients (23 non-HIV and 20 AIDS) the IgG response against 3 BCG and 2 MAC antigens was assessed. The response to four antigens in patients with AIDS was considerably lower than in non-HIV infected patients. Therefore, antibody production against MAC glycolipid antigens was impaired in AIDS patients.     

Activation of the ubiquitin proteolytic system in murine acquired immunodeficiency syndrome affects IkappaBalpha turnover.

Murine acquired immunodeficiency syndrome (MAIDS) is a complex immunopathology caused by a defective murine leukemia virus (LP-BM5) that mainly targets B-lymphocytes. Lymphadenophathy, splenomegaly, hypergammaglobulinemia and progressive immunodeficiency are prominent features of MAIDS. Previously, we showed that the ubiquitin proteolytic system was upregulated in infected lymph nodes [Crinelli, R., Fraternale, A., Casabianca, A. & Magnani, M. (1997) Eur. J. Biochem. 247, 91-97]. In this report, we demonstrate that increased 26S proteasome activity is responsible for accelerated turnover of the IkappaBalpha inhibitor in lymph node extracts derived from animals with MAIDS. The molecular mechanisms mediating IkappaBalpha proteolysis involved constitutive phosphorylation of IkappaBalpha at Ser32 and Ser36 and subsequent ubiquitination, suggesting persistent activation of an NF-kappaB inducing pathway. Interestingly, enhanced IkappaBalpha degradation did not result in enhanced NF-kappaB DNA binding activity, but rather in a different subunit composition. The modulation of NF-kappaB/IkappaB system may affect multiple immunoregulatory pathways and may in part explain the mechanisms leading to the profound immune dysregulation involved in MAIDS pathogenesis.     

Analysis of specificity in the serodiagnosis of acquired immunodeficiency syndrome

Analysis of serum samples for the presence of antibody to AIDS-inducing virus was carried out with the use of the Virognostika diagnosticum manufactured by Organon (the Netherlands). As a result, 6.1% of sera from patients with hematologic diseases, 5.7% of sera from oncologic patients, and 9.2% of sera from hepatitis B patients proved to be "positive" according to the criteria of the manufacturer. However the positively reacting sera could be neutralized by sorption on human red cells, groups AB and 0 and by treatment with the lysate of human lymphocyte culture, which was indicative of the fact that false positive reactions were probably due to the contamination of the antigenic preparation by components of the producer-cell membrane.     

Interleukin 2 enhances the natural killer cell activity of acquired immunodeficiency syndrome patients through a gamma-interferon-independent mechanism

Patients with the acquired immunodeficiency syndrome (AIDS) exhibit a variety of disorders of cellular immunity, including a deficient ability to generate cytotoxic T cells and depressed levels of natural killer (NK) cell activity. Interleukin 2 (IL 2) in vitro can markedly augment these depressed immune functions. Because IL 2 can induce the release of interferon-gamma (IFN-gamma) from normal peripheral blood lymphocytes (PBL), and because IFN-gamma may play a role in the regulation of NK cell activity, this study was performed to determine if the IL 2 enhancement of the NK cell activity of patients with AIDS was an IFN-gamma-dependent effect. PBL from eight healthy heterosexual donors and from nine patients with AIDS were studied for their ability to release IFN-gamma in response to IL 2 at a concentration of 100 U/ml. After 60 hr of culture, the PBL of all eight healthy donors produced IFN-gamma with a mean titer of 113 U/ml (range 40 to 320 U/ml). In contrast, the PBL from only two of nine patients with AIDS released measurable amounts of IFN-gamma (40 U/ml each) in response to IL 2 with a mean titer of 13.5 U/ml for all nine. Although the PBL from patients with AIDS were deficient in their capacity to produce IFN-gamma in response to 100 U/ml of IL 2, significant enhancement of NK cell activity could be obtained after only 1 hr of PBL treatment with 10 U/ml of IL 2, with an optimal NK enhancing effect occurring at doses of 50 to 100 U/ml of IL 2. The use of an anti-IFN-gamma monoclonal antibody resulted in complete neutralization of the IFN released from the normal PBL cultured with IL 2, but failed to inhibit the IL 2 enhancement of NK cell activity. Exogenous IFN-gamma exhibited different kinetics of enhancement of NK cell activity when compared to IL 2, requiring substantially more than 1 hr of pretreatment of PBL. These results indicate that the PBL from patients with AIDS usually do not release IFN-gamma when cultured with IL 2, and that IL 2 enhancement of the depressed NK cell activity of these patients may be an IFN-gamma-independent event. These results may have important implications for the therapy of AIDS.